Early crime writing and the state: Jonathan Wild, Daniel Defoe and Bernard Mandeville in 1720s London

This article argues that the early development of crime writing needs to be understood in relation to the consolidation of the modern state. It demonstrates that London in the 1720s constitutes a significant moment in this early development for three main reasons. First, the period witnessed a crime epidemic which reached its climax in the 1720s and which precipitated a set of particularly aggressive counter-measures by the state; second, it saw the rise and eventual fall of the infamous Jonathan Wild who acted as both thief and surrogate policeman; and third, it was also marked by a surge in interests on the part of writers like Daniel Defoe and Bernard Mandeville in the related matters of crime and punishment. This article explores the ways in which accounts of crime and punishment in this period deployed and in some instances interrogated the rhetoric of social contract theory and writings on statecraft, particularly by Thomas Hobbes and Mandeville. But while the criminal biographies and gallows sermons produced by the Newgate prison’s ‘ordinaries’ provided crude and reductive accounts of the efficacy of the state, the article shows how two accounts of the life of Jonathan Wild (by Defoe and H.D) responded in highly complex ways to the issues of crime and policing and provided a consistently and self-consciously ambivalent reading of the state and state power. To conclude, I suggest that this ambivalence can be read as a critique of the impartial or neutral state and that it constitutes one of the key features of what we would later understand to be crime writing as a dedicated literary genre.

Struell Wells: pagan past and Christian present

The complex of buildings at Struell Wells, near Downpatrick, Co. Down, is the most extensive at a holy well in Ireland. It comprises two wells, two bath-houses and the ruins of a church. Nearby is a natural rock feature known as St Patrick’s Chair. The earliest reference to the wells is likely to be in the 8th century Fíacc’s Hymn which records the site being visited by St Patrick. The earliest reference to their healing powers can be dated to the 11th/12th century and the site continued to be a focus of pilgrimage at midsummer until its suppression in the nineteenth century. The site seems to be unique in that bathing in the wells constituted an integral part of the rituals performed by pilgrims. A recent study of the holy well phenomenon in Ireland has suggested that the rituals associated with them have their origins in the Counter-Reformation (Carroll 1999). The evidence from Struell, however, strongly suggests that it was an important sacred site in pre-Christian times.

Plasma HDL cholesterol and risk of myocardial infarction: A mendelian randomisation study

Background: High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian random isation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal.
Methods: We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20 913 myocardial infarction cases, 95 407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12 482 cases of myocardial infarction and 41 331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol.
Findings: Carriers of the LIPG 396Ser allele (2·6% frequency) had higher HDL cholesterol (0·14 mmol/L higher p=8×10-13) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with noncarriers. This difference in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84-0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88-1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58-0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93 95% CI 0·68-1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45-1·63) was concordant with that from genetic score (OR 2·13 95% CI 1·69-2·69, p=2×10 -10).
Interpretation: Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.