For most of these gene defects the mechanisms linking mutation to phenotype remain to be elucidated.
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The JO phenotype can be caused by mutations in LRP5 and PLS3, but also by mutations in some of the genes that cause OI. Patients with heritable bone fragility who do not have extraskeletal manifestations of OI are often diagnosed with JO. Specific phenotypes are caused by mutations in SERPINF1 (recessive OI type VI), P4HB (Cole-Carpenter syndrome) and SEC24D (‘Cole-Carpenter like’). TMEM38B), or interfere with osteoblast function (SP7, WNT1).
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Most of the involved genes code for proteins that play a role in the processing of collagen type I protein (BMP1, CREB3L1, CRTAP, LEPRE1, P4HB, PPIB, FKBP10, PLOD2, SERPINF1, SERPINH1, SEC24D, SPARC, OI is usually caused by dominant mutations affecting one of the two genes that code for two collagen type I, but a recessive form of OI is present in 5-10% of individuals with a clinical diagnosis of OI.
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Heritable forms of primary bone fragility in children typically lead to a clinical diagnosis of either osteogenesis imperfecta (OI) or juvenile osteoporosis (JO). I will discuss these developments from both a scientific and public policy perspective.įrank Rauch Shriners Hospitals for Children The World Health Assembly in May 2016 adopted the report of the Commission on Ending Childhood Obesity and this has major implications for national and global health policy. This led the WHO and an increasing number of governments to start to formulate developmental strategies to confront obesity. However in part because of the Millennium Development Goals that brought an emphasis to maternal and girls’ health and because of scientific progress as reflected in the “ first 1000 days” movement, the first recognition of the developmental and epigenetic component to obesity was noted in the political declaration of the UN General Assembly in 2011. These issues have largely been addressed to the extent needed for policy recommendations although there are areas of research that need further promotion – in particular those related to the development of eating behaviours and satiety control. These barriers included an over-simplistic understanding of the phenomenon, a failure to appreciate its normative nature and multiple mechanisms that are best understood in a evolutionary medicine context, a lack of compelling biological mechanistic explanations and estimates of the size of the developmental component.
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A number of barriers, both scientific and societal, existed to the incorporation of this knowledge into public policy. But while this evidence emerged over 30 years ago, it is only in the past 5 years it has gained traction in the policy domain. There is considerable evidence showing that the fetus and neonate are affected by the environment created by its mother and these have longer-term metabolic consequences including obesity and the implications for non-communicable disease (NCD). The marked individual differences in the sensitivity to the obesogenic environment need to be understood at both the individual and population level. Indeed the evidence that biological, developmental and contextual factors are operating from the earliest stages in development and indeed across generations is compelling. Peter Gluckman Office of Chief Science Advsor to the Prime MinisterĪttempts to deal with the obesity epidemic based solely on adult behavioural change have been rather disappointing.