Child Health Conference Research Articles

McMaster Child Health Conference 2023

The McMaster Child Health Conference (MCHC) is an annual symposium for stakeholders, faculty, and students from multiple disciplines to discuss issues, policies, and novel research relevant to child health and development. For their 8th year, the conference invited the Hamilton community to explore the theme “Food for Thought: Nutrition & Health in Child Development" at the first in-person conference since the COVID-19 pandemic, on March 11, 2023. Keynote speakers and workshop leaders covered a range of topics from consequences of maternal nutritional on perinatal development to food insecurity among children in Hamilton, and more!

McMaster Child Health Conference

McMaster Child Health Conference

Power, policy and abortion care in Uganda.

Unsafe abortion practices remain the major contributor to maternal death in Uganda, impeding the achievement of universal health coverage and quality of maternal health care. Using an ethnographic design and critical discourse analysis, we explored the operations of power in setting maternal healthcare priorities, as evident at the 2018 Reproductive, Maternal, Neonatal, Child and Adolescents Health Conference. Observational data were collected of the policy-making activities, processes and events and key informant interviews were conducted with 27 participants. We describe how neoliberal and state governance through the structure and organization of policy-making, epistemic governance and universal concepts of ‘high-impact’ interventions, results-based financing, cost-effectiveness and accountability converge to suppress the articulation of local conditions associated with unsafe and risky abortion. By defining maternity along the continuum of birth and emphasizing birthing women, priority-setting was directed towards interventions promoting women’s normative role as mothers while suppressing unmet abortion care needs. Finally, discursive and communicative materials controlled how women of reproductive age in Uganda managed reproduction.

The 5th International Child and Adult Behavioral Health Conference Abu-Dhabi, UAE

The 5th International Child and Adult Behavioral Health Conference Abu-Dhabi, UAE

Abstracts from the Northern Undergraduate Child Health Conference

Abstracts from the Northern Undergraduate Child Health Conference

Stress Response and Child Health Meeting Information : The European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health took place in Heraklion, Crete, Greece, 18 to 20 May 2012.

Stress is defined as a state of real or perceived threat to homeostasis. The principal effectors of the stress system are corticotropin-releasing hormone (CRH), arginine vasopressin, the proopiomelanocortin-derived peptides α-melanocyte-stimulating hormone and β-endorphin, the glucocorticoids, and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for various endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of stressful event(s). Prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors. This review summarizes the topics presented at the fifth New Inroads to Child Health (NICHe) Conference "Stress Response and Child Health" held at Heraklion, Crete, Greece, in May 2012.

Prenatal Stress, Telomere Biology, and Fetal Programming of Health and Disease RiskA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

A substantial body of epidemiological, clinical, cellular, and molecular evidence converges to suggest that conditions during the intrauterine period of life play a critical role in developmental programming to influence subsequent health and susceptibility for common, complex disorders. Elucidation of the biological mechanisms underlying these effects is an area of considerable interest and investigation, and it is important to determine whether these mechanisms are distinct for different health outcomes or whether there are some common underlying pathways that may account for the effects of disparate prenatal and early postnatal conditions on various health and disease risk phenotypes. We propose that telomere biology may represent a common underlying mechanism connecting fetal programming and subsequent health outcomes. It appears that the initial establishment of telomere length and regulation of telomere homeostasis may be plastic and receptive to the influence of intrauterine and other early life conditions. Moreover, telomere homeostasis in various cell types may serve as a fundamental integrator and regulator of processes underlying cell genomic integrity and function, aging, and senescence over the life span. We advance the hypothesis that context- and time-inappropriate exposures to various forms of physiological stress (maternal-placental-fetal endocrine aberrations and immune, inflammatory, and oxidative stresses) during the intrauterine period of development may alter or program the telomere biology system in a manner that accelerates cellular dysfunction, aging, and disease susceptibility over the life span.

Protein Complexes and Target Genes Identification by in Vivo Biotinylation: The STAT5 ParadigmA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Signal transducers and activators of transcription (STATs) are implicated in physiological cellular processes, stress-related responses, and malignancies. This Presentation provides an overview on STATs, focusing on STAT5, and describes an in vivo biotinylation methodology applied in mammalian cells for identification of STAT5-containing protein complexes and STAT5 target genes. Our results show that in vivo biotinylation can be used efficiently to elucidate the complex STAT5-dependent transcriptional mechanisms.

