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Childhood obesity is a major global issue. Its incidence is constantly increasing, thereby offering a threatening public health perspective. The risk of developing the numerous chronic diseases associated with this condition from very early in life is significant. Although complex and multi-factorial, the pathophysiology of obesity recognizes essential roles of nutritional and metabolic aspects. Particularly, several risk factors identified as possible determinants of later-life obesity act within the first 1000 days of life (i.e., from conception to age 2 years). The purpose of this manuscript is to review those key mechanisms for which a role in predisposing children to obesity is supported by the most recent literature. Throughout the development of the human feeding environment, three different stages have been identified: (1) the prenatal period; (2) breast vs. formula feeding; and (3) complementary diet. A deep understanding of the specific nutritional challenges presented within each phase might foster the development of future preventive strategies.

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PURPOSE: We seek to identify pathogenic mechanisms for diabetic retinopathy that can become therapeutic targets beyond hyperglycemia and hypertension. We investigated if a defective myogenic response of retinal arteries to increased perfusion pressure, which exposes capillaries to increased pressure and flow, is associated with the onset of clinical retinopathy. METHODS: We examined prospectively the incidence of retinopathy in type 1 diabetic individuals tested 4 years earlier for the retinal arterial myogenic response, and in a cross-sectional study the prevalence of defective myogenic response in type 1 patients who had diabetic retinopathy. Among these, we contrasted early-onset (after 15 ± 2 years of diabetes, E-DR; n = 5) to late-onset (after 26 ± 3 years of diabetes, L-DR; n = 7) retinopathy. We measured the myogenic response using a laser Doppler blood flowmeter after a change in posture from sitting to reclining, which increases retinal perfusion pressure. RESULTS: Five of seven participants who 4 years prior had a defective myogenic response had now developed clinical retinopathy; as compared with only one of six participants who 4 years prior had a normal response (P = 0.10). In the cross-sectional study, all participants had normal retinal hemodynamics at steady state. In response to the postural change, only the E-DR group showed defective myogenic response (P = 0.005 versus controls, P = 0.02 versus L-DR) and abnormally high retinal blood flow (P = 0.016 versus controls). CONCLUSIONS: In type 1 diabetic patients, a defective myogenic response of retinal arteries to pressure is not required for the development of clinical retinopathy, but is prominently associated with an accelerated onset of retinopathy.

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Despite large improvements in the management of glucose levels and in the treatment of cardiovascular risk factors, the mortality rate in individuals with type 1 diabetes (T1D) is still high. Recently, Lind et al found that T1D individuals with glycated hemoglobin levels of 6.9% or lower had a risk of death from any cause or from cardiovascular causes that is twice as high as the risk for matched controls. T1D is a chronic disease with an early onset (e.g., pediatric age) and thus in order to establish a clear correlation between death rate and the glycometabolic control, the whole history of glycemic control should be considered; particularly in the early years of diabetes. The switch from a normo- to hyperglycemic milieu in an individual with T1D in the pediatric age, represents a stressful event that may impact outcomes and death rate many years later. In this paper we will discuss the aforementioned issues, and offer our view on these findings, paying a particular attention to the several alterations occurring in the earliest phases of T1D and to the many factors that may be associated with the chronic history of T1D. This may help us to better understand the recently published death rate data and to develop future innovative and effective preventive strategies.

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Celiac disease is a frequent chronic inflammatory small bowel disease which may present itself with associated autoimmune comorbidities. Among these comorbidities, thyroid disorders show a significant prevalence; even in the pediatric population. However, the exact epidemiology and clinical significance of such alterations are yet to be fully elucidated. The most updated guidelines do not currently offer any specific support. Focusing on the pediatric population, we will review the recent available literature that we believe might be helpful in advancing the clinician's knowledge-base regarding this issue. We also discuss which, to our knowledge, are the key pathophysiologic concepts behind the association between these two entities. Finally, we offer our own clinical perspective, recommending routine laboratory thyroid screening, possibly followed by an echographic thyroid evaluation as we believe such an approach to be appropriate when caring for children with celiac disease.