Archaeal Symbiosis and Digoxin Status Modulates Evolution of Homo Sapiens and Homo Neanderthalis - Digoxin Is a Neanderthal Hormone

Introduction: The climate change and global warming/ice age results in endosymbiotic actinidic archaeal growth in the human system and cholesterol catabolism resulting in endogenous digoxin synthesis. The increased endosymbiotic archaeal growth detected in autism and matrilineal communities with increased incidence of autism and neanderthalic origin leads to the conclusion that digoxin acts as neanderthalic hormone. The increased endosymbiotic archaeal growth and resultant endogenous digoxin synthesis in relation to climate change and global warming results in neanderthalisation of homo sapiens and human disease resulting in homo sapien extinction. Digoxin can inhibit reverse transcriptase activity and RNA editing resulting in suppression of endogenous retroviral growth. This produces inhibition of HERV expression and jumping gene phenomena producing in adynamicity of the human genome. HERV related jumping genes are crucial in synaptic diversity, HLA expression and immunomodulation as well as metabolic diversity. Digoxin produces alteration in sodium-hydrogen exchange producing an acidic pH and acts like a growth factor producing stem cell transformation of adult cells. Stem cells have a distinct metabolism with increased glycolysis and suppression of PDH and mitochondrial function. This can result in cancer and metabolic syndrome. The digoxin interference with RNA editing can lead to mutated RNA viruses and wide spread RNA viral epidemics. The digoxin interference with HERV expression and RNA editing and resultant inhibition of genomic, metabolic, neural and immune diversity produces autoimmune disease, cancer, metabolic syndrome, degenerations, schizophrenia and autism which are increasing at epidemic rates in human population. Materials and Methods: Endogenous digoxin levels and serum cytochrome F420 levels as a marker of archaeal growth were estimated in matrilineal communities, SLE, multiple sclerosis, parkinson’s disease, alzheimer’s disease, CNS glioma, multiple myeloma, metabolic syndrome x with CAD and CVA, schizophrenia and autism. 15 numbers were included in each group and each patient had an age and sex matched control. Endogenous digoxin was estimated by Elisa and cytochrome F420 estimated by spectrophotometry. The statistical analysis was done by ANOVA. Results: Endogenous digoxin levels and cytochrome F420 levels were elevated in matrilineal neanderthalic communities, SLE, multiple sclerosis, parkinson’s disease, alzheimer’s disease, CNS glioma, multiple myeloma, metabolic syndrome x with CAD and CVA, schizophrenia and autism. Endogenous