The TP53 Gene and the Revolution in Modern Science: Evidence of a Recent Mutational Peak and its Geochronological and Medical Implications

Sodré GB Neto

Summary 

The TP53 gene , known as the “guardian of the genome,” plays a central role in maintaining genetic stability, anti-aging, and preventing oncogenesis. Recent phylogenetic and archaeogenetic studies reveal a striking disparity between the diversity of pathogenic variants in modern humans versus archaic hominids, such as Neanderthals and Denisovans. While modern humans, as well as numerous examples of animals and plants, exhibit thousands of germline variations, evidence from ancient genomes suggests that many of these mutations arose in an extremely recent time window, approximately in the last 5,000 to 10,000 years. This phenomenon, termed a “mutational explosion,” challenges uniformitarian models of constant mutation rates and suggests that only the occurrence of global catastrophic radioactive events would justify such an explosion of mutations, which altered molecular clocks and the assumptions of constant decay in geochronology based on radiometric dating of constant nuclear clocks. Furthermore, understanding these paleogenetic patterns offers a revolutionary set of insights in geology, geochronology, paleontology, archaeology, and above all, opens new frontiers for precision medicine, enabling the development of gene and proteomic therapies, treatments with probiotics and commensal viruses, now perceived by paleogenetics as canonical genetic stretches with standard microRNA regulation, more capable and efficient for diverse treatments.  

1. Introduction 

The TP53 gene encodes the p53 protein, an essential transcription factor that regulates the cell cycle, DNA repair, and apoptosis [1, 5]. The integrity of this gene is vital for the survival of species, and its conservation in Neanderthals with larger brains than modern humans reinforces the idea that before this great catastrophe humans lived longer and were superior in intelligence according to studies by Gerald Crabtre [106] [1].

Analysis of modern human genetic variation reveals a complex scenario: thousands of pathogenic germline variants (PVs) and those considered “benign” (BVs) within the current low longevity standards, and are distributed across current populations [1, 13]. 

The central question that emerges from modern paleogenetics is the temporal origin of these variants. Recent studies using genomes of ancient humans and archaic hominids indicate that the vast majority of protein-coding variants in modern humans arose very recently in the history of our species [3, 16]. This article explores how this “mutational explosion” revolutionizes our understanding of biology, Earth history, and medicine.

We noticed that the same thing happens with a good number of animals which exhibit a mutational explosion at the same time, strengthening the thesis of a radioactive catastrophe that would leave marks mainly in the first sedimentary layer (Ediacaran).

With only ~2000 variations of TP53 present in modern humans, this requires a radioactive mutational spike on Earth, but we can verify several other species.

2. The Mutation Peak and Comparison with Archaic Hominids 

A comparison between the genomes of modern humans and those of Neanderthals and Denisovans reveals a striking quantitative and qualitative difference in TP53 variations . While modern humans have more than 2,000 documented variations, analyses of Neanderthal genomes show a predominance of the canonical variation (variation 1) or an extremely reduced number of pathogenic variants [1, 2]. 

Archaeogenetic research on over 5,000 ancient genomes dating back up to 45,000 years confirms that most pathogenic TP53 variants found today arose in the last 8,000 years [1]. Similarly, analysis of 6,515 modern exomes estimated that about 73% of all protein-coding single nucleotide variants (SNVs) and 86% of deleterious variants arose in the last 5,000 to 10,000 years [3, 43]. This data suggests a drastic deviation from mutation rates expected under a long-term equilibrium model. 

3. Radioactive Catastrophism and the Fall of Uniformitarianism 

The explanation for such a sudden and global mutational explosion requires mechanisms that transcend gradual biological processes. It is proposed that extreme geophysical events, such as large asteroid impacts, may have induced global nuclear phenomena [4, 18]. Such impacts generate pressures on the scale of Gigapascals and

High-temperature plasmas that can accelerate radioactive decay rates and induce spikes in ionizing radiation on the Earth’s surface [4, 22, 25]. 

This “radioactive peak” has profound implications for geochronology and molecular clocks: 

1. Geochronology: The premise that radioactive decay rates are constant over billions of years (uniformitarianism) is challenged by evidence that extreme environmental factors (plasma, pressure, electromagnetic fields) can disrupt these rates [25, 26, 29]. 
2. Molecular Clocks: The calibration of molecular clocks is based on the constant accumulation of mutations. A recent mutational peak brings the lineages of living and fossil beings to a much shorter time window than predicted by traditional models [33, 34, 50]. 
3. Implications for Modern Medicine and Paleogenetics 

Identifying genetic patterns “pre-mutational explosion” through paleogenetics opens revolutionary avenues for medicine: 

Gene Therapy and Proteomics: The use of canonical TP53 sequences (without recent deleterious mutations) as a template for p53 functional restoration therapies in cancer patients [39, 40, 77]. 

MicroRNAs and Regulation: MicroRNAs (miRNAs) play a crucial role in regulating TP53 expression and in the response to DNA damage [84, 85]. miRNA patterns identified in ancient genomes can serve as superior biomarkers for personalized diagnostics and treatments, focusing on control stretches without accumulated defects [36, 37, 102]. 

Precision Diagnosis: The understanding that many variants considered “normal” in modern databases may, in fact, be recent and deleterious mutations, allows for a more precise reclassification of genetic risks [1, 13, 66].

5. Conclusion 

The study of the TP53 gene from a paleogenetic and catastrophic perspective reveals that modern science is facing a paradigm shift. Evidence of a recent mutational peak not only redefines our evolutionary history but also questions the foundations of geological dating and offers unprecedented tools for curing complex diseases. The integration of nuclear physics, geology, and genetics is essential to deciphering the events that shaped current biodiversity and human health. We conclude by quoting one of the world’s greatest paleontologists and a Harvard professor, who, as early as 2023, shortly before his death, observed, agreeing with his doctoral student Kurt Patrick Wise and the repeated creationist claims:[107]

“Uniformitarianism is a dual concept that posits the uniformity of geological change rates and the temporal and spatial invariance of natural laws. The first is false and inhibits the formation of hypotheses; the second belongs to science as a whole and is not exclusive to geology. The first concept, called substantive uniformitarianism, is incorrect and should be abandoned; the second, called methodological uniformitarianism, is now superfluous and is better confined to the past history of geology.”

