PARADIGM SHIFT NEEDED IN PREVENTION MEDICINE!

IF ONE CAN DIE BECAUSE A DYSFUNCTION IN THE NOTCH OR THE WNT PATHWAYS? WHY MONITOR CHOLESTEROL!
AN NHI RFA ASKED:" In particular, “sudden death” among dialysis patients, even in the pediatric age range, is largely unexplained and needs further study.". Well we monitor in Chronic renal failure K,Na,Ca,BUN,Creatinine,GFR,cholesterol,PTH...how come we still have these sudden death.  Nobody checked the status of amplification on the Wnt, the NOTCH, PI3K,AKT, NITRIC OXIDE, which we know to be affected in this disease. I tell you right now this will be medicine of the future!

Case in point:  The trade off Hypothesis
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"When Chronic Kidney disease impairs the kidney's ability to excrete phosphate, Phosphate accumulate in the intracellular and extracellular fluid and lead to the physicochemical formation of Calcium-phospate complexes that reduce the level of ionized calcium". Low serum calcium will trigger release of PTH which suppress the reabsorption of Phosphate by the proximal tubule of the kidney and increase renal excretion of phosphate but as the process continue, the level of Phosphate drops and the relative increase of Calcium suppresses the PTH but the new steady state is achieved at a higher PTH threshold.  The recognition that a higher PTH is needed tells us that other receptor susceptible to PTH are now Hyperstimulated.  At Bone level, the bone continue to be affected and RENAL BONE DISEASE WILL PROGRESS EVEN AS CALCIUM AND PHOSPHATE ARE CORRECTED IN THE SERUM!
QUESTION FOR YOU, WHAT NEEDS TO BE MONITORED, CALCIUM OR PHOSPHATE Vs THE PTH GENE?
OVER EXPRESSION OF A GENE WILL IMPACT OTHER GENES AND UNTIL THAT OVEREXPRESSION IS CORRECTED WE HAVE NOT ACCOMPLISHED MUCH PREVENTION!
UNTIL WE START MONITORING GENE EXPRESSION, AMPLIFICATION OR SUPPRESSION, WE ARE NOWHERE IN PREVENTIVE MEDICINE FOR STROKE, CORONARY ARTERY DISEASE OR DIABETES MELITUS FOR THAT MATTER!