Consistent evidence associates IGF-1 deficiency and metabolic syndrome. In this review, we will focus on the metabolic effects of IGF-1, the concept of metabolic syndrome and its clinical manifestations (impaired lipid profile, insulin resistance, increased glucose levels, obesity, and cardiovascular disease), discussing whether IGF-1 replacement therapy could be a beneficial strategy for these patients. The search plan was made in Medline for Pubmed with the following mesh terms: IGF-1 and “metabolism, carbohydrate, lipids, proteins, amino acids, metabolic syndrome, cardiovascular disease, diabetes” between the years 1963–2015. The search includes animal and human protocols. In this review we discuss the relevant actions of IGF-1 on metabolism and the implication of IGF-1 deficiency in the establishment of metabolic syndrome. Multiple studies (in vitro and in vivo) demonstrate the association between IGF-1 deficit and deregulated lipid metabolism, cardiovascular disease, diabetes, and an altered metabolic profile of diabetic patients. Based on the available data we propose IGF-1 as a key hormone in the pathophysiology of metabolic syndrome; due to its implications in the metabolism of carbohydrates and lipids. Previous data demonstrates how IGF-1 can be an effective option in the treatment of this worldwide increasing condition. It has to distinguished that the replacement therapy should be only undertaken to restore the physiological levels, never to exceed physiological ranges.

Insulin growth factor 1 (IGF-1) has multiple effects on metabolism. Much evidence suggests that the deficiency of this hormone increases insulin resistance, impairs lipid metabolism, augments oxidative damage and deregulates the neuro-hormonal axis. An inverse relationship between IGF-1 levels and the prevalence of Metabolic Syndrome (MetS) with its cardiovascular complications has been identified. However, the underlying mechanisms linking IGF-1 and MetS are still poorly understood. In order to elucidate such mechanisms, the aim of this work was to study, in mice with partial IGF-1 deficiency, liver expression of genes involved in glucose and lipid metabolism as well as serum levels of glucose, triglycerides and cholesterol, as well as liver malondialdehyde (MDA) levels, as a marker for oxidative damage. Three experimental groups were studied in parallel: Controls (CO), wild type mice (igf-1 +/+); untreated heterozygous mice (Hz, igf-1 +/−) and Hz (igf-1 +/−) mice treated with low doses of IGF-1 for 10 days (Hz + IGF-1). A reduction of IGF-1 serum levels in the Hz group was found, which was normalized by IGF-1 therapy. Serum levels of glucose, triglycerides and cholesterol were significantly increased in the untreated Hz group as compared to both controls and Hz + IGF-1 groups. The expression of genes involved in gluconeogenesis, glycogenolysis, lipid synthesis and transport, and catabolism were altered in untreated Hz animals and the expression of most of them was normalized by IGF-1 therapy; MDA was also significantly increased in the Hz untreated group. The mere partial IGF-1 deficiency is responsible for the reduction in the expression of genes involved in glucose and lipid metabolism, resulting in dyslipidemia and hyperglycemia. Such genetic alterations may seriously contribute to the establishment of MetS.

Neurodegenerative diseases (NDs) represent a growing public health challenge worldwide. While their clinical manifestations typically emerge late in life, increasing evidence suggests that biological vulnerability may originate much earlier in life. Early childhood adversity, expressed through mechanisms of toxic stress and allostatic load, has been associated with chronic activation of the hypothalamic–pituitary–adrenal axis, mitochondrial dysfunction, oxidative stress, and persistent inflammation—molecular pathways that overlap with those implicated in neurodegeneration. This narrative review highlights recent advances linking early adversity with long-term brain health. It discusses stress-related biomarkers, such as hair cortisol, inflammatory cytokines, and epigenetic modifications, as potential early indicators of neurodegenerative risk. Remarkably, protective and benevolent childhood experiences may mitigate these biological trajectories, underscoring the role of resilience in shaping neurobiological outcomes. We argue that integrating pediatric cohorts, particularly in underrepresented regions such as Latin America, with longitudinal biomarker approaches and omics technologies offers a unique opportunity to identify early predictors and preventive strategies. Understanding neurodegeneration as a lifespan process opens new avenues for early intervention and public health policy.

Background: Although most cases of childhood cancer are unlikely to be prevented, by today’s standards, most children with cancer can now be cured. However, disparities about survival exist among countries; in Mexico, the overall survival is 49.6%, with 70% of childhood cancers diagnosed at advanced stages. Therefore, parents and caregivers must have optimal knowledge of the early signs and symptoms of childhood malignancies as they are largely non-specific. This study was designed to explore the current knowledge of childhood cancer among parents and caregivers in Mexico and identify the need for education and health promotion in low- and middle-income countries. Methods: An online survey of 112 parents and caregivers was performed to assess their knowledge of childhood cancer, focusing on the signs and symptoms and early diagnostic strategies. Results: Sixty-nine (61.6%) mothers, 23 (20.5%) fathers, 17 (15.2%) familiar caregivers, and 3 (2.7%) non-familiar caregivers responded. Forty-six (41.1%) respondents said that they knew a child diagnosed with cancer, 92.9% mentioned leukemia as the most common type of cancer among children, the most highly ranked option when asked which sign/symptom they considered as a warning for suspicion was growth/lump in any part of the body, 97.3% considered that an early diagnosis is related to a higher cure rate, and 92.9% expressed the desire to receive reliable information about childhood cancer. Conclusions: Although parents and caregivers have some knowledge of childhood cancer, there are concepts that should be reinforced to improve their understanding of this group of diseases, as they are the frontline for children to seek medical attention. In the future, the use of tools that help educate more caregivers will strengthen knowledge and contribution regarding this issue and promote the generation of public policies that support the early diagnosis of childhood cancer.

Objective This study aimed to determine parents’ and school-aged children’s mental well-being after experiencing confinement and prolonged school closures during the COVID-19 pandemic. Design Using a cross-sectional design, an online survey was applied to parents of school-aged children inquiring about their mental well-being and COVID-19 pandemic changes in their home and working lives. To assess the presence of depression, anxiety and stress in parents, the participants responded to the Depression, Anxiety and Stress Scale - 21 scale. To assess psychosocial dysfunction and sleep disturbances in children, participants responded to the Pediatric Symptom Checklist and the Children Sleep Habits Questionnaire. Results A total of 209 parents answered the questionnaire, most of them were female (87.1%) with a mean age of 40 years. The prevalence of anxiety, stress and parental depression symptoms were 35.9%, 28.2% and 25.4%, respectively. Children’s mean age was 8.9 years, the prevalence of children’s psychosocial dysfunction was 12%, while their sleep disturbance symptoms were 59.8%. 10.5% of children were suffering both outcomes. We found a bidirectional relationship between parents’ and children’s mental health outcomes. Parental depression symptoms were associated with experiencing COVID-19 infection within the household, having children with pre-existing medical diagnoses, children’s psychosocial dysfunction and sleep disturbances. Children’s psychosocial dysfunction was associated with parental depression and changes in their school routine. Children’s sleep disturbances were associated with parental anxiety, younger age, increased use of electronic devices, night-time awakenings and shorter sleep time. Conclusion Our results support the impact of long confinement and school closure due to the COVID-19 pandemic in Mexican children and parents’ mental well-being. We advocate for specific mental health interventions tailored to respond to parents and children at risk of mental well-being distress.