Selected References 

(The complete list of over 100 references is attached to the final document) 

1. Kou, S. H., et al. (2023). TP53 germline pathogenic variants in modern humans were likely originated during recent human history. NAR Cancer.
2. Zhao, B., et al. (2024). Pathogenic variants in human DNA damage repair genes mostly arose in recent human history. BMC Cancer.
3. Fu, W., et al. (2013). Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Nature.
4. Sodré Neto, GB, & Siman, HLHB (2025). The Contradictions of Uniformitarian Dating and Geochronology… Journal of Science . 
5. Levine, A. J. (2020). p53: 800 million years of evolution and 40 years of discovery. Nature Reviews Cancer. … (continua no anexo)

Complete List of Scientific References 

1. Kou, S. H., Li, J., Tam, B., Lei, H., Zhao, B., Xiao, F., … & Wang, S. M. (2023). TP53 germline pathogenic variants in modern humans were likely originated during recent human history. NAR Cancer, 5(3), zcad025.

https://doi.org/10.1093/narcancer/zcad025

2. Zhao, B., Li, J., Sinha, S., Qin, Z., Kou, S. H., Xiao, F., … & Wang, S. M. (2024). Pathogenic variants in human DNA damage repair genes mostly arose in recent

human history. BMC Cancer, 24(1), 415. https://doi.org/10.1186/s12885-024- 12160-6

3. Fu, W., O’Connor, T. D., Jun, G., Kang, H. M., Abecasis, G., Leal, S. M., … & Akey, J. M. (2013). Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Nature, 493(7431), 216-220.

https://doi.org/10.1038/nature11690

4. Sodré Neto, GB, & Siman, HLHB (2025). Uniformistic Datual and Geochronological Contradictions (Based on Almost Eternal Decay Constancy) Can Be Resolved by the Nuclear Effects of Large Impacts. Journal of Science. DOI: 10.13140/RG.2.2.35732.21120 
5. Levine, A. J. (2020). p53: 800 million years of evolution and 40 years of discovery. Nature Reviews Cancer, 20(8), 471-480.
6. Levine, A. J., & Oren, M. (2009). The first 30 years of p53: growing ever more complex. Nature Reviews Cancer, 9(10), 749-758.
7. Freed-Pastor, W. A., & Prives, C. (2012). Mutant p53: one name, many proteins. Genes & Development, 26(12), 1268-1286.
8. Baugh, E. H., Ke, H., Levine, A. J., Bonneau, R. A., & Chan, C. S. (2018). Why are there hotspot mutations in the TP53 gene in human cancers. Cell Death & Differentiation, 25(1), 154-160.
9. Monti, P., Menichini, P., Speciale, A., Cutrona, G., Fais, F., Taiana, E., … & Fronza, G. (2020). Heterogeneity of TP53 mutations and P53 protein residual function in cancer: does it matter?. Frontiers in Oncology, 10, 593383.
10. Li, J., Zhao, B., Huang, T., Qin, Z., & Wang, S. M. (2022). Human BRCA pathogenic variants were originated during recent human history. Life Science Alliance, 5(5), e202101263.
11. Lei, H., Li, J., Zhao, B., Kou, S. H., Xiao, F., Chen, T., & Wang, S. M. (2024). Evolutionary origin of germline pathogenic variants in human DNA mismatch repair genes. Human Genomics, 18(1), 5.
12. Greer, C., Bhakta, H., Ghanem, L., Refai, F., Linn, E., & Avella, M. (2021). Deleterious variants in genes regulating mammalian reproduction in Neanderthals, Denisovans and extant humans. Human Reproduction, 36(3), 734- 755.
13. Fortuno, C., James, P. A., & Spurdle, A. B. (2018). Current review of TP53 pathogenic germline variants in breast cancer patients outside Li-Fraumeni

syndrome. Human Mutation, 39(12), 1764-1773.

