Our latest manuscript from the KetoSAge trial has successfully completed the peer review process and is now accepted for publication in Frontiers Nutrition! 💫 This study examines the suppression of physiological ketosis (euketonaemia), the resulting state of hypoketonaemia, and the associated alterations in sex hormones and sex hormone binding globulin (SHBG). These findings have direct relevance to cancer biology because SHBG exerts regulatory control over intracellular signalling dynamics to sex steroids that without SHBG can drive oncogenic signalling. SHBG functions as a central endocrine modulator, that governs the availability and the signalling pathways (hormone + SHBG results in a different signalling cascade) of bioactive hormones capable of activating proliferative pathways (when there is lack of SHBG). Reduced SHBG increases unbound hormone signalling (different to bound with SHBG co-signalling), which intensifies oncogene driven behaviour and strengthens the cancer phenotype. Lower SHBG = higher c-Myc and higher Bcl2 = more oncogene expression and activity, more proliferation less apoptosis capacity. Preserving higher SHBG expression therefore supports a more protective anti-cancer endocrine environment. ➡️ Insulin directly regulates hepatic SHBG synthesis. Higher circulating insulin suppresses SHBG production and allows stronger mitogenic signalling. ➡️ Lowering insulin restores euketonaemia, elevates SHBG, and produces a metabolic endocrine pattern associated with reduced oncogenic activity. Euketonaemia with foods low in insulin mimetics and other mitogenic phyto-estrogens and growth factors, supports metabolic endocrine oncology therapy in more ways than restricting glucose for fuel. @Yvoni_Kyr @AdrianSotoMota @tnseyfried @drtomasduraj @_LucyPetagine @I_mitochondria