Proof of Concept-The Miraculous Cancer Cure Approach WORKS!
HYPOTHESIS: SP1 AND MAO-B AS MISSING PIECES IN HORVATH’S FRAMEWORK
Horvath’s universal mammalian clock identifies ~35-48 genes (e.g., LHFPL4, ZIC family) near CpGs gaining methylation with age, enriched in developmental TFs and PRC2 sites. Bowles highlights SP1 from Horvath’s data as regulating MAO-A/B, yet Horvath’s list excludes such integrators, focusing on autosomal loci to emphasize conserved drift over programmed intent. This narrowing might avoid “rocking the boat”: admitting programmed aging (e.g., MAO-B as evolved for species-level benefits like genetic diversity against predators) contradicts selfish gene theory, where deleterious traits shouldn’t persist without early advantages.
Creatively, envision aging as evolution’s “diversity engine”: MAO-B, upregulated by SP1 post-puberty, depletes FAD symmetrically to CD38’s NAD+ hit, crippling 80% of ETC protons and enforcing senescence. In asexual/non-aging species (e.g., planaria), uniformity leads to extinction via evolving threats; sexual/aging species (via switches like MAO-B) foster variation, migrating to fill niches. KS’s extra X disrupts this switch—extra MAO copies, modulated by escapees or hormones, “jam” the program, slowing clocks. Horvath’s list, by omitting SP1/MAO regulators, sidesteps this, portraying aging as stochastic byproduct rather than adaptive code.