The sociogenomics revolution is upon us, we are told. Whether revolutionary or not, sociogenomics is poised to flourish given the ease of incorporating polygenic scores (or PGSs) as “genetic propensities” for complex traits into social science research. Pointing to evidence of ubiquitous heritability and the accessibility of genetic data, scholars have argued that social scientists not only have an opportunity but a duty to add PGSs to social science research. Social science research that ignores genetics is, some proponents argue, at best partial and likely scientifically flawed, misleading, and wasteful. Here, I challenge arguments about the value of genetics for social science and with it the claimed necessity of incorporating PGSs into social science models as measures of genetic influences. In so doing, I discuss the impracticability of distinguishing genetic influences from environmental influences because of non-causal gene–environment correlations, especially population stratification, familial confounding, and downward causation. I explain how environmental effects masquerade as genetic influences in PGSs, which undermines their raison d’être as measures of genetic propensity, especially for complex socially contingent behaviors that are the subject of sociogenomics. Additionally, I draw attention to the partial, unknown biology, while highlighting the persistence of an implicit, unavoidable reductionist genes versus environments approach. Leaving sociopolitical and ethical concerns aside, I argue that the potential scientific rewards of adding PGSs to social science are few and greatly overstated and the scientific costs, which include obscuring structural disadvantages and cultural influences, outweigh these meager benefits for most social science applications.

Neurodegeneration with brain iron accumulation (NBIA) is a term used for a group of hereditary neurological disorders with abnormal accumulation of iron in basal ganglia. It is clinically and genetically heterogeneous with symptoms such as dystonia, dysarthria, Parkinsonism, intellectual disability, and spasticity. The age at onset and rate of progression are variable among individuals. Current therapies are exclusively symptomatic and unable to hinder the disease progression. Approximately 16 genes have been identified and affiliated to such condition with different functions such as iron metabolism (only two genes: Ferritin Light Chain (FTL) Ceruloplasmin (CP)), lipid metabolism, lysosomal functions, and autophagy process, but some functions have remained unknown so far. Subgroups of NBIA are categorized based on the mutant genes. Although in the last 10 years, the development of whole-exome sequencing (WES) technology has promoted the identification of disease-causing genes, there seem to be some unknown genes and our knowledge about the molecular aspects and pathogenesis of NBIA is not complete yet. There is currently no comprehensive study about the NBIA in Iran; however, one of the latest discovered NBIA genes, GTP-binding protein 2 (GTPBP2), has been identified in an Iranian family, and there are some patients who have genetically remained unknown.

Absolute pitch is a rare pitch-naming ability with unknown etiology. Some scientists maintain that its manifestation depends solely on environmental factors, while others suggest that genetic factors contribute to it. We sought to further investigate the hypothesis that genetic factors support the acquisition of absolute pitch and to better elucidate the inheritance pattern of this trait. To this end, we conducted a twin study and a segregation analysis using data collected from a large population of absolute pitch possessors. The casewise concordance rate of 14 monozygotic twin pairs, 78.6%, was significantly different from that of 31 dizygotic twin pairs, 45.2%, assuming single ascertainment (x2 = 5.57, 1 df, p = .018), supporting a role for genetics in the development of absolute pitch. Segregation analysis of 1463 families, assuming single ascertainment, produced a segregation ratio pD = .089 with SEpD = 0.006. Unlike an earlier segregation analysis on a small number of absolute pitch probands from musically educated families, our study indicates that absolute pitch is not inherited in a simple Mendelian fashion. Based on these data, absolute pitch is likely genetically heterogeneous, with environmental, epigenetic, and stochastic factors also perhaps contributing to its genesis. These findings are in agreement with the results of our recent linkage analysis.