The Effect of Acute and Chronic Stress on GrowthA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Impaired bone growth is observed in many children exposed to stress, but whether the underlying cause is psychological or secondary to a variety of chronic disorders is unclear. The growth plate is specifically targeted by stress through many different mechanisms, including increased serum concentrations of proinflammatory cytokines and cortisol, as well as impaired actions of the growth hormone (GH)-insulin-like growth factor-1 (IGF-1) axis. Both glucocorticoids, such as cortisol, and proinflammatory cytokines adversely affect several aspects of chondrogenesis in the growth plate, and these effects can be ameliorated by raising local IGF-1 concentrations. However, this intervention does not completely normalize growth. In children with stress related to chronic inflammation, the cornerstone of improving stress-impaired growth remains the judicious use of glucocorticoids while ensuring effective control of the disease process. Specific immunomodulatory therapy that targets the actions of tumor necrosis factor-α (TNFα) is at least partially effective at rescuing linear growth in many children with juvenile idiopathic arthritis (JIA). Patients who do not respond to anti-TNF treatment may be candidates for therapeutic agents that target other proinflammatory cytokines and for GH intervention. Although GH treatment rescues linear growth in some patients with JIA, it is unknown whether GH can rescue growth in those patients who do not respond to anticytokine therapy. Further experimental and clinical studies are needed to explore these and other new potential treatment strategies that could improve bone growth in patients who do not respond to conventional therapy.

P450 Oxidoreductase Deficiency: A Disorder of Steroidogenesis with Multiple Clinical ManifestationsA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Cytochrome P450 enzymes catalyze the biosynthesis of steroid hormones and metabolize drugs. There are seven human type I P450 enzymes in mitochondria and 50 type II enzymes in endoplasmic reticulum. Type II enzymes, including both drug-metabolizing and some steroidogenic enzymes, require electron donation from a two-flavin protein, P450 oxidoreductase (POR). Although knockout of the POR gene causes embryonic lethality in mice, we discovered human POR deficiency as a disorder of steroidogenesis associated with the Antley-Bixler skeletal malformation syndrome and found mild POR mutations in phenotypically normal adults with infertility. Assay results of mutant forms of POR using the traditional but nonphysiologic assay (reduction of cytochrome c) did not correlate with patient phenotypes; assays based on the 17,20 lyase activity of P450c17 (CYP17) correlated with clinical phenotypes. The POR sequence in 842 normal individuals revealed many polymorphisms; amino acid sequence variant A503V is encoded by ~28% of human alleles. POR A503V has about 60% of wild-type activity in assays with CYP17, CYP2D6, and CYP3A4, but nearly wild-type activity with P450c21, CYP1A2, and CYP2C19. Activity of a particular POR variant with one P450 enzyme will not predict its activity with another P450 enzyme: Each POR-P450 combination must be studied individually. Human POR transcription, initiated from an untranslated exon, is regulated by Smad3/4, thyroid receptors, and the transcription factor AP-2. A promoter polymorphism reduces transcription to 60% in liver cells and to 35% in adrenal cells. POR deficiency is a newly described disorder of steroidogenesis, and POR variants may account for some genetic variation in drug metabolism.

The Effects of Acute and Chronic Stress on Diabetes ControlA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Stress is an important contributor to pathological conditions in humans. Hormonal changes that occur during acute and chronic stress situations can affect glucose homeostasis in both healthy people and in those with diabetes. Several studies have reported a negative effect of acute stress on maintenance of blood glucose concentrations in patients with type 1 and type 2 diabetes. The effect of stress on glycemic control in people with diabetes may be related to a direct effect of stress hormones on blood glucose levels and an indirect effect of stress on patient behaviors related to diabetes treatment and monitoring and meal and exercise plans. In contrast, there is no clear evidence that stressful life events promote the development of diabetes in children or in adults. Stress hyperglycemia, the development of hyperglycemia during acute illness, represents another interesting connection between the stress system and glucose homeostasis. A large body of evidence supports an association between stress hyperglycemia and increased morbidity and mortality in critically ill patients. Interestingly, there is some evidence supporting a beneficial effect of insulin in reducing morbidity and mortality in patients admitted to intensive care units. Finally, stress can influence the development of type 2 diabetes indirectly by promoting obesity and metabolic syndrome.

Neurosteroids and Microneurotrophins Signal Through NGF Receptors to Induce Prosurvival Signaling in Neuronal CellsA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

The neurosteroid dehydroepiandrosterone (DHEA) exerts a portion of its neuroprotective effects by directly interacting with the nerve growth factor (NGF) receptors TrkA and p75(NTR) to induce prosurvival signaling. DHEA is an intermediate in the biosynthesis of estrogens and androgens that affects the endocrine system and potentially increases the risk for developing estrogen- and androgen-dependent tumors. We have synthesized 17-spiro analogs of DHEA that lack estrogenic or androgenic properties and bind to and activate NGF receptors, thus exerting potent neuroprotective effects without the tumor risk. These synthetic DHEA derivatives may serve as lead molecules to develop small agonists of NGF receptors that can penetrate the blood-brain barrier (microneurotrophins) with potential applications in the treatment of neurodegenerative diseases. The neuroprotective properties of microneurotrophins are now being tested in various animal models of neurodegenerative diseases.