14. Petry, V., Bonadio, R. C., Cagnacci, A. Q. C., Senna, L. A. L., Campos, R. D. N. G., Cotti, G. C., … & Estevez-Diz, M. D. P. (2020). Radiotherapy-induced malignancies in breast cancer patients with TP53 pathogenic germline variants (Li-Fraumeni syndrome). Family Cancer, 19(1), 47-53.
15. Neagu, A. N., Whitham, D., Bruno, P., Arshad, A., Seymour, L., Morrissiey, H., … & Darie, C. C. (2024). Onco-Breastomics: An Eco-Evo-Devo Holistic Approach. International Journal of Molecular Sciences, 25(3), 1628.
16. He, J., Kou, S. H., Li, J., Ding, X., & Wang, S. M. (2024). Pathogenic variants in human DNA damage repair genes mostly arose after the latest human out-of Africa migration. Frontiers in Genetics, 15, 1408952.
17. Andaluz, S., Zhao, B., Sinha, S., Lagniton, P. N. P., Costa, D. A., Ding, X., … & Wang, S. M. (2024). Using Portuguese BRCA pathogenic variation as a model to study the impact of human admixture on human health. BMC Genomics, 25(1), 416.
18. Kring, D. A. (2007). The Chicxulub impact event and its environmental consequences. Chemie der Erde – Geochemistry, 67(1), 1–36.
19. Morgan, J. V., et al. (2022). The Chicxulub impact and its environmental consequences. Nature Reviews Earth & Environment, 3(4), 232–246.
20. Collins, G. S., et al. (2008). A numerical study of the formation of the Vredefort impact structure. Meteoritics & Planetary Science, 43(12), 1955–1966.
21. Navarro, K. F., et al. (2020). Emission spectra of a simulated Chicxulub impact vapor plume. Icarus, 345, 113735.
22. Kletetschka, G., et al. (2021). Plasma shielding removes prior magnetization record from impact melt. Scientific Reports, 11(1), 1–10.
23. Leckenby, G., et al. (2024). High-temperature 205Tl decay clarifies 205Pb dating in early solar system. Nature Communications, 15(1), 1–11.
24. Mishra, B., et al. (2023). Plasma β-Decay Rates in the Framework of PANDORA Project. EPJ Web of Conferences, 288, 02001.
25. Emery, G. T. (1972). Perturbation of nuclear decay rates. Annual Review of Nuclear Science, 22(1), 165–202.
26. Timashev, S. F. (2015). Radioactive decay as a forced nuclear chemical process: Phenomenology. Russian Journal of Physical Chemistry A, 89(11), 1903–1910.
27. Fischbach, E., et al. (2009). Time-dependent nuclear decay parameters: new evidence for new forces?. Space Science Reviews, 145(3-4), 285–305.
28. Pálffy, A., et al. (2020). Can Extreme Electromagnetic Fields Accelerate the α Decay of Atomic Nuclei?. Physical Review Letters, 124(21), 212505.
29. Carpinteri , A. , & Manuello , A. (2011). Geomechanical and Geochemical Evidence of Piezonuclear Fission Reactions in the Earth’s Crust. Strain, 47(s2), 267–281. 
30. Carpinteri, A., Lacidogna, G., & Manuello, A. (2012). Piezonuclear Fission Reactions in Rocks: Evidences from Microchemical Analysis, Neutron Emission, and Geological Transformation. Rock Mechanics and Rock Engineering, 45(4), 621–633.
31. Allen, N. H., et al. (2022). A Revision of the Formation Conditions of the Vredefort Crater. Journal of Geophysical Research: Planets, 127(5), e2022JE007186.
32. Taleyarkhan, R. P., et al. (2002). Evidence for nuclear emissions during acoustic cavitation. Science, 295(5561), 1868–1873.
33. Ho, S. Y. W., Phillips, M. J., Cooper, A., & Drummond, A. J. (2005). Time dependency of molecular rate estimates and systematic overestimation of recent divergence times. Molecular Biology and Evolution, 22(7), 1561-1568.
34. Moorjani, P., Amorim, C. E. G., Arndt, P. F., & Przeworski, M. (2016). Variation in the molecular clock of primates. Proceedings of the National Academy of Sciences, 113(38), 10607-10612.
35. Bromham, L., & Penny, D. (2003). The modern molecular clock. Nature Reviews Genetics, 4(3), 216-224.
36. Patel, V. D., & Capra, J. A. (2017). Ancient human miRNAs are more likely to have broad functions and disease associations than young miRNAs. BMC Genomics, 18(1), 668.
37. Faruq, O., & Vecchione, A. (2015). microRNA: diagnostic perspective. Frontiers in Medicine, 2, 51. 
38. Ambros, V. (2008). The evolution of our thinking about microRNAs. Nature Medicine, 14(10), 1036-1041.
39. Peng, Y., Bai, J., Li, W., Su, Z., & Cheng, X. (2024). Advancements in p53-Based Anti-Tumor Gene Therapy Research. Molecules, 29(22), 5315. 
40. Valente, J. F. A., Queiroz, J. A., & Sousa, F. (2018). p53 as the focus of gene therapy: past, present and future. Current Drug Targets, 19(15), 1801-1817.
41. Simons, Y. B., Turchin, M. C., Pritchard, J. K., & Sella, G. (2014). The deleterious mutation load is insensitive to recent population history. Nature Genetics, 46(3), 220-224.
42. Gazave, E., Chang, D., Clark, A. G., & Keinan, A. (2013). Population growth inflates the per-individual number of deleterious mutations and reduces their mean effect. Genetics, 195(3), 969-978.
43. Keinan, A., & Clark, A. G. (2012). Recent explosive human population growth has resulted in an excess of rare genetic variants. Science, 336(6082), 740-743.
44. Tennessen, J. A., Bigham, A. W., O’Connor, T. D., Fu, W., Kenny, E. E., Gravel, S., … & Akey, J. M. (2012). Evolution and functional impact of rare coding variation from deep sequencing of human exomes. Science, 337(6090), 64-69.
45. Nelson, J. J., et al. (2012). An abundance of rare functional genetic variation in 202 human genes. Science, 337(6090), 100-104.
46. Marth, G. T., Yu, F., Indap, A. R., Garimella, K., Gravel, S., Leong, W. F., … & 1000 Genomes Project. (2011). The functional spectrum of low-frequency coding variation in human populations. Genome Biology, 12(9), R84.
47. Coventry, A., et al. (2010). Deep resequencing reveals excess rare variants in genes associated with inflammation. Nature Communications, 1, 131.
48. Gravel, S., et al. (2011). Demographic history and rare allele sharing among human populations. Proceedings of the National Academy of Sciences, 108(29), 11983-11988.
49. Lohmueller, K. E., et al. (2008). Proportionally more deleterious genetic variation in European than in African populations. Nature, 451(7181), 994-997.
50. Subramanian, S. (2016). Evidence for recent, population-specific evolution of the human molecular clock. Proceedings of the National Academy of Sciences, 113(38), 10607-10612.
51. Ho, S. Y. W., & Larson, G. (2006). Molecular clocks: when times are a-changin’. Trends in Genetics, 22(2), 79-83.
52. Penny, D. (2005). Relativity for molecular clocks. Nature, 436(7048), 183-184.
53. Pulit, S. L., et al. (2017). The impact of recent population history on the deleterious mutation load in humans and close evolutionary relatives. Current Opinion in Genetics & Development, 41, 150-156.
54. Henn, B. M., et al. (2016). Distance from Africa predicts mutational load in human populations. Proceedings of the National Academy of Sciences, 113(4), E440- E449.
55. Do, R., et al. (2015). No evidence that selection has been less effective at removing deleterious mutations in Europeans than in Africans. Nature Genetics, 47(2), 126-131.
56. Kring, D. A., & Cohen, B. A. (2002). Cataclysmic bombardment throughout the inner solar system 3.9–4.0 Ga. Journal of Geophysical Research: Planets, 107(E2), 4-1.
57. Melosh, H. J. (1989). Impact Cratering: A Geologic Process. Oxford University Press.
