A geological model of the chalk of East Kent

This report describes the geological modelling of the Chalk in the North Downs of East Kent, within the catchment of River Great Stour and eastwards to the coast, including the Isle of Thanet. This work was funded by the Environment Agency to support investigations of the local hydrogeology and thereby to enhance catchment management. The whole area is underlain by the Upper Cretaceous Chalk Group, with the Palaeogene succession of the Thanet Sand Formation, the Lambeth Group and the Thames Group overlying it in the northern and central eastern parts. The project included a desk study revision of the Chalk of the North Downs, using the new Chalk lithostratigraphy. The revisions to the geology are shown on the 1:50 000 scale geological map which accompanies this report. Together with evidence from boreholes and from seismic surveys, the new outcrop patterns have been incorporated into a geological model, using both computer software (EarthVision) and manual methods. The introduction describes the background to the project. The second chapter describes the sources for the data used in the model: published and unpublished geological maps, borehole records (both lithological and geophysical), seismic surveys, biostratigraphic records, digital topographic information, and the published literature. Each Chalk formation present in the area is then briefly described in the third chapter, noting its relationship to the older lithostratigraphic divisions, and to biostratigraphic zones. The local Chalk succession extends from the base of the Chalk Group to the Newhaven Chalk Formation, here represented by the Margate Chalk Member. Evidence for the thickness of each formation is reviewed. The early Palaeogene formations (the Thanet Sand, Upnor, Harwich and London Clay formations) are also briefly described (Chapter 4) and the local superficial deposits mentioned, with references to detailed descriptions (Chapter 5). Apart from minor adjustments to the outcrop of the basal Palaeogene surface, no revision of these formations was done for this study

Do brain regions involved in threat processing mediate the association between developmental trauma and psychosis

Background: There is growing evidence that developmental trauma - psychologically traumatic events during childhood and/or adolescence – is causally associated with increased risk of psychosis in adulthood [1]. However, an understanding of the precise mechanisms underlying this is lacking. Consistent with biopsychosocial and computational theories of psychosis [2,3], multiple lines of evidence converge on the role of altered threat processing in the pathway linking developmental trauma and psychosis [4,5]. Here, in a well-characterised birth cohort, we investigate prospectively, the effect of developmental trauma on volumes of brain structures involved in threat processing, and examine their roles in the association between developmental trauma and psychotic experiences in adulthood. Methods: We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) study, a large population-based cohort in the United Kingdom. Data from 418 participants were derived from parent- or self-reported assessments. Trauma variables represent trauma exposure (between 0-17 years), the number of types, and timing of trauma: childhood (0-10.9 years) or adolescence (11-17 years). Psychotic experiences were assessed using the psychosis-like symptoms semi-structured interview at 12 and 18 years. Magnetic resonance imaging was used to measure volumes of the whole brain, amygdala, vmPFC, and striatum at age 18. We used logistic and linear regression, and mediation analyses to examine associations. In addition, we explored whether these associations could be explained by genetic confounding or reverse causation, by repeating analyses (1) whilst adjusting for schizophrenia polygenic risk scores (PRS), and (2) in a subgroup of individuals who did not report psychotic experiences at age 12 (n=304). Results: Exposure to developmental trauma was associated with an increased odds of psychotic experiences at age 18 (OR=1.80; 95% CI=1.17-2.81, p<.001), with evidence supporting dose-response effects for exposure to multiple trauma types (B=.18, p<.001, R2=.05), and at both age periods (B=.15, p<.001, R2=.03). Developmental trauma was associated with reduced left amygdalar volumes in adulthood (B=-.01, p<.01, R2=.02), with evidence supporting a dose-response association, whereby exposure to three or more types of trauma (B=-.004, p<.05, R2=.01), and exposure to trauma during both childhood and adolescence (B=-.003, p<.05, R2=.01), had a greater effect compared with exposure during childhood or adolescence only. Developmental trauma was not associated with alterations in vmPFC and striatal volumes. Reduced left amygdalar volumes mediated 16% (95% CI=2%-80%, p=.03) of the association between developmental trauma and psychotic experiences (mediation effect: 0.04, 95% CI=0.01-0.08, p=.015). These findings substantively remained the same in sensitivity analyses aimed to minimise the effects of reverse causation and genetic confounding. Conclusions: In this study, we found evidence of a dose-response association between developmental trauma and reduced left amygdalar volumes in adulthood, and of a mediating role of left amygdalar volumes in the trauma-psychosis association. These findings were not explained by reverse causation or genetic confounding. These findings provide observational evidence for the hypothesis that a causal association between developmental trauma and altered threat processing underlies vulnerability to psychosis. Importantly, our identification of a neurobiological mediator of the trauma-psychosis relationship informs strategies for secondary and tertiary prevention of psychosis associated with developmental trauma