Here is the link to the transcript of Rush’s opening brief on his cancer:
https://www.rushlimbaugh.com/daily/2020/10/19/an-update-on-my-health-its-a-roller-coaster/
MAYBE TOO LATER FOR THIS RESEARCH FOR RUSH LIMBAUGH, BUT MAYBE SOMEONE CAN FIND A WAY TO CONVEY IT TO HIM. RESEARCH INDICATES THAT TAKING INOSITOL CAN STOP LUNG CANCER.
TITLE: Inositol–Trisphosphate Reduces Alveolar Apoptosis and Pulmonary Edema in Neonatal Lung Injury
JOURNAL: American Journal of Respiratory Cell and Molecular Biology
DATE: February 2012
Clinical Relevance
In neonatal acute lung injury (nALI), pulmonary ceramide content is augmented because of increased acid sphingomyelinase activity. Ceramide induces alveolar epithelial apoptosis and edema. The suppression of acid sphingomyelinase by inositol-1,2,6-trisphosphate almost restores lung function, when given together with surfactant (“surfactant fortification”), in a porcine nALI model of hypoxemic respiratory failure.
Conclusion
In the present study, we introduced a new neonatal piglet model of triple-hit nALI with severe pulmonary inflammation, and demonstrated that the intermediate-term effects of surfactant are not sufficient to improve gas exchange, lung mechanics, and pulmonary edema when compared with no intervention. The admixture of inositol with surfactant neither amended lung function nor exerted any clinical effects on aSMase activity and the generation of ceramide, in contrast to the admixture of D-myo-inositol-1,2,6-trisphosphate (S + IP3) that effectively suppressed aSMase and caspase-8 activities. We observed significantly reduced alveolar epithelial apoptosis, a finding of critical importance for improved gas exchange, lung mechanics, and pulmonary edema. Despite limited knowledge about its dose and kinetics, IP3 seems to be effective in the alveolar space even 10 hours after its local administration, and demonstrated anti-inflammatory effects throughout this study period. Except for delayed creatinine clearance, no systemic side effects were identified. The present findings reinforce the notion that aSMase plays a key role in inflammatory nALI, and that the magnitude of aSMase suppression is paralleled by a reduction of epithelial apoptosis. We conclude that surfactant supplementation with IP3 is a promising pharmacologic option for the treatment of neonates with hypoxemic respiratory failure, and deserves clinical evaluation.