@Neo I read through thread on CR but didn’t verify, these things are pretty new to me, Dunedin pace and the other clocks sound interesting. So what I think:
Michael Lustgarten’s approach probably works in so far the markers he optimize have causality and correct curve (e.g I believe he has the wrong curve on apoB and LDL-c which I’m sure you agree with). CR probably works in humans since biomarkers improve in studies, however like any intervention, I’d want to check in regularly how biomarkers move and how I feel.
I’m curious, you mentioned in your thread, outside of how you feel, is the restriction on amount of calories basically dependent on muscle mass, or is it something else? Sudden deaths in e.g anorexia or liquid protein diets (has anyone mentioned this?) I see a lot of case reports and news in the 70’s and 80’s.
What’s causing suddent death etc in anorexia, can this happen on CR at some point? What is measured?
At least one-third of all deaths in patients with anorexia nervosa are estimated to be due to cardiac causes, mainly sudden death.14,16,20 Cardiovascular complications are common, and they have been reported in up to 80% of the cases; up to 10% of these complications were mainly bradycardia, hypotension, arrhythmias, repolarization abnormalities, and sudden death.14,16,17,21–23 It must be noted that food restriction can lead to increased vagal tone, bradycardia, orthostatic hypotension, syncope, arrhythmias, congestive heart failure, and sudden death.24 Bradycardia presents particularly during the night but neither mean QT nor corrected mean QT length over 24-hour monitoring seem to be different compared with controls.25
With respect to QT abnormalities, QT interval is a measure of myocardial repolarization and its length is associated with life-threatening ventricular tachycardia. Thus, a prolonged QT interval is a biomarker for ventricular tachyarrhythmia and a risk factor for sudden death.17 In EDs, QT interval abnormalities have been studied as a marker of sudden death and also to assess the effect of refeeding. It has been proposed that sudden deaths are a result of cardiac arrhythmias for which a long QT interval on the electrocardiogram would be a marker. The necropsy and clinical findings in three cases of sudden death reported by Isner et al provided evidence that sudden death in anorexia nervosa, like sudden death in liquid-protein dieting, might result from ventricular tachyarrhythmia related to QT interval prolongation.16,26 Nevertheless, the QT interval seems to have a poor predictive value for the recognition of patients who are at particular risk of sudden death. Only QT intervals >600 milliseconds are clearly associated with a significant risk of sudden death, but few ED patients usually have such long QT intervals.27 Considering the QT dispersion, an increase of the QT interval dispersion represents regional differences in myocardial excitability recovery and may lead to an increased arrhythmogenic substrate, with a higher risk for clinically significant ventricular arrhythmia and sudden death. In this case, the predictive value of the increased QT interval dispersion as a marker of sudden acute ventricular arrhythmia or death has been demonstrated.16,22 Both prolonged QT interval and increased QT interval dispersion tend to normalize after refeeding, along with heart rate and heart-rate variability.5,28
Reason I am asking, I’m wondering about the feasibility to be on higher CR might increase (you mentioned hunger feelings) – because we have GLP-1 agonists and other drugs? But of course probably a safer level to not get in anorexia territory for body fat or muscle mass (and as optimal BMI as possible)? Just wondering about the limits and how to track it as well.
But do you think 10-20% long term CR might be more possible with GLP-1 agonists (provided it’s still safe body composition, etc), would that be good?