58. Reimold, W. U., & Gibson, R. L. (2010). Meteorite Impact!: The Danger from Space and South Africa’s Mega-Impact The Vredefort Structure. Springer Science & Business Media.
59. Gentry, R. V. (1986). Creation’s Tiny Mystery. Earth Science Associates.
60. Snelling, A. A. (2005). Radioisotopes and the Age of the Earth: Results of a Young Earth Creationist Research Initiative. Institute for Creation Research.
61. Vardiman, L., Snelling, A. A., & Chaffin, E. F. (2000). Radioisotopes and the Age of the Earth: A Young-Earth Creationist Research Initiative. Institute for Creation Research.
62. Chaffin, E. F. (2003). Accelerated Decay: Theoretical Considerations. Proceedings of the Fifth International Conference on Creationism.
63. Humphreys, D. R. (2003). New evidence for accelerated nuclear decay. Proceedings of the Fifth International Conference on Creationism.
64. Austin, S. A. (2005). Do radioisotope clocks need repair? Testing the assumptions of isochron dating using K-Ar, Rb-Sr, Sm-Nd, and Pb-Pb isotopes. Radioisotopes and the Age of the Earth, 2, 325-392.
65. Baumgardner, J. R. (2005). Carbon-14 evidence for a recent global flood and a young earth. Radioisotopes and the Age of the Earth, 2, 587-630.
66. De Andrade, K. C., et al. (2021). Cancer incidence, patterns, and genotype– phenotype associations in individuals with pathogenic or likely pathogenic germline TP53 variants: an observational cohort study. The Lancet Oncology, 22(11), 1595-1610.
67. Khincha, P. P., et al. (2019). Genetic and clinical characteristics of individuals with Li-Fraumeni syndrome. Journal of Clinical Oncology, 37(15), 1500.
68. Malkin, D. (2011). Li-Fraumeni syndrome. Genes & Cancer, 2(4), 475-484.
69. Olivier, M., et al. (2010). The IARC TP53 database: new features and updates. Human Mutation, 31(6), 631-640.
70. Petitjean, A., et al. (2007). Impact of mutant p53 functional properties on TP53 mutation patterns and clinical outcomes: lessons from the IARC TP53 database. Human Mutation, 28(6), 622-629.
71. Soussi, T., & Lozano, G. (2005). p53 mutation heterogeneity in cancer: can the immune response provide a clue for personalized medicine? Cancer Cell, 8(5), 349-351.
72. Hainaut, P., & Pfeifer, G. P. (2016). Somatic TP53 Mutations as a Signature of Environmental Carcinogens. Seminars in Cancer Biology, 38, 77-87.
73. Kandoth, C., et al. (2013). Mutational landscape and significance across 12 major cancer types. Nature, 502(7471), 333-339.
74. Lawrence, M. S., et al. (2014). Discovery and saturation analysis of cancer genes across 21 tumour types. Nature, 505(7484), 495-501.
75. Vogelstein, B., et al. (2013). Cancer genome landscapes. Science, 339(6127), 1546- 1558.
76. He, H. (2025). Targeting TP53TG1: A promising prognostic biomarker and therapeutic target for personalized cancer therapy. Discover Oncology, 16(1), 1- 15.
77. Xu, B., et al. (2025). The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs. Biomolecules, 15(8), 1088.
78. Patel, V. D., & Capra, J. A. (2017). Ancient human miRNAs are more likely to have broad functions and disease associations than young miRNAs. BMC Genomics, 18(1), 668.
79. Ambros, V. (2004). The functions of animal microRNAs. Nature, 431(7006), 350- 355.
80. Bartel, D. P. (2004). MicroRNAs: genomics, biogenesis, mechanism, and function. Cell, 116(2), 281-297.
81. Lu, J., et al. (2005). MicroRNA expression profiles classify human cancers. Nature, 435(7043), 834-838.
82. Calin, G. A., & Croce, C. M. (2006). MicroRNA signatures in human cancers. Nature Reviews Cancer, 6(11), 857-866.
83. Esquela-Kerscher, A., & Slack, F. J. (2006). Oncomirs—microRNAs with a role in cancer. Nature Reviews Cancer, 6(4), 259-269.
84. He, L., et al. (2007). A microRNA component of the p53 tumour suppressor network. Nature, 447(7148), 1130-1134.
85. Raver-Shapira, N., et al. (2007). Transcriptional activation of miR-34a by p53 mediates p53-induced apoptosis. Molecular Cell, 26(5), 731-743.
86. Tarasov, V., et al. (2007). Differential regulation of microRNAs by p53 revealed by genome-wide expression profiling: p53-regulated microRNAs can suppress proliferation of colon cancer cells. Cell Cycle, 6(13), 1586-1593.
87. Chang, T. C., et al. (2007). Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Molecular Cell, 26(5), 745-752.
88. Hermeking, H. (2010). The miR-34 family in cancer and apoptosis. Cell Death & Differentiation, 17(2), 193-199.
89. Kim, V. N., Han, J., & Siomi, M. C. (2009). Biogenesis of small RNAs in animals. Nature Reviews Molecular Cell Biology, 10(2), 126-139.
90. Friedman, R. C., et al. (2009). Most mammalian mRNAs are conserved targets of microRNAs. Genome Research, 19(1), 92-105.
91. Lewis, B. P., Burge, C. B., & Bartel, D. P. (2005). Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets. Cell, 120(1), 15-20.
92. Grimson, A., et al. (2007). MicroRNA targeting specificity in mammals: determinants beyond seed pairing. Molecular Cell, 27(1), 91-105.
93. Garcia, D. M., et al. (2011). Weak seed-pairing stability and high target-site abundance decrease the proficiency of lsy-6 and other microRNAs. Nature Structural & Molecular Biology, 18(10), 1139-1146.
94. Betel, D., et al. (2010). Comprehensive modeling of microRNA targets predicts functional non-conserved and conserved targets. BMC Bioinformatics, 11(1), 431.
95. Agarwal, V., et al. (2015). Predicting effective microRNA target sites in mammalian mRNAs. eLife, 4, e05005.
96. Krol, J., Loedige, I., & Filipowicz, W. (2010). The widespread regulation of microRNA biogenesis, function and decay. Nature Reviews Genetics, 11(9), 597- 610.
97. Pasquinelli, A. E. (2012). MicroRNAs: deviants from the model. Nature Reviews Genetics, 13(4), 273-282.
98. Ha, M., & Kim, V. N. (2014). Regulation of microRNA biogenesis. Nature Reviews Molecular Cell Biology, 15(8), 509-524.
99. Jonas, S., & Izaurralde, E. (2015). Towards a molecular understanding of microRNA-mediated gene silencing. Nature Reviews Genetics, 16(7), 421-433.
100. Gebert, L. F., & MacRae, I. J. (2019). Regulation of microRNA function in animals. Nature Reviews Molecular Cell Biology, 20(1), 21-37.
101. O’Brien, J., et al. (2018). Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Clinical Applications. Frontiers in Endocrinology, 9, 402.
102. Rupaimoole, R., & Slack, F. J. (2017). MicroRNA therapeutics: towards a new era for the management of cancer and other diseases. Nature Reviews Drug Discovery, 16(3), 203-222.
103. Ling, H., Fabbri, M., & Calin, G. A. (2013). MicroRNAs and other non-coding RNAs as targets for anticancer drug development. Nature Reviews Drug Discovery, 12(11), 847-865.
104. Hayes, J., Peruzzi, P. P., & Lawler, S. (2014). MicroRNAs in cancer: biomarkers, functions and therapy. Trends in Molecular Medicine, 20(8), 460-469.
105. Hummel, R., et al. (2010). MicroRNAs: precursors and indicators of cancer. Molecular Oncology, 4(2), 137-161.
106. Crabtree GR. Our fragile intellect. Part I. Trends Genet. 2013 Jan;29(1):1-3. doi: 10.1016/j.tig.2012.10.002. Epub 2012 Nov 12. PMID: 23153596. https://pubmed.ncbi.nlm.nih.gov/23153596/
107. Gould, SJ (March 1, 1965).  “Is uniformitarianism necessary?” .  American Journal of Science  (in English) (3): 223–228.  ISSN  0002-9599 .  doi : 10.2475/ajs.263.3.223 . Retrieved March 20, 2023

