Translational Epigenomic Public Health: Gene and Environment Interaction and Disease Causation, Prevention and Control

Public health reflects what we can do as a society to remain healthy, with the core function of public health, indicative of assessment, policy, and assurance. Since human health does not merely involve an absence of physical disease process, but a complete state of social, economic, and mental well-being, hence global environment and health outcomes. Substantially, every day there is an encounter or daily interaction with the human environment, which affects the way in which the human gene is expressed and the subsequent gene product as protein molecules. Basically, social conditions such as social isolation, discrimination, racism, low SES, social adversity, and unemployment, as well as toxic waste, air pollutants, poor water and air qualities, climate warming, etc. have the tendency to alter human gene expression in a negative direction, implying increased disease development, poor prognosis, survival disadvantage, and excess mortality. Since social determinants of health (SDH) reflect social hierarchy and social gradient as the cause of causes in health disparities understanding and health disparities narrowing, however the ultimate elimination, as expressed by Healthy People, 2030 requires Epigenomic Determinants of Health (EDH) in health disparities narrowing and ultimate elimination, hence health equity transformation.  

Genes remain hereditary materials acquired through 23 pairs of chromosomes and exert fundamental functions in cellular development, differentiation, and maturation. Human proteins that serve as cell membranes, enzymes that catalyze biological activities and drug receptors that are molecules required for drug binding and response are all products of human gene expression, and if drug receptors are unenviable, there is no drug response, hence marginalized health outcome, excess mortality in childhood and adult disease.  

 Medicine and health  remain an inexact science, since the only known diagnosis is mortality, when and how is not very fully understood, indicative of mutualistic, collaborative, transdisciplinary, symbiotic, translational, team science and dynamic initiatives in the understanding of disease risk determinants, morbidity, therapeutics, prognosis, survival, and mortality. Since the disease process is significantly driven by environment and not gene, as DNA sequence (genomics), but gene and environment interaction, as epigenomic modulations in disease etiology, therapeutics, prognosis, and survival, there is a need to understand specific environments associated with DNA, and the application of such understanding in disease prevention and control, as well as therapeutics.There is a need for human beings  to understand specific environments and interactions with human gene as DNA sequence in impaired gene expression, protein synthesis, and cellular proliferation as cell synthesis, division, and maturation.

Specifically, epigenomic modulations reflect genes as DNA and environment interaction, such as stress, isolation, nutritional imbalance, air pollutants, toxic waste, poor water quality, etc., in transcriptomes elaboration, amino acid (AA) and protein synthesis, gene expression and cell synthesis, division and maturation in cellular proliferation. Human’s stress, isolation, anxiety, and depression trigger social signal transduction (SST), resulting in catecholamine elaboration and DNA methylation, which is explained by the DNA as helix transformation into tRNA, mRNA, transcriptomes with the methyl group, CH3 binding with the C-p-G (CH3-C-p-G), as DNA methylation, driven by DNA methylate enzyme as well as the RNA polymerase. The observed methyl-cytosine inhits transcriptomes elaboration, resulting in impaired protein synthesis, gene expression downregulation, and abnormal cellular proliferation, hence malignant neoplasm and other conditions including though not limited to Type II diabetes mellitus (T2DM), hypertension (Htn), major depressive disorder MDD), asthma, cardiovascular disease (CVDs), cerebrovascular disease (stroke), Parkinsonism, Dementia,  etc.  

Epigenomic public health (EPH) is a novel trajectory in the application of normal epigenomic modulations in disease understanding, as well as the utilization of abnormal epigenomic modulations knowledge in disease causation, control and prevention. With patients presenting with wheezing, shortness of breath, and coughing as the chief complaint, history taking remains vital as well as system review. These clinical features reflect malignancy, which requires confirmation with laboratory data/information. However, there are a number of cancer subtypes that present with different clinical manifestations and different responses to treatment and preventive measures, such as prostate cancer, ALL, AML, retinoblastoma, lymphoma, bronchial carcinoma, cervical carcinoma, breast cancer,  etc.

 With respect to epigenomic public health, the specific gene involved in prostate cancer requires epigenomic modulation via laboratory assessment, such as DNA methylation and histone modification through methylation, acetylation, or phosphorylation. Upon this aberrant epigenomic modulation and inverse gene expression of a specific gene, protein synthesis as certain drug receptors marginalizes, resulting in impaired drug response, poor disease outcome, and mortality. Since < 6.0% of the clinical condition is driven by genomic aberration, as abnormal DNA sequencing, DNA sequence (gene), and environment interaction predispose to multiple disease causation, such as malignant neoplasm (cancer) prostate, breast, lymphoma, bronchial, brain/CNS, ependymoma, hypertension, T2DM, obesity, CVAs, CVDs, asthma, there is a need for epigenomic public health initiative. This approach implies the understanding of drug transcriptome as drug receptors, protein synthesis, and normal cell proliferation, and the application of induction therapy in enhancing health improvement, hence epigenomic public health trajectory. Since gene expression enhances protein synthesis, this process facilitates drug receptors, indicative of drug response and improved therapeutics.