The intelligence of heritability.

Abstract: The influences of heredity and environment on behaviour are sometimes quantified as a heritability ratio, which assigns a percentage of variation in test scores to variation in the genotypes of individuals. There are compelling reasons, both biological and statistical, to doubt the validity of the common practice of partitioning variance in this manner. This paper outlines the conceptual foundations and explains the weaknesses of heritability analysis, reviews evidence of heredity-environment interaction during development, and argues for an alternative research strategy to detect and understand the functions of specific genes relevant for individual differences in behaviour. Article: The importance of heredity for human intelligence and other mental attributes is a perennial topic of debate in psychology with a history extending to Rousseau and earlier. Since 1970 these questions have been addressed by a specialization in psychology calling itself behaviour genetics and having its own professional society and journal. The dominant school of thought in this subdiscipline asserts that almost every human characteristic is determined by both the genetic inheritance and the life experience of the individual, and it seeks to estimate the relative strengths of these two factors. The index commonly used to summarize the results for a specific behaviour is the heritability coefficient, which is the most salient feature of the academic discipline of behaviour genetics. Studies of twins and adopted children have claimed substantial heritability of everything from time spent watching television to religious conservatism and what brand of beer you prefer (Plomin ct al., 1990; Heritability in the broad sense (h B 2 ) is said to estimate the proportion of variance in a measure of behaviour or other phenotype (V Y ) in a breeding population that is attributable to genetic variation (h B 2 = V G / V Y ). The estimation of this parameter involves a model based on the inheritance of genes via the principles of Mendel, which are well established, plus assumptions about how genetic effects are related to environment and behaviour, which are still contentious. Genetic Facts Before presenting the main argument, a few genetic facts should be considered. A gene is a segment of a DNA molecule occurring at a specific locus or place along the DNA, and it codes for the structure of a polypeptide molecule that may function as a protein, enzyme or hormone. A person's genotype is the pair of genes he or she has at the locus, one coming from each parent. There are perhaps 50,000 (possibly as many as 100,000) different genes in the 23 human chromosomes, each coding for a specific polypeptid

Growth of the mouse corpus callosum.

Abstract: Brains of BALB/cCF inbred mice were examined at 15 ages ranging from 16.5 to 50.5 days from conception and cross-sectional areas of major forebrain fibre tracts at the midsagittal plane were measured. The anterior commissure appeared prior to the corpus callosum (CC), which was first seen at midplane at 17.0 days, and both tracts underwent a very rapid increase in size in the prenatal and early postnatal period, reaching the adult range of size at about 1 week after birth or several days prior to the onset of myelination. The growth spurt of these fibre tracts was much more pronounced than that of whole brain. By comparing BALB/c mice with hybrid mice that always have normal CC, it was found that some BALB/c mice at 18.5 days of age which have very small or absent CC do so because the growth of the whole brain is retarded whereas others have CC that is small for the brain size. Evidence also suggested that many mice with no CC but normal brain size at 18.5 days prenatally do eventually acquire at least a small CC. Observations at 3 postnatal ages of BALB/c mice weighed and marked at birth revealed that the 'runts' with low birth weight, which were presumably retarded prenatally, either die or catch up with mice of normal birth weight and do not have unusually small adult CC

Retarded Formation of the Hippocampal Commissure in Embryos From Mouse Strains Lacking a Corpus Callosum

formation of the hippocampal commissure in embryos from mouse strains lacking a corpus callosum. Hippocampus, 1997, 7, 2- A precise description of the timing and route traveled by axons traversing the telencephalic midline through the ventral hippocampal commissure (HC) is essential for understanding the role it plays in the formation of the corpus callosum (CC). A normal baseline of HC development was described in B6D2F 2 hybrid mice and then compared with two inbred strains of mice displaying callosal agenesis, BALB/cWah1 (50% CC defect) and 129/J (70% CC defect), their F 2 hybrid (C129F 2 -33% CC defect), and a recombinant inbred strain (RI-1-100% CC defect) derived from pairs of C129F 2 mice. Embryos weighing from 0.25 gto0.70 g(E14.5-E17) were collected and fixed by perfusion. Axon tracts were labeled using crystals of the lipophilic dyes DiI and DiA inserted into the hippocampal fimbria and cerebral cortex. HC axons in B6D2F 2 mice first cross the midline at about 0.350 g body weight (E14.8) by traveling over the dorsal septum and along the pia membrane lining the longitudinal fissure. Earlier crossing was prevented by the presence of a deep cleft formed by the longitudinal fissure extending down into the septal region. Subsequent axons fasciculated along existing axons, gradually building the dorsoventral height of the HC to about 200 μm by 0.600 g. The earliest callosal axons from frontal cortex crossed the midline at 0.620 g and were clearly seen fasciculating along and between existing hippocampal axons at the dorsal surface of the HC as they crossed. In the acallosal strains, HC formation was delayed by the continued presence of the cleft deep in the septal region. This delay in time of crossing was correlated with later CC defect expression. Initial HC crossing occurred at about 0.470 g (E1 6.25) in BALB mice and about 0.520 g (E1 6.5) in 129 mice. In the RI-1 embryos, first HC crossing was estimated at about 0.750 g (E1 7.5), although several older embryos showed no crossing. These results show the importance of the HC for successful CC formation and suggest that absent CC arises as a consequence of a developmental defect which affects the formation of the hippocampal commissure prior to arrival of CC axons at midplane