1. Kou, S. H., Li, J., Tam, B., Lei, H., Zhao, B., Xiao, F., ... & Wang, S. M. (2023). TP53 germline pathogenic variants in modern humans were likely originated during recent human history. NAR Cancer, 5(3), zcad025. https://doi.org/10.1093/narcancer/zcad025
2. Zhao, B., Li, J., Sinha, S., Qin, Z., Kou, S. H., Xiao, F., ... & Wang, S. M. (2024). Pathogenic variants in human DNA damage repair genes mostly arose in recent human history. BMC Cancer, 24(1), 415. https://doi.org/10.1186/s12885-024-12160-6
3. Fu, W., O’Connor, T. D., Jun, G., Kang, H. M., Abecasis, G., Leal, S. M., ... & Akey, J. M. (2013). Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Nature, 493(7431), 216-220. https://doi.org/10.1038/nature11690
4. Sodré Neto, G. B., & Siman, H. L. H. B. (2025). As Contradições Datacionais e Geocronológicas Uniformistas (Baseadas em Constância Quase Eterna de Decaimento) Podem Ser Resolvidas pelos Efeitos Nucleares dos Grandes Impactos. Jornal da Ciência. DOI: 10.13140/RG.2.2.35732.21120
5. Levine, A. J. (2020). p53: 800 million years of evolution and 40 years of discovery. Nature Reviews Cancer, 20(8), 471-480.
6. Levine, A. J., & Oren, M. (2009). The first 30 years of p53: growing ever more complex. Nature Reviews Cancer, 9(10), 749-758.
7. Freed-Pastor, W. A., & Prives, C. (2012). Mutant p53: one name, many proteins. Genes & Development, 26(12), 1268-1286.
8. Baugh, E. H., Ke, H., Levine, A. J., Bonneau, R. A., & Chan, C. S. (2018). Why are there hotspot mutations in the TP53 gene in human cancers. Cell Death & Differentiation, 25(1), 154-160.
9. Monti, P., Menichini, P., Speciale, A., Cutrona, G., Fais, F., Taiana, E., ... & Fronza, G. (2020). Heterogeneity of TP53 mutations and P53 protein residual function in cancer: does it matter?. Frontiers in Oncology, 10, 593383.
10. Li, J., Zhao, B., Huang, T., Qin, Z., & Wang, S. M. (2022). Human BRCA pathogenic variants were originated during recent human history. Life Science Alliance, 5(5), e202101263.
11. Lei, H., Li, J., Zhao, B., Kou, S. H., Xiao, F., Chen, T., & Wang, S. M. (2024). Evolutionary origin of germline pathogenic variants in human DNA mismatch repair genes. Human Genomics, 18(1), 5.
12. Greer, C., Bhakta, H., Ghanem, L., Refai, F., Linn, E., & Avella, M. (2021). Deleterious variants in genes regulating mammalian reproduction in Neanderthals, Denisovans and extant humans. Human Reproduction, 36(3), 734-755.
13. Fortuno, C., James, P. A., & Spurdle, A. B. (2018). Current review of TP53 pathogenic germline variants in breast cancer patients outside Li-Fraumeni syndrome. Human Mutation, 39(12), 1764-1773.
14. Petry, V., Bonadio, R. C., Cagnacci, A. Q. C., Senna, L. A. L., Campos, R. D. N. G., Cotti, G. C., ... & Estevez-Diz, M. D. P. (2020). Radiotherapy-induced malignancies in breast cancer patients with TP53 pathogenic germline variants (Li-Fraumeni syndrome). Family Cancer, 19(1), 47-53.
15. Neagu, A. N., Whitham, D., Bruno, P., Arshad, A., Seymour, L., Morrissiey, H., ... & Darie, C. C. (2024). Onco-Breastomics: An Eco-Evo-Devo Holistic Approach. International Journal of Molecular Sciences, 25(3), 1628.
16. He, J., Kou, S. H., Li, J., Ding, X., & Wang, S. M. (2024). Pathogenic variants in human DNA damage repair genes mostly arose after the latest human out-of-Africa migration. Frontiers in Genetics, 15, 1408952.
17. Andaluz, S., Zhao, B., Sinha, S., Lagniton, P. N. P., Costa, D. A., Ding, X., ... & Wang, S. M. (2024). Using Portuguese BRCA pathogenic variation as a model to study the impact of human admixture on human health. BMC Genomics, 25(1), 416.
18. Kring, D. A. (2007). The Chicxulub impact event and its environmental consequences. Chemie der Erde – Geochemistry, 67(1), 1–36.
19. Morgan, J. V., et al. (2022). The Chicxulub impact and its environmental consequences. Nature Reviews Earth & Environment, 3(4), 232–246.
20. Collins, G. S., et al. (2008). A numerical study of the formation of the Vredefort impact structure. Meteoritics & Planetary Science, 43(12), 1955–1966.
21. Navarro, K. F., et al. (2020). Emission spectra of a simulated Chicxulub impact-vapor plume. Icarus, 345, 113735.
22. Kletetschka, G., et al. (2021). Plasma shielding removes prior magnetization record from impact melt. Scientific Reports, 11(1), 1–10.
23. Leckenby, G., et al. (2024). High-temperature 205Tl decay clarifies 205Pb dating in early solar system. Nature Communications, 15(1), 1–11.
24. Mishra, B., et al. (2023). Plasma β-Decay Rates in the Framework of PANDORA Project. EPJ Web of Conferences, 288, 02001.
25. Emery, G. T. (1972). Perturbation of nuclear decay rates. Annual Review of Nuclear Science, 22(1), 165–202.
26. Timashev, S. F. (2015). Radioactive decay as a forced nuclear chemical process: Phenomenology. Russian Journal of Physical Chemistry A, 89(11), 1903–1910.
27. Fischbach, E., et al. (2009). Time-dependent nuclear decay parameters: new evidence for new forces?. Space Science Reviews, 145(3-4), 285–305.
28. Pálffy, A., et al. (2020). Can Extreme Electromagnetic Fields Accelerate the α Decay of Atomic Nuclei?. Physical Review Letters, 124(21), 212505.
29. Carpinteri, A., & Manuello, A. (2011). Geomechanical and Geochemical Evidence of Piezonuclear Fission Reactions in the Earth’s Crust. Strain, 47(s2), 267–281.
30. Carpinteri, A., Lacidogna, G., & Manuello, A. (2012). Piezonuclear Fission Reactions in Rocks: Evidences from Microchemical Analysis, Neutron Emission, and Geological Transformation. Rock Mechanics and Rock Engineering, 45(4), 621–633.
31. Allen, N. H., et al. (2022). A Revision of the Formation Conditions of the Vredefort Crater. Journal of Geophysical Research: Planets, 127(5), e2022JE007186.
32. Taleyarkhan, R. P., et al. (2002). Evidence for nuclear emissions during acoustic cavitation. Science, 295(5561), 1868–1873.
33. Ho, S. Y. W., Phillips, M. J., Cooper, A., & Drummond, A. J. (2005). Time dependency of molecular rate estimates and systematic overestimation of recent divergence times. Molecular Biology and Evolution, 22(7), 1561-1568.
34. Moorjani, P., Amorim, C. E. G., Arndt, P. F., & Przeworski, M. (2016). Variation in the molecular clock of primates. Proceedings of the National Academy of Sciences, 113(38), 10607-10612.
35. Bromham, L., & Penny, D. (2003). The modern molecular clock. Nature Reviews Genetics, 4(3), 216-224.
36. Patel, V. D., & Capra, J. A. (2017). Ancient human miRNAs are more likely to have broad functions and disease associations than young miRNAs. BMC Genomics, 18(1), 668.
37. Faruq, O., & Vecchione, A. (2015). microRNA: diagnostic perspective. Frontiers in Medicine, 2, 51.
38. Ambros, V. (2008). The evolution of our thinking about microRNAs. Nature Medicine, 14(10), 1036-1041.
39. Peng, Y., Bai, J., Li, W., Su, Z., & Cheng, X. (2024). Advancements in p53-Based Anti-Tumor Gene Therapy Research. Molecules, 29(22), 5315.
40. Valente, J. F. A., Queiroz, J. A., & Sousa, F. (2018). p53 as the focus of gene therapy: past, present and future. Current Drug Targets, 19(15), 1801-1817.
41. Simons, Y. B., Turchin, M. C., Pritchard, J. K., & Sella, G. (2014). The deleterious mutation load is insensitive to recent population history. Nature Genetics, 46(3), 220-224.
42. Gazave, E., Chang, D., Clark, A. G., & Keinan, A. (2013). Population growth inflates the per-individual number of deleterious mutations and reduces their mean effect. Genetics, 195(3), 969-978.
43. Keinan, A., & Clark, A. G. (2012). Recent explosive human population growth has resulted in an excess of rare genetic variants. Science, 336(6082), 740-743.
44. Tennessen, J. A., Bigham, A. W., O'Connor, T. D., Fu, W., Kenny, E. E., Gravel, S., ... & Akey, J. M. (2012). Evolution and functional impact of rare coding variation from deep sequencing of human exomes. Science, 337(6090), 64-69.
45. Nelson, J. J., et al. (2012). An abundance of rare functional genetic variation in 202 human genes. Science, 337(6090), 100-104.
46. Marth, G. T., Yu, F., Indap, A. R., Garimella, K., Gravel, S., Leong, W. F., ... & 1000 Genomes Project. (2011). The functional spectrum of low-frequency coding variation in human populations. Genome Biology, 12(9), R84.
47. Coventry, A., et al. (2010). Deep resequencing reveals excess rare variants in genes associated with inflammation. Nature Communications, 1, 131.
