Abstract
It is of great interest to understand how diet may influence the onset and progression of metabolic syndrome (MetS) in pediatric age groups, as MetS in childhood and adolescence is associated with an increased risk of cardiovascular disease and type-2 diabetes in adulthood. Recently, Azemati and colleagues (2020) reported no association between junk food intake and MetS in Iranian children and adolescents aged 7–18 years; however, we have identified some methodological limitations in this study, which are important to consider when examining MetS risk, especially in samples of this age. In response, we have developed a letter to the editor detailing the issues associated with defining MetS in pediatric age groups and how pubertal maturation and visceral adipose tissue are important variables to assess.
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Dear Editor,
Recently Azemati and colleagues [1] reported the associations between junk food consumption and cardiometabolic outcomes in a large cross-sectional dataset of Iranian children and adolescents. This is one of the largest studies in such regions and extends on the current evidence of poor diet in countries where obesity is increasingly becoming an issue. However, we have identified gaps and it would be important to consider these when developing an evidence base. Firstly, the authors defined the metabolic syndrome (MetS) according to the Adult Treatment Panel III criteria modified for the pediatric population. To date, there is no clear consensus as to whether MetS should be defined in children and adolescents; and considering the progressive nature of the condition, controversy surrounds the dichotomization of continuous cardiometabolic variables, as such an approach results in a loss of data and statistical power and can underestimate future disease risk [2, 3]. Consequently, it is recommended that research in pediatric populations focus on the clustering of continuous cardiometabolic variables [2] and this should be considered by the authors when interpreting their findings, as although they conclude that junk food intake was not related to MetS, it is indeed possible that junk food intake in this age group contributes to the progression of MetS in later life.
Additionally, the authors studied an age group with great variation in sexual maturation; however, data regarding participant’s pubertal stage was not collected nor adjusted for in the statistical analyses. This may have influenced the authors’ findings, as during puberty, children develop transient insulin resistance—a known determinant of MetS [3]. Finally, there are limitations inherent in using BMI as a measure of obesity and MetS risk, as individuals with a high BMI can present without metabolic abnormalities, particularly when they have little abdominal visceral adipose tissue (VAT) [4]. As such, VAT is thought to drive the cardiometabolic health risks associated with obesity [4] and so we argue that VAT should be assessed in Iranian children as a more reliable marker of MetS risk. Although authors did assess WHtR, this measure is not enough to quantify VAT and as discussed above, this measure was not adjusted for pubertal stage and was dichotomised, thereby reducing its predictive reliability. In summary, whilst Azemati and colleagues (2020) do provide insights into the role of junk food on metabolic syndrome in countries with changing dietary patterns, such studies should assess cardiometabolic risk factors as continuous variables and need to carefully consider puberty and VAT to provide the most accurate and reliable estimates.
References
Azemati B et al (2020) Association between junk food consumption and cardiometabolic risk factors in a national sample of Iranian children and adolescents population: the CASPIAN-V study. Eat Weight Disord 25(2):329–335. https://doi.org/10.1007/s40519-018-0591-1
Magge SN, Goodman E, Armstrong SC (2017) The metabolic syndrome in children and adolescents: shifting the focus to cardiometabolic risk factor clustering. Pediatrics 140(2):5–17. https://doi.org/10.1542/peds.2017-1603
Reinehr T (2016) Metabolic syndrome in children and adolescents: a critical approach considering the interaction between pubertal stage and insulin resistance. Curr Diab Rep 16(1):1–9. https://doi.org/10.1007/s11892-015-0695-1
Després J-P (2006) Is visceral obesity the cause of the metabolic syndrome? Ann Med 38(1):52–63. https://doi.org/10.1080/07853890500383895
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Gallagher, C., Moschonis, G. & Erbas, B. Current methods inadequate in assessing the association between junk food intake and metabolic syndrome in children and adolescents: letter to editor. Eat Weight Disord 26, 1277–1278 (2021). https://doi.org/10.1007/s40519-020-01011-5
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DOI: https://doi.org/10.1007/s40519-020-01011-5