High Prevalence of Stunting and CKD-1/Obesity in Low- and Middle-nSES Population: A Review Article Support by p53-p21-p16 Axis
Abstract
Introduction: Stunting /pygmy or growth impairment parallel with obesity, is in high prevalence in the Aflatoxins exposure population, based on p16 upregulation. Mutation of p16 or epigenetic silencing, gives proliferation of BAT (UCP 132), SMCs (CKD-1), and later cancer cell proliferation and metastasis.
Method: Review articles using my Library, and academic search engines like PubMed, Science Direct, and EBSCOhost.
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Introduction
There is an urgent need to inform the public and political decision-maker (mainly the legislative) to lead people to mitigate AFB1exposure, and promote the technique in preparing clean food, and the useful of good foodstuff management 1,2,3,4 infighting most diseases5,6,7,8 especially stunting in low-and middle-neighborhood Socioeconomic Status (nSES) population.9 The people should throwaway the AFB1 exposure food which is not success to do until now.10,11 Moreover, don’tgive it to animals because Aflatoxin doesn’tdestruct with high temperatures till 250oC and metabolite to AFM1.11 Stunting/pygmy or growth impairment, associated with the p53-p21-p16 axis has been broadly known. This study focuses on upregulated p169,12,13 as tumor suppressor induce growth impairment mechanism, not the later stage which knockout of p16, induced proliferation.14,15,16,17,18,19,20,21 and cancer.22 Post-weaning associated with stunting23 and paradox downregulation,24 has been reported. Stern, 2001, has reported p53 mutation codon 249 in HCC patients in China (AFB1 Meta-Analysis).19 Leong, 2009: downregulated p53 induced upregulated p16 (p53-p21-p16) axis pathway.14
Conclusion
Evidence-Based Diagnosis of AFB1 exposure by urine AFM1 sub-ppb marker for public services, could decrease the prevalence of stunting which should be paralleled with Indonesian heritage management from A to Z to get zero-level food free of AFB1 exposure. Various molecular pathophysiological effect was already known as p53-p21-p16 axis pathways, that upregulation of p16INK4a slowdown the G1 S cell cycle and support the cause of stunting.
Urine AFM1 level represents aflatoxin B1 exposure is needed for public services simply to convince people, policymakers, legislation is urgent to fight stunting. We propose that legislation should address the role of AFB1 exposure in the pathogenesis of stunting and evaluate interventions to limit AFB1 exposure directly (UPLC) or indirectly (BMI/WC/SsST/refrigerator fullness) to reduce childhood stunting. Stunting and obesity are markers especially vulnerable to mycotoxin exposure.