A segment of the ribosomal RNA gene of Schistosoma mansoni and a DNA fragment specific to Echinococcus granulosus, cloned in plasmids, have been used as DNA probes to assess the extent of genetic variability within E. granulosus and some distinct strains have been identified. The DNA analysis, involving restriction endonuclease digestion and Southern blot hybridization with the probes, did not demonstrate any significant genetic variation within the U.K. horse/dog or sheep/dog strains but confirmed the distinctiveness of the two strains shown in previous studies. The sheep/dog strain was shown to be cosmopolitan in its distribution and fertile bovine material originating from the United Kingdom, Kenya, Spain and India conformed to this strain by DNA hybridization. In contrast, cattle isolates from Holland produced markedly different DNA hybridization banding profiles indicating that cattle can harbour more than one strain of E. granulosus. Similarly, it was shown that goats can harbour two different strains of E. granulosus, the sheep/dog strain and a form which infects camels. The strain of E. granulosus infecting equines in Spain and Ireland is genetically identical to that infecting horses in the United Kingdom. There is also a different strain infecting pigs in Poland and Yugoslavia. This pig/dog strain appears to be very similar genetically to the forms of E. granulosus which use camels and goats as intermediate hosts and is similar, though not identical, to the variant infecting Dutch cattle. It has been shown that E. granulosus material, fixed for a prolonged period in ethanol, or lyophilized, is amenable to DNA analysis and that it is possible to characterize the DNA of a single adult worm.

The previous paper in this issue Computer model of the maintenance and selection of genetic heterogeneity in polygamous helminths by Saul uses an individual-based computer simulation to explore aspects of the transmission and maintenance of genetic heterogeneity among polygamous intestinal helminths, both in the absence and in the presence of external selection pressures resulting from chemotherapy. Saul finds that, in the absence of any selective effects, genetic heterogeneity persists, contradicting the results presented by Anderson, May & Gupta (1989) that mating probability functions create density-dependent and frequency-dependent selective pressures against a rare allele, which eventually leads to its elimination.

A stochastic simulation model of the transmission and maintenance of genetic heterogeneity in the absence and presence of external selection pressures is presented for polygamous intestinal helminths such as Ascaris. The model assumes that the density distribution of the adult parasites is highly aggregated and that density-dependent effects on fecundity are important. The model gives rise to stable infection rates in the host. Where the parasite population contains genetic heterogeneity, with the exception of stochastic fluctuations which models genetic drift, the ratio of the different alleles remained constant over extended periods of time. This result contrasts with that of an earlier analytical model (Anderson, R. M., May, M. R. & Gutpa S. (1989) Parasitology 99, S59–S79), in which uneven mating probabilities for the different combinations of worm possible in a host was postulated to inevitably lead to fixation of the most abundant allele. New results suggest that in spite of the restricted choice of mating available to a worm in the confines of a host, selection pressure always leads to enrichment of the parasites carrying resistant alleles.

The present genome era is characterized by speedy progress and prompt transfer of results into clinical practice. This creates the need for rapid disclosure of results and renewal of laboratory's protocols. Molecular cytogenetics has provided and increased ability to identify chromosomes, correlate chromosome structure with gene location, find out cryptic aberrations, and detect specific DNA sequences. These advances have allowed the confident discovery of a number of contiguous gene syndromes. The positional cloning and positional candidate strategies have greatly expedited the search process of disease genes, and become relevant methods for genes' discovery. Understanding the molecular basis of diseases has shown an unpredicted wide genetic heterogeneity, which has splitted single disorders into many clinically similar conditions, and added complexity to the nosology of human diseases. The opposite process, allelism, where clinical diversity results from allelic mutations, has lumped together many distinct disorders, by showing that different clinical entities are not necessarily due to mutations in different genes. Dynamic mutations have provided the molecular understanding of interindividual and intrafamilial variability including anticipation, in a number of diseases. The discovery of distinct correlations between the molecular pattern and disease severity is providing a unique opportunity for using molecular results to assess the clinical outcome. Diagnostic, presymptomatic and predictive molecular testing are becoming widely used and provide enormous opportunities for improving the lot of our patients.