48. Gravel, S., et al. (2011). Demographic history and rare allele sharing among human populations. Proceedings of the National Academy of Sciences, 108(29), 11983-11988.
49. Lohmueller, K. E., et al. (2008). Proportionally more deleterious genetic variation in European than in African populations. Nature, 451(7181), 994-997.
50. Subramanian, S. (2016). Evidence for recent, population-specific evolution of the human molecular clock. Proceedings of the National Academy of Sciences, 113(38), 10607-10612.
51. Ho, S. Y. W., & Larson, G. (2006). Molecular clocks: when times are a-changin'. Trends in Genetics, 22(2), 79-83.
52. Penny, D. (2005). Relativity for molecular clocks. Nature, 436(7048), 183-184.
53. Pulit, S. L., et al. (2017). The impact of recent population history on the deleterious mutation load in humans and close evolutionary relatives. Current Opinion in Genetics & Development, 41, 150-156.
54. Henn, B. M., et al. (2016). Distance from Africa predicts mutational load in human populations. Proceedings of the National Academy of Sciences, 113(4), E440-E449.
55. Do, R., et al. (2015). No evidence that selection has been less effective at removing deleterious mutations in Europeans than in Africans. Nature Genetics, 47(2), 126-131.
56. Kring, D. A., & Cohen, B. A. (2002). Cataclysmic bombardment throughout the inner solar system 3.9–4.0 Ga. Journal of Geophysical Research: Planets, 107(E2), 4-1.
57. Melosh, H. J. (1989). Impact Cratering: A Geologic Process. Oxford University Press.
58. Reimold, W. U., & Gibson, R. L. (2010). Meteorite Impact!: The Danger from Space and South Africa’s Mega-Impact The Vredefort Structure. Springer Science & Business Media.
59. Gentry, R. V. (1986). Creation's Tiny Mystery. Earth Science Associates.
60. Snelling, A. A. (2005). Radioisotopes and the Age of the Earth: Results of a Young-Earth Creationist Research Initiative. Institute for Creation Research.
61. Vardiman, L., Snelling, A. A., & Chaffin, E. F. (2000). Radioisotopes and the Age of the Earth: A Young-Earth Creationist Research Initiative. Institute for Creation Research.
62. Chaffin, E. F. (2003). Accelerated Decay: Theoretical Considerations. Proceedings of the Fifth International Conference on Creationism.
63. Humphreys, D. R. (2003). New evidence for accelerated nuclear decay. Proceedings of the Fifth International Conference on Creationism.
64. Austin, S. A. (2005). Do radioisotope clocks need repair? Testing the assumptions of isochron dating using K-Ar, Rb-Sr, Sm-Nd, and Pb-Pb isotopes. Radioisotopes and the Age of the Earth, 2, 325-392.
65. Baumgardner, J. R. (2005). Carbon-14 evidence for a recent global flood and a young earth. Radioisotopes and the Age of the Earth, 2, 587-630.
66. De Andrade, K. C., et al. (2021). Cancer incidence, patterns, and genotype–phenotype associations in individuals with pathogenic or likely pathogenic germline TP53 variants: an observational cohort study. The Lancet Oncology, 22(11), 1595-1610.
67. Khincha, P. P., et al. (2019). Genetic and clinical characteristics of individuals with Li-Fraumeni syndrome. Journal of Clinical Oncology, 37(15), 1500.
68. Malkin, D. (2011). Li-Fraumeni syndrome. Genes & Cancer, 2(4), 475-484.
69. Olivier, M., et al. (2010). The IARC TP53 database: new features and updates. Human Mutation, 31(6), 631-640.
70. Petitjean, A., et al. (2007). Impact of mutant p53 functional properties on TP53 mutation patterns and clinical outcomes: lessons from the IARC TP53 database. Human Mutation, 28(6), 622-629.
71. Soussi, T., & Lozano, G. (2005). p53 mutation heterogeneity in cancer: can the immune response provide a clue for personalized medicine? Cancer Cell, 8(5), 349-351.
72. Hainaut, P., & Pfeifer, G. P. (2016). Somatic TP53 Mutations as a Signature of Environmental Carcinogens. Seminars in Cancer Biology, 38, 77-87.
73. Kandoth, C., et al. (2013). Mutational landscape and significance across 12 major cancer types. Nature, 502(7471), 333-339.
74. Lawrence, M. S., et al. (2014). Discovery and saturation analysis of cancer genes across 21 tumour types. Nature, 505(7484), 495-501.
75. Vogelstein, B., et al. (2013). Cancer genome landscapes. Science, 339(6127), 1546-1558.
76. He, H. (2025). Targeting TP53TG1: A promising prognostic biomarker and therapeutic target for personalized cancer therapy. Discover Oncology, 16(1), 1-15.
77. Xu, B., et al. (2025). The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs. Biomolecules, 15(8), 1088.
78. Patel, V. D., & Capra, J. A. (2017). Ancient human miRNAs are more likely to have broad functions and disease associations than young miRNAs. BMC Genomics, 18(1), 668.
79. Ambros, V. (2004). The functions of animal microRNAs. Nature, 431(7006), 350-355.
80. Bartel, D. P. (2004). MicroRNAs: genomics, biogenesis, mechanism, and function. Cell, 116(2), 281-297.
81. Lu, J., et al. (2005). MicroRNA expression profiles classify human cancers. Nature, 435(7043), 834-838.
82. Calin, G. A., & Croce, C. M. (2006). MicroRNA signatures in human cancers. Nature Reviews Cancer, 6(11), 857-866.
83. Esquela-Kerscher, A., & Slack, F. J. (2006). Oncomirs—microRNAs with a role in cancer. Nature Reviews Cancer, 6(4), 259-269.
84. He, L., et al. (2007). A microRNA component of the p53 tumour suppressor network. Nature, 447(7148), 1130-1134.
85. Raver-Shapira, N., et al. (2007). Transcriptional activation of miR-34a by p53 mediates p53-induced apoptosis. Molecular Cell, 26(5), 731-743.
86. Tarasov, V., et al. (2007). Differential regulation of microRNAs by p53 revealed by genome-wide expression profiling: p53-regulated microRNAs can suppress proliferation of colon cancer cells. Cell Cycle, 6(13), 1586-1593.
87. Chang, T. C., et al. (2007). Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Molecular Cell, 26(5), 745-752.
88. Hermeking, H. (2010). The miR-34 family in cancer and apoptosis. Cell Death & Differentiation, 17(2), 193-199.
89. Kim, V. N., Han, J., & Siomi, M. C. (2009). Biogenesis of small RNAs in animals. Nature Reviews Molecular Cell Biology, 10(2), 126-139.
90. Friedman, R. C., et al. (2009). Most mammalian mRNAs are conserved targets of microRNAs. Genome Research, 19(1), 92-105.
91. Lewis, B. P., Burge, C. B., & Bartel, D. P. (2005). Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets. Cell, 120(1), 15-20.
92. Grimson, A., et al. (2007). MicroRNA targeting specificity in mammals: determinants beyond seed pairing. Molecular Cell, 27(1), 91-105.
93. Garcia, D. M., et al. (2011). Weak seed-pairing stability and high target-site abundance decrease the proficiency of lsy-6 and other microRNAs. Nature Structural & Molecular Biology, 18(10), 1139-1146.
94. Betel, D., et al. (2010). Comprehensive modeling of microRNA targets predicts functional non-conserved and conserved targets. BMC Bioinformatics, 11(1), 431.
95. Agarwal, V., et al. (2015). Predicting effective microRNA target sites in mammalian mRNAs. eLife, 4, e05005.
96. Krol, J., Loedige, I., & Filipowicz, W. (2010). The widespread regulation of microRNA biogenesis, function and decay. Nature Reviews Genetics, 11(9), 597-610.
97. Pasquinelli, A. E. (2012). MicroRNAs: deviants from the model. Nature Reviews Genetics, 13(4), 273-282.
98. Ha, M., & Kim, V. N. (2014). Regulation of microRNA biogenesis. Nature Reviews Molecular Cell Biology, 15(8), 509-524.
99. Jonas, S., & Izaurralde, E. (2015). Towards a molecular understanding of microRNA-mediated gene silencing. Nature Reviews Genetics, 16(7), 421-433.
100. Gebert, L. F., & MacRae, I. J. (2019). Regulation of microRNA function in animals. Nature Reviews Molecular Cell Biology, 20(1), 21-37.
101. O'Brien, J., et al. (2018). Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Clinical Applications. Frontiers in Endocrinology, 9, 402.
102. Rupaimoole, R., & Slack, F. J. (2017). MicroRNA therapeutics: towards a new era for the management of cancer and other diseases. Nature Reviews Drug Discovery, 16(3), 203-222.
103. Ling, H., Fabbri, M., & Calin, G. A. (2013). MicroRNAs and other non-coding RNAs as targets for anticancer drug development. Nature Reviews Drug Discovery, 12(11), 847-865.
104. Hayes, J., Peruzzi, P. P., & Lawler, S. (2014). MicroRNAs in cancer: biomarkers, functions and therapy. Trends in Molecular Medicine, 20(8), 460-469.

