Kaydedildi:
| Yazar: | |
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| Materyal Türü: | Recurso digital |
| Dil: | |
| Baskı/Yayın Bilgisi: |
Zenodo
2026
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| Konular: | |
| Online Erişim: | https://doi.org/10.5281/zenodo.20075490 |
| Etiketler: |
Etiketle
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İçindekiler:
- <p class="MsoNormal">The Redacted Science framework (Craddock, <em>Redacted Science</em>) originally proposed that modern humans coevolved with a fungal symbiont, specifically <em>Candida</em>, producing a physiologically distinct phenotype designated <em>Homo candidus</em>. This paper extends that framing. The conserved mammalian interface systems through which the symbiont operates, including the hypothalamic-pituitary axis, the endocannabinoid system, sodium-potassium pump dynamics, renal concentrating mechanisms, and phagocytic immune pathways, are not uniquely human. They are shared across all land mammals and have been preserved across approximately 200 million years of mammalian evolution.</p> <p class="MsoNormal">Recent comparative mycobiome studies document that each mammalian lineage carries its own host-adapted Saccharomycetaceae fungal symbiont: <em>C. albicans</em> in humans, <em>C. natalensis</em> in dogs, <em>C. tropicalis</em> in mice, <em>Kazachstania slooffiae</em> (the teleomorphic state of <em>Candida slooffiae</em>) in pigs. The conserved feature across the mammalian clade is the interface architecture, not the identity of any single organism. This paper therefore proposes that the coevolution did not originate with humans but with the mammalian body plan itself, and designates the full clade <em>Mammalia candidus</em>, with the specific organism varying by host lineage.</p> <p class="MsoNormal"><em>Homo candidus</em> is a subset of that broader category, distinguished not by the presence of the symbiosis but by the capacity for conscious, volitional participation in its physiological program. The Pan-Mammalian Coevolution hypothesis is argued to be complementary to the Methylation/Neural Selection hypothesis, describing respectively the structural and runtime layers of the same symbiotic architecture.</p> <p class="MsoNormal">The paper also addresses the detection variability problem documented across mammalian mycobiome surveys, arguing that conventional detection rates reflect methodology limits rather than true absence. Implications for human and veterinary medicine, mycobiome research, and the framing of idiopathic disease are discussed. A specific environmental mechanism for this coevolution is developed in the companion paper on the Saline Oscillation Hypothesis (Craddock, Saline Oscillation).</p>