Fetal Programming of Brain Development: Intrauterine Stress and Susceptibility to PsychopathologyA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

The fetal brain is highly plastic and is not only receptive to but requires cues from its environment to develop properly. Based on an understanding of evolutionary biology, developmental plasticity, and life history theory, one can predict that stressors are an important environmental condition that may influence brain development. In fact, the available empirical evidence appears to support the notion that exposure to excess stress in intrauterine life has the potential to adversely affect short- and long-term neurodevelopmental outcomes with implications for altered susceptibility for mental health disorders in childhood and adult life. In this presentation, we provide a rationale for proposing that endocrine and inflammatory stress mediators are key candidate pathways for programming brain development. These mediators are responsive to a diverse set of intrauterine perturbations and alter key signaling pathways critical for brain development, including but not limited to mammalian target of rapamycin, Wnt (wingless), Sonic hedgehog, and reelin signaling. We suggest that recent advances in neuroimaging and other methods now afford us an unprecedented opportunity to advance our understanding of this important topic. Additionally, we provide empirical evidence from two recently published papers for fetal programming of human brain development. We conclude by suggesting some future directions for expanding this field of research.

Posttraumatic Stress Disorder in Children and Adolescents: Neuroendocrine PerspectivesA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Posttraumatic stress disorder (PTSD) is a syndrome of distress that develops after exposure to traumatic life experiences. Dysregulation of both the hypothalamic-pituitary-adrenal (HPA) axis and the locus caeruleus/norepinephrine-sympathetic nervous system (LC/NE-SNS) is associated with the pathophysiology of the disorder. Studies have demonstrated a neuroendocrine profile unique to adults with PTSD, with centrally elevated corticotropin-releasing hormone (CRH), low cortisol in the periphery, and elevated catecholamines. Traumatic stress experiences in early life are strong predisposing factors for later PTSD development. In addition, early life stress programs the developing brain to overreact to future stressors. In children and adolescents involved in motor vehicle accidents, we found that high evening salivary cortisol and morning serum interleukin 6 concentrations were predictive of PTSD development 6 months later. We demonstrated a progressive divergence of the HPA and LC/NE-SNS axes of the stress system, which may be part of the pathophysiologic mechanism responsible for PTSD maintenance. An initial elevation of cortisol in the aftermath of the trauma, followed by a gradual normalization and finally low cortisol secretion, together with a gradual elevation of catecholamines over time, may represent the natural history of neuroendocrine changes in pediatric PTSD. Thus, the low cortisol concentrations found in adults with PTSD may reflect prior trauma and might represent a biologic vulnerability factor for later PTSD development.

Circadian Rhythms of Glucocorticoid Hormone Actions in Target Tissues: Potential Clinical ImplicationsA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Organisms face unforeseen short- and long-term changes in the environment (stressors). To defend against these changes, organisms have developed a stress system that includes the hypothalamic-pituitary-adrenal (HPA) axis, which employs glucocorticoids and the glucocorticoid receptor (GR) for signal transduction. In addition, organisms live under the strong influence of day-night cycles and, hence, have also developed a highly conserved circadian clock system for adjusting their activities to recurring environmental changes. This regulatory system creates and maintains internal circadian rhythmicity by employing a self-oscillating molecular pacemaker composed of the Clock-Bmal1 heterodimer and other transcription factors. The circadian clock consists of a central master clock in the suprachiasmatic nucleus of the brain hypothalamus and peripheral slave clocks in virtually all organs and tissues. The HPA axis and the circadian clock system communicate with each other at multiple levels. The central clock controls the HPA axis, creating the diurnal oscillation of circulating adrenocorticotropic hormone and cortisol, and the HPA axis adjusts the circadian rhythmicity of the peripheral clocks in response to various stressors through the GR. Further, Clock-Bmal1 regulates the response to glucocorticoids in peripheral tissues through acetylation of the GR, possibly antagonizing the biologic actions of diurnally fluctuating circulating cortisol. Importantly, dysregulation in the clock system and the HPA axis may cause similar pathologic manifestations--including obesity, metabolic syndrome, and cardiovascular disease--by uncoupling circulating cortisol concentrations from tissue sensitivity to glucocorticoids.

Primary Generalized Glucocorticoid Resistance and Hypersensitivity: The End-Organ Involvement in the Stress ResponseA Presentation from the European Society for Paediatric Endocrinology (ESPE) New Inroads to Child Health (NICHe) Conference on Stress Response and Child Health in Heraklion, Crete, Greece, 18 to 20 May 2012.

