Climate Change and Global Warming Is Produced by Human Endosymbiotic Archaeal Overgrowth and Methanogenesis

Ravikumar Kurup, Parameswara Achutha Kurup

Abstract


ntroduction: The previous reports from this laboratory have demonstrated the existence and growth of endosymbiotic actinidic archaea in human population which has been related to disease states like schizophrenia, autism, metabolic syndrome, cancer, autoimmune disease and degenerations. The overgrowth of endosymbiotic actinidic archaea results in neanderthalisation of humans. The overgrowth of endosymbiotic archaea results from the growth of homo sapien civilization. The homo sapien civilization results in industrialization and production of carbon dioxide, a greenhouse gas. The homo sapien civilization also results in widespread use of electronic devices like mobile phones and internet producing interconnectivity and a globalised world. The resultant low level EMF pollution also results in endosymbiotic archaeal growth. Carbon dioxide is a major greenhouse gas whose effects are long term but moderate. The archaea are methanogenic organisms. Methanogenesis results from the production of methane from carbon dioxide and hydrogen. Methanogenesis can also occur from formate and acetate. Acetate is the end product of carbohydrate, protein and lipid catabolism in humans. The human nutritional sources get metabolically converted to acetate and acetyl CoA which can enter the citric acid cycle and mitochondrial oxidative phosphorylation. The presence of endosymbiotic actinidic archaea results in conversion of acetate to formate and methane. It also results in conversion of the ubiquitous carbon dioxide and hydrogen to methane. Thus the human body due to endosymbiosis by archaea becomes the principal source of methanogenesis. Methane is an important greenhouse gas. The effect of methane is short term as compared to carbon dioxide. Methane being a larger molecule can produce absorption of long range radiation and its global warming potential is 29 times that of carbon dioxide. Thus the principal culprit for global warming and eventual catastrophic extinction of human society is methane produced by human endosymbiotic archaea. The archaeal overgrowth due to global warming can affect ocean beds and lakes. This results in warming of the ocean and instability of methane hydrates in the ocean bed releasing methane. The arctic permafrost decays releasing organic carbon which can be a source of methanogenesis by archaea. The study was conducted to evaluate the growth of actinidic archaea in humans.
Materials and Methods: Cytochrome F420 levels were studied in the homo sapien population as well as human populations exhibiting the Neanderthal phenotype. Fifteen cases each of the above mentioned groups were chosen for the study. The blood samples were drawn in the fasting state. Cytochrome F420 was estimated flourimetrically (excitation wavelength 420 nm and emission wavelength 520 nm). The permission from the Ethics Committee of the Institute was obtained for this study.
Results: The study showed that there was increased cytochrome F420 levels in the population with Neanderthal phenotype in the blood. This indicated the growth of archaeal endosymbionts in the Neanderthal phenotype. There was also increased cytochrome F420 level in the normal homo sapien population but the extent of increase was small. The blood samples were drawn in the fasting state.
Discussion: Thus the increased production of greenhouse gases predominantly methane is from human sources alone due to increased growth of endosymbiotic 

archaea consequent to global warming triggered by industrial overproduction of carbon dioxide and EMF pollution. The homo sapien industrialisation is a small trigger but is rapidly taken over and dominated by endosymbiotic archaeal growth in humans. The archaeal overgrowth and neanderthalisation of homo sapiens converts the somatic cells to stem cells leading to cancer, autoimmune disease, degeneration and autism/schizophrenia in the neoneanderthal species. The Warburg phenotype of stem cells also produces the metabolic syndrome. The neoneanderthals becomes prone to civilisational disease. The neanderthalised humans stem cells phenotypes are retroviral resistant due to digoxin induced RNA editing, reverse transcriptase inhibition due to magnesium deficiency and membrane raft changes due to cholesterol depletion. The neanderthalised human stem cells serve as a reservoir for other species virus and bacteria resulting in breakage of the species barrier for infection. The archaeal symbionts can secrete RNA and DNA virus like particles which can recombine with expressed viral remnants in the genome as well as parts of the human genome per se producing new viruses and bacteria. The neanderthalised humans stem cells are resistant to infection which ravages the sensitive homo sapien phenotype exterminating them. Thus archaeal symbiosis, global warming, generation of new emerging viruses, pandemics of viral infections, homo sapien extinction and homo neanderthalis dominance becomes the rule. The realm of the homo neanderthalis sets in. The archaeal overgrowth in the oceanic beds and oceanic warming results in instability of methane hydrates in the ocean bed releasing methane. This produces global catastrophe. It results in oceanic earthquakes, continental shifts, tsunamis and flooding leading to eventual extinction of the human race of both species.
Conclusion: Thus the human body due to endosymbiosis by archaea becomes the principal source of methanogenesis. Methane is an important greenhouse gas. The effect of methane is short term as compared to carbon dioxide. Methane being a larger molecule can produce absorption of long range radiation and its global warming potential is 29 times that of carbon dioxide. Thus the principal culprit for global warming and eventual catastrophic extinction of human society is methane produced by human endosymbiotic archaea.


Keywords


Global warming; Greenhouse gas; Methane; Endosymbiotic; Archaea; Neanderthals; Retroviral resistance

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References


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DOI: http://dx.doi.org/10.3968/6030

DOI (PDF): http://dx.doi.org/10.3968/g6812

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