Neck pain is a prevalent health problem, largely reported in adult patients. However, very recent data show that new technologies are inducing a shift in the prevalence of this relevant issue from adulthood to all of the pediatric ages. In fact, the precocious and inappropriate use of personal computers and especially cell phones might be related to the development of a complex cluster of clinical symptoms commonly defined as “text neck syndrome”. The purpose of this article is to analyze the new phenomenon of the “text neck syndrome”, the underlying causes and risk factors of musculoskeletal pain, that can be modified by changes in routine life, in different cultures and habits, and on the “text neck syndrome” as increased stresses on the cervical spine, that can lead to cervical degeneration along with other developmental, medical, psychological, and social complications. Findings support the contention that an appropriate approach for an early diagnosis and treatment is crucial to properly evaluate this emerging issue worldwide in children and adolescents who spend a lot of time watching smartphones and computers; additional research with more rigorous study designs and objective measures of musculoskeletal pain are needed to confirm significant relationships. Existing evidence is limited by non-objective measures and the subjective nature of musculoskeletal pain.

Oxidant-antioxidant status was investigated in a group of severely obese prepubertal children in comparison with healthy subjects and in relation to a dietary restriction-weight loss program. All subjects underwent anthropometric measurements and determination of lipid profile, lag phase, malondialdehyde (MDA), and vitamin E. Compared with controls, obese children had a significantly higher body mass index (BMI) (28.97 ± 2.42 vs. 16.03 ± 1.88 kg/m²; P = 0.0002) and waist-to-hip ratio (WHR) (0.89 ± 0.03 vs. 0.80 ± 0.01; P = 0.0004); lag phase and vitamin E levels were significantly decreased [24.05 ± 16.21 vs. 43.16 ± 10 min (P = 0.004) and 21.12 ± 14.96 vs. 35.54 ± 13.62 μmol/liter (P = 0.02), respectively], whereas MDA was significantly increased (0.90 ± 0.31 vs. 0.45 ± 0.24 nmol/mg; P = 0.001). Both lag phase and MDA significantly correlated with BMI [respectively, r = −0.34 (P = 0.004) and r = 0.57 (P = 0.002)] and WHR [respectively, r = −0.63 (P = 0.0001) and r = 0.38 (P = 0.04)]. Oxidant status normalized after 6 months of dietary restriction [lag phase, 59.11 ± 14.74 min (P = 0.002); MDA, 0.47 ± 0.09 nmol/mg (P = 0.003)], which was associated with a reduction of BMI (27.34 ± 1.87 kg/m²; P = 0.003), WHR (0.87 ± 0.02; P = 0.001), and fat mass (34.49 ± 2.68%; P = 0.008), but returned to baseline levels together with fatness indexes after another 6 months of free diet. Altered oxidant-antioxidant status is already present in prepubertal severely obese children and is reversible with a dietary restriction-weight loss program, which should be highly encouraged and maintained over time in this age group.

Objective: To investigate whether there is an association of the triglyceride-to-HDL cholesterol (TG:HDL-C) ratio with cardiovascular risk factors and early signs of vascular damage in obese prepubertal children.Design and methods: In 50 obese (27 boys, 7.8±1.4 years) and 37 normal-weight (20 boys; 7.3±1.5 years) prepubertal children, anthropometric measurements, oxidative stress markers (urinary isoprostanes (PGF2α (prostaglandin F2α)), soluble receptor for advanced glycation end-products (sRAGE)) and insulin sensitivity (homeostasis model assessment of insulin resistance (HOMA-IR) and whole-body insulin sensitivity index (WBISI)) were evaluated. Lipids profile was assessed and the TG:HDL-C ratio was calculated. In addition, high-resolution ultrasound was performed to assess carotid intima-media thickness (cIMT).Results: Obese children showed significantly higher values of the TG:HDL-C ratio (1.9±1.1 vs 1.2±0.6, P=0.002) compared with controls. After dividing the population in tertiles of the TG:HDL-C ratio (1.67), cIMT (P=0.0003), and HOMA-IR (P=0.0001) progressively increased from the lower to the upper tertile, whereas WBISI (P=0.0003) and sRAGE (P=0.05) progressively decreased. In a regression model, the TG:HDL ratio was significantly and positively associated with cIMT (r=0.493; P=0.0005). A cutoff point for TG:HDL-C ratio of 1.12 had 81% sensitivity and 49% specificity in the identification of children with cIMT values in the upper quartile (Area under the curve values from receiver operating characteristic curves=0.633±0.065, P=0.045).Conclusion: This study confirms the reliability of the TG:HDL-C ratio as a useful marker of cardiovascular risk. Interestingly, our results underline that the TG:HDL-C ratio is directly related with early signs of vascular damage already present in prepubertal children.