The model we present here, based on the thesis of Sodré GB Neto, suggests that the impact of a fragmented asteroid triggered a cascade of events, including the generation of nuclear piezoelectricity that accelerated radioactive decay, resulting in a global radiation pulse. This radiation, in turn, would have induced a mutational explosion in living organisms and contributed to the rapid formation of sedimentary strata, which trapped and preserved soft tissues. This approach not only offers a coherent explanation for the synchronicity of these anomalies but also resolves the paradox of morphological stasis, reinterpreting the fossil record as a snapshot of a pre-catastrophe biota, and invalidates conventional radiometric dating that assumes constant decay rates. Our goal is to present a compelling argument for a fundamental reassessment of geochronology and evolutionary biology, proposing an alternative model that better aligns with the available empirical evidence.

2. Methods

To develop this integrative model, we employed a multidisciplinary approach, combining critical analysis of existing literature with the synthesis of data from diverse scientific areas. The criteria for selecting evidence were based on its direct relevance to the phenomena of mutagenesis, radioactive anomalies, and soft tissue preservation, as well as its ability to challenge or complement uniformitarian models. Temporal synchronization analysis was performed by correlating events dated by independent methods, seeking convergences in the window of 5,000 to 10,000 years before present (ka BP).

Specifically, the methods included:

1. Systematic Literature Review:  A comprehensive search was conducted in scientific databases (PubMed, Web of Science, Scopus, Google Scholar) using keywords such as “TP53 mutation explosion”, “Ediacaran radiation anomaly”, “soft tissue preservation fossils”, “piezonuclear fission”, “asteroid impact Holocene”, and “non-uniformitarian geology”. We prioritized articles with DOI, PMID, or PMC to ensure the traceability and verifiability of the sources.

2. Comparative Genomic Analysis:  We examined studies on the mutation rate and evolution of the TP53 gene in humans and large mammals, focusing on data indicating a recent and rapid increase in variant diversity. The expansion of TP53 retrogenes in elephants and whales was analyzed as an example of evolutionary convergence under intense selective pressure  .

3. Geochronological and Geochemical Reassessment:  We analyzed geochemical data from Ediacaran strata, particularly those related to Uranium (U) and Thorium (Th) anomalies, and evidence of nuclear piezoelectricity in high-pressure environments. The interpretation of these data was made in light of the impact-induced radioactive decay acceleration model  .

4. Study of Soft Tissue Preservation:  We reviewed the literature on the occurrence of organic soft tissues in fossils, including collagen, osteocytes, and blood vessels. We assessed the implications of biomolecule degradation rates for conventional dating and their consistency with a scenario of rapid and recent burial  .

5. Integrative Modeling:  The different lines of evidence were synthesized into a conceptual model that posits a fragmented asteroid impact event as the trigger for the observed phenomena. Temporal synchronicity was visualized through an event graph, illustrating the overlapping windows of anomaly occurrence (Figure 1).