Different Rankings of Inbred Mouse Strains on the Morris Maze and a Refined 4-Arm Water Escape Task

The submerged platform or Morris water escape task is widely used to study genetic variation in spatial learning and memory, but interpretation is sometimes difficult because of wall hugging, jumping off the platform, floating or non-spatial swim strategies. We modified the task by introducing four wide arms into the circular tank and adding features that reduced, eliminated, or compensated for several competing behaviors. Three versions of the 4-arm task were evaluated in detail, and the third version yielded good results for six of eight inbred strains. Furthermore, the 4-arm task could be scored adequately without computerized video tracking. Although performance on the 4-arm task was generally superior to the Morris maze, the extent of the improvement was strain dependent. Two strains with retinal degeneration (C3H/HeJ, FVB/NJ) performed poorly on both the Morris and 4-arm mazes, whereas C57BL/6J and DBA/2J did well on both mazes. A/J performed poorly on the Morris task but became very proficient on the 4-arm maze, despite its strong tendency to hug the walls of the tank. The BALB/cByJ strain, on the other hand, exhibited the best probe trial performance on the Morris maze but was very slow in acquiring the 4-arm task. We conclude that no single task can reveal the full richness of spatially guided behavior in a wide range of mouse genotypes

Hybrid vigour and maternal environment in mice. III. Hippocampal mossy fibres and behaviour

Inbred BALB/c and C57BL/6 mice as well as their F1 hybrids were reared in either an inbred or hybrid maternal environment prenatally and/or postnatally, and were later tested for several behaviours prior to histological study of the brain at 100 days after birth. Whereas measures of spatial memory showed hybrid vigour or overdominance, measures of hippocampal mossy fibres showed intermediate inheritance. Brain-behaviour correlations within a strain were generally very small, and effects of maternal environment on hippocampal morphology were not significant

Race, the heritability of IQ, and the intellectual scale of nature

A critical response to selected arguments presented by Arthur Jensen regarding intelligence testing, race, and heritability

Reply: A Note on the Roman and Tryon Selected Lines of Rats

We would like to make several brief comments on Professor Broadhurst's letter. The sentence from Wahlsten's chapter in the Anisman and Bignami volume which Professor Broadhurst is contesting was based on Anisman's personal experiences in 1970-1972, when he failed to obtain selected lines of rats following two attempts. On the other hand, both of us have been impressed by the rapid response of Dr. DeFries and the staff of the Institute for Behavioral Genetics to requests for special mouse strains or lines

The genetic kaleidoscope of vision

Site-specific phenotypic effects of the 73 known alleles in the rhodopsin gene that cause retinal degeneration are difficult to interpret because most alleles are documented in only one case or one family, which means variation in effects could actually arise from interactions with other loci. However, sample sizes necessary to detect epistatk. interaction may place an answer to this question beyond our grasp

Shock-Induced Activity Changes, Adrenal Lipid Depletion and Brain Weight in Mice: A Genetic Study

Motor activity was evaluated before and after a brief electric shock. Whereas small genetic differences in activity were apparent prior to shock, large group differences occurred following shock. C57 mice did not freeze following a shock; DBA mice showed prolonged freezing; and the F1 hybrids froze only briefly. Backcross groups revealed segregation for postshock activity. Adrenal lipid depletion, as revealed by the absence of Sudan staining in the adrenal cortex, was detected in many male mice, but no correlation with either pre- or postshock activity was detected. Inheritance of adrenal lipid depletion clearly was not monogenetic

Digit Ratio (2D:4D) Differences between 20 Strains of Inbred Mice

The second to fourth digit ratio (2D:4D) is sexually differentiated in a variety of species, including humans, rats, birds, and lizards. In humans, this ratio tends to be lower in males than in females. Lower digit ratios are believed to indicate increased prenatal testosterone exposure, and are associated with more masculinized behavior across a range of traits. The story seems more complicated in laboratory mice. We have previously shown that there is no sex difference in the digit ratios of inbred mice, but found behavioral evidence to suggest that higher 2D:4D is associated with more masculinized behaviors. Work examining intrauterine position effects show that neighbouring males raise pup digit ratio, suggesting again that higher digit ratios are associated with increased developmental androgens. Other work has suggested that masculinization is associated with lower digit ratios in lab mice. Here, we examine the fore- and hindlimb digit ratios of 20 inbred mouse strains. We find large inter-strain differences, but no sexual dimorphism. Digit ratios also did not correlate with mice behavioral traits. This result calls into question the use of this trait as a broadly applicable indicator for prenatal androgen exposure. We suggest that the inbred mice model presents an opportunity for researchers to investigate the genetic, and gene-environmental influence on the development of digit ratios