Primary generalized glucocorticoid resistance (PGGR or Chrousos syndrome) and primary generalized glucocorticoid hypersensitivity (PGGH) are rare genetic disorders characterized by generalized, partial target-tissue insensitivity or hypersensitivity to glucocorticoids, respectively, while also causing compensatory alterations in the activity of the hypothalamic-pituitary-adrenal axis. The molecular basis of Chrousos syndrome and PGGH has been ascribed to mutations in the gene encoding the human glucocorticoid receptor (hGR), which impair glucocorticoid signal transduction and alter tissue sensitivity to glucocorticoids. Alterations in hGR action may have important implications for many critical biological processes, such as the behavioral and physiologic responses to stress, immune responses, growth, and reproduction. This Presentation summarizes the pathophysiology, clinical manifestations, and molecular mechanisms of the PGGR and PGGH states.

Vaginal Birth After Cesarean Delivery

Once a woman is delivered by cesarean, her options in a subsequent pregnancy are either a planned trial of labor or a planned elective repeat cesarean. There are no randomized trials comparing these two choices to definitively guide patients and physicians. The primary cesarean rate is increasing and vaginal birth after cesarean delivery (VBAC) rates are decreasing. Nonmedical factors have had a major effect on these trends. The 2010 Eunice Kennedy Shriver National Institute of Child Health and Human Development Conference on VBAC, after presenting a detailed analysis of benefits compared with risks, recommended that measures should be taken to assure women that VBAC is available to them. This will require an organized and concerted effort on the part of patients, physicians, and hospitals. To meet patient expectations for a safe and successful outcome with a trial of labor after cesarean delivery (TOLAC), specific management plans, checklists, practical coverage arrangements, and simulation drills are necessary.

A Structured Public Health Approach to Increasing Rates and Duration of Breastfeeding in Romania

Studies indicate that since 1990, rates of breastfeeding initiation and duration in Eastern Europe, including Romania, have decreased. Most breastfeeding promotion efforts in Romania have focused on in-hospital care, with an emphasis on training clinicians. Prior studies report that about 88% of Romanian mothers initiate breastfeeding in the hospital; however, these same studies report limited breastfeeding duration. We posit that an important problem is lack of support and education in the weeks and months following the birth. The nature of this problem suggests the need for an integrated and structured public health solution. Based on our independent research, the results of an international maternal and child health (MCH) conference, and consultation with Romanian and American experts, we propose use of the public health problem-solving paradigm to support breastfeeding in Romania. This article presents a conceptual model showing the integration of input, output, and process components and a logic model explicating possible interventions (or needs) and barriers to breastfeeding. We propose a public health solution that begins with a new MCH within the public health training structure at a major Romanian university and a summer course bringing together Romanian and American students to study MCH, including breastfeeding. We believe that these two courses will promote enthusiasm and generate ideas to develop community-based interventions as well as policy recommendations to increase breastfeeding duration in Romania. We suggest that this public health problem-solving approach provides an integrated way of maintaining and increasing breastfeeding; furthermore, this approach could be broadly used in Eastern Europe.

Offline: Naming and shaming

“We are killing thousands of women”, said one participant at the Pledges to Action for maternal, newborn, and child health conference in Delhi last week. She was furious that the meeting was not discussing the quality of care given to women and children. The gathering was part of the UN Secretary General’s global strategy on MDGs 4 and 5. Well over 8 million mothers and their children die of preventable causes worldwide each year. November 14 was Children’s Day in India and also the birthday of Jawaharlal Nehru, one of the founding spirits of modern India. There is an alarming schism between what Indian politicians say and what they do. The Minister of Health, Ghulam Nabi Azad, claimed that “India pledges its commitment to achieve the MDG health goals within the timeframe of 2015”. Yet over 5000 children under 5 die each day in India. The President of India, Pratibha Devisingh Patil, said she was “conscious of this enormous challenge”. Newspapers regularly note lack of government action on maternal and child health. One report last weekend described how the Prime Minister’s National Council on nutrition had not met for two years.

Proceedings from the National Institute of Child Health and Human Development Conference on the Uterine Fibroid Research Update Workshop

The purpose of the National Institutes of Health conference Fibroid Research Workshop in September 2007 was to bring Eunice Kennedy Shriver National Institute of Child Health and Human Development-funded fibroid investigators together to discuss basic science and clinical research advances on uterine leiomyomata. General topics included advances in epidemiology, etiology, therapeutic approaches, and clinical trial challenges; suggestions for advancement of basic understanding, clinical intervention, clinical trials, and future directions were highlighted.