3. Results

Our analysis revealed a remarkable temporal and causal convergence between the three lines of evidence, which consistently align with the model of a recent global catastrophic event. Below, we detail the results for each category of evidence and their integration.

3.1. The Holocene Mutational Peak of the TP53 Gene

Genomic literature demonstrates that most coding protein variants in modern humans, including deleterious ones, arose in the last 5,000 to 10,000 years  . This mutational explosion is significantly faster than expected from background mutation rates and cannot be fully explained by demographic factors such as post-migration population growth out of Africa  . The TP53 gene, a vital tumor suppressor, exhibits an unprecedented expansion of mutated variants in modern humans, contrasting with the lower diversity observed in Neanderthals  .

In parallel, we observe evolutionary convergence in large mammals. Elephants and mammoths, for example, have developed enhanced cancer suppression mechanisms, including the expansion of multiple copies of the TP53 gene (retrogenes), a relatively recent evolutionary event  . Similarly, cetaceans (whales) exhibit an increased  turnover rate  of tumor suppressor genes  . This synchronicity of mutational events in diverse mammalian lineages, regardless of their specific cultural or ecological history, suggests an intense global environmental selective pressure, like a pulse of radiation  .

3.2. Radioactive Anomalies and Nuclear Piezoelectricity in the Ediacaran Strata

The reassessment of Ediacaran strata, traditionally dated to hundreds of millions of years ago, reveals geochemical evidence of radioactive spikes and nuclear piezoelectricity that are more consistent with a recent catastrophic event than with uniform processes of slow deposition  . Anomalous concentrations of Uranium (U) and Thorium (Th) have been detected in formations such as the Doushantuo (China) and the Nama Group (Namibia), with levels incompatible with gradual sedimentary deposition  .

The proposed mechanism involves nuclear piezoelectricity, where gigapascal (GPa) pressures generated by asteroid impacts induce phono-fission reactions in rocks. These reactions release neutrons and accelerate the decay of radioactive isotopes, creating the illusion of a much longer geological time than has actually elapsed  . The presence of redox-sensitive element enrichment (RSTE) and δ238U anomalies reinforces the idea of ​​a sudden global perturbation, which would have led to the rapid formation of these strata  .

3.3. Preservation of Soft Tissues in Fossils

The discovery of organic soft tissues, such as collagen, osteocytes, blood vessels, and even cells in fossils of dinosaurs and other organisms supposedly tens or hundreds of millions of years old, represents a significant challenge to biomolecule degradation models  . Known degradation rates of proteins and other organic macromolecules make their preservation for such extended periods extremely unlikely, even under ideal burial conditions  .

Our interpretation is that the exceptional preservation of these soft tissues is not a rare anomaly, but rather evidence of the rapid and synchronized burial of a vast number of organisms during the catastrophic event. The anoxic conditions and rapid sedimentation created by megatsunamis and post-impact turbidity currents would have favored mass fossilization, trapping and protecting biomolecules from degradation for a period consistent with the 5,000 to 10,000-year window  .

3.4. Synchronization of Events

Figure 1 illustrates the temporal overlap of the three lines of evidence, all converging on a window of 5,000 to 10,000 years before the present. This synchronicity is the cornerstone of our model, suggesting a common cause for phenomena that, from a uniformitarian perspective, would be considered independent events distant in time.

Figure 1:  Synchronized chronology of evidence supporting the recent radioactive catastrophe model. The TP53 mutational peak, the Ediacaran radioactive anomalies (reinterpreted), and the preservation of soft tissues in fossils converge on a time window of 5,000 to 10,000 years before present, challenging conventional dating.

4. Discussion

The model proposed by Sodré GB Neto offers a coherent and unified explanation for a series of anomalies that have challenged conventional scientific paradigms. The idea of ​​a catastrophic fragmented asteroid impact event, generating nuclear piezoelectricity and a global radiation pulse, provides a proximate mechanism for the acceleration of mutation rates and the rapid formation of sedimentary strata.

4.1. Theoretical Implications and Paradox Resolution

This model has profound implications for geochronology and evolutionary biology. The main one is the invalidation of radiometric dating methods that assume constant decay rates. If decay rates can be accelerated under extreme pressure and plasma conditions, then the millions-of-year “ages” attributed to geological formations and biological events can be drastically reduced to much more recent timescales. This means that the Ediacaran, with its radioactive signatures, could be a record of catastrophic events that occurred in a much more recent past than previously thought, temporally coupling with the Holocene mutational peak.

Furthermore, the model resolves the  paradox of morphological stasis . The absence of gradual changes and the sudden appearance of complex forms in the fossil record, which are difficult to explain by Darwinian gradualism, are reinterpreted. Instead of slow and continuous evolution, the fossil record captures the diversity of ancestral basic types that were simultaneously buried during the catastrophic event. The “explosion” of new forms is not evolution, but the manifestation of mutated variations (as in TP53) occurring in response to extreme environmental stress and radiation, leading to rapid diversification and adaptation in a short period of time  .

4.2. The Proposed Mechanism: A Synthesis

The central mechanism of our model can be summarized as follows: the fragmentation of a large asteroid upon entering Earth’s atmosphere resulted in multiple impacts. These impacts generated gigapascal (GPa) pressures, which, in turn, induced nuclear piezoelectricity in mineral-rich rocks. This phenomenon led to the emission of neutrons and the acceleration of radioactive decay of isotopes, resulting in a global radiation pulse. This radiation had twofold effects:

1. Geological:  It caused the accelerated “aging” of rocks, creating the illusion of millions of years in strata that were formed rapidly. The synchronized formation of sedimentary strata, such as those of the Ediacaran period, occurred due to megatsunamis and turbidity currents generated by the impacts, which quickly buried vast amounts of material.

2. Biological:  It induced an explosion of mutations in living organisms, as evidenced by the proliferation of TP53 gene variants in humans and large mammals. The rapid burial and anoxic conditions resulting from the catastrophic event also favored the exceptional preservation of organic soft tissues in thousands of fossils, which would otherwise have degraded on conventional geological timescales.

5. Conclusion

The synchronized radioactive catastrophism model, proposed by Sodré GB Neto, offers a robust and coherent framework for integrating evidence that, in isolation, represents significant challenges to uniformitarian models. The convergence of the Holocene mutational peak of TP53, the Ediacaran radioactive anomalies, and the preservation of soft tissues in fossils points to a recent global catastrophic event that occurred between 5,000 and 10,000 years ago. This event, driven by asteroid impacts and their nuclear piezoelectric effects, demands a fundamental reassessment of geochronology and evolutionary biology.

By resolving the paradox of morphological stasis and invalidating the assumptions of constant radioactive decay rates, our model opens new avenues for research and a more accurate understanding of the history of Earth and life. We encourage the scientific community to seriously consider this alternative perspective, which aligns more consistently with the multiple lines of empirical evidence. We believe this manuscript represents a significant step toward a more integrative and non-uniformist scientific paradigm.