Macroprudential Ideas and Contested Social Purpose: A Response to Terrence Casey

In response to Terrence Casey's argument that the emergence of macroprudential regulation since the financial crash can and should save neoliberalism we raise five objections. 1). The Debt-Driven Growth Hypothesis (DDG) and the Financial Instability Hypothesis (FIH), as Casey terms them, are just as likely to be complementary as they are oppositional and they are by no means incompatible. 2) Casey's empirics are too thin and static, drawn from the 1980s and 1990s, while Anglo Liberal Financialised Capitalism (ALFC) is a complex adaptive system that has continued to evolve throughout the 2000s. 3) Casey overlooks the dynamic relationship between potentially excessive financialisation and the performance of the wider economy, which is becoming a growing concern for many policy makers using the macroprudential frame. 4) Macroprudential as a series of ideas about the economy are often incompatible with neoliberal premises and their ontological foundations. 5) Many of the policy makers who have acted as the biggest champions of macroprudential regulation have also been highly critical of ALFC and view the macroprudential turn as making a contribution to a much needed deeper financial reformation that would over time transform some of the constituent economic and social relations of the existing political economy. We conclude that what we call the social purpose of macroprudential regulation (the question of whether it is intended to patch up or transform the existing system) is contested, and that macroprudential regulation has much potential beyond saving ‘neoliberalism’.

Defining the role of common variation in the genomic and biological architecture of adult human height

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated 1/42,000, 1/43,700 and 1/49,500 SNPs explained 1/421%, 1/424% and 1/429% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/I 2-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.

New genetic loci link adipose and insulin biology to body fat distribution

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms.

Genetic studies of body mass index yield new insights for obesity biology

Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.