Lucy Faulkner and the 'ghastly grin': Reworking the title page illustration to Goblin Market

An article that recovers the work of the craftswoman Lucy Faulkner Orrinsmith. It demonstrates her role in the re-cutting of the title page illustration to Christina Rossetti’s poem ‘Goblin Market’ designed by D. G. Rossetti in 1862-5

Early life events and their consequences for later disease: a life history and evolutionary perspective

Biomedical science has little considered the relevance of life history theory and evolutionary and ecological developmental biology to clinical medicine. However, the observations that early life influences can alter later disease risk--the "developmental origins of health and disease" (DOHaD) paradigm--have led to a recognition that these perspectives can inform our understanding of human biology. We propose that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course. Such adaptive processes allow genotypic variation to be preserved through transient environmental changes. Cues for plasticity operate particularly during early development; they may affect a single organ or system, but generally they induce integrated adjustments in the mature phenotype, a process underpinned by epigenetic mechanisms and influenced by prediction of the mature environment. In mammals, an adverse intrauterine environment results in an integrated suite of responses, suggesting the involvement of a few key regulatory genes, that resets the developmental trajectory in expectation of poor postnatal conditions. Mismatch between the anticipated and the actual mature environment exposes the organism to risk of adverse consequences-the greater the mismatch, the greater the risk. For humans, prediction is inaccurate for many individuals because of changes in the postnatal environment toward energy-dense nutrition and low energy expenditure, contributing to the epidemic of chronic noncommunicable disease. This view of human disease from the perspectives of life history biology and evolutionary theory offers new approaches to prevention, diagnosis and interventio

Non-genomic transgenerational inheritance of disease risk

That there is a heritable or familial component of susceptibility to chronic non-communicable diseases such as type 2 diabetes, obesity and cardiovascular disease is well established, but there is increasing evidence that some elements of such heritability are transmitted non-genomically and that the processes whereby environmental influences act during early development to shape disease risk in later life can have effects beyond a single generation. Such heritability may operate through epigenetic mechanisms involving regulation of either imprinted or non-imprinted genes but also through broader mechanisms related to parental physiology or behaviour. We review evidence and potential mechanisms for non-genomic transgenerational inheritance of 'lifestyle' disease and propose that the 'developmental origins of disease' phenomenon is a maladaptive consequence of an ancestral mechanism of developmental plasticity that may have had adaptive value in the evolution of generalist species such as Homo sapien

Developmental perspectives on individual variation: implications for understanding nutritional needs

Genetic research has focused on identifying linkages between polymorphisms and phenotypic traits to explain variations in complex biologies. However, the magnitude of these linkages has not been particularly high. Conversely, the ability of developmental plasticity to generate biological variation from one genotype is well understood, while interest has emerged in the clinical significance of epigenetic processes, particularly those influenced by the external environment. Environmental cues in early development may induce responses that provide adaptive advantage later in life. The benefit of such responses depends on the fidelity of the prediction of the future environment. Life history and physiological changes mediated through epigenetic processes then follow, determining the later phenotype. Developmental mismatch, leading to disease, can arise from discordance between the fetal environment, which is relatively constant across generations, and the postnatal nutritional environment, which can change drastically within and between generations. Metabolic disorders represent the outcome of an individual living in an energetically inappropriate environment. Experimental and clinical evidence suggests that individual capacity to live in a given energetic environment is influenced by developmental factors acting through epigenetic mechanisms. Epigenetic biomarkers may be able to identify a risk of developmental mismatch and thus offer the opportunity for nutritional or other interventio

Fetal and neonatal pathways to obesity

Evolutionary and developmental perspectives add considerably to our understanding of the aetiology of obesity and its related disorders. One pathway to obesity represents the maladaptive consequences of an evolutionarily preserved mechanism by which the developing mammal monitors nutritional cues from its mother and adjusts its developmental trajectory accordingly. Prediction of a nutritionally sparse environment leads to a phenotype that promotes metabolic parsimony by favouring fat deposition, insulin resistance, sarcopenia and low energy expenditure. But this adaptive mechanism evolved to accommodate gradual changes in nutritional environment; rapid transition to a situation of high energy density results in a mismatch between predicted and actual environments and increased susceptibility to metabolic disease. This pathway may also explain why breast and bottle feeding confer different risks of obesity. We discuss how early environmental signals act through epigenetic mechanisms to alter metabolic partitioning, glucocorticoid action and neuroendocrine control of appetite. A second pathway involves alterations in fetal insulin levels, as seen in gestational diabetes, leading to increased prenatal fat mass which is subsequently amplified by postnatal factors. Both classes of pathway may coexist in an individual. This developmental approach to obesity suggests that potential interventions will vary according to the target population