@blsm All I know is above
Perhaps it’s just a one off experiment for the Candida IgG
Anyone else feel like Michael Lustgarten’s approach might actually work since CR has a net benefit on like 7 biomarkers (except lymphocytes), iirc?
Isn’t this possibly some signal that it, and that CR works as well?
@AnUser Yes, I think that aspect is core and helping him (and one of the most valuable things in Bryan Johnson’s protocol too).
And in general would be good even if it does not drives clicks or sell as much as taking people to eat loads of protein and gain big muscle
Have you seen my posts on CR(ON)
(And fasting)
I meant that his approach might both work and that CR itself.
Because CR is expected to work in animal models, and now both method and CR validated in N=1 according to human epidemiological data (ACM). I might be thinking incorrectly on the CR validation part though.
7 or so biomarkers improve on ACM, 1 negative, that means his method in itself might be valid and that’s important.
It was long ago but I will take a look, I think important is to have the correct method of evaluating strategies.
Wonder if the benefits in human CR studies were on biomarkers showing a net benefit on short term ACM risk.
Would love the read about this - can you share more
I don’t have any studies per se, what I meant was:
Mike has a method he believes will improve his longevity.
This method of optimizing biomarkers according to ACM epidemiological or youth data show that CR works really well for him with lots of biomarkers going in the right direction.
Is his method good? I’m thinking that his one actually works and there’s signal in the epidemiological data for ACM and youth because it shows that CR works well. Which validates his approach.
Does that make sense? If so:
Next would be to see if short term studies on calorie restriction improves biomarkers for better epidemiological ACM, including ones he saw improvement in.
I might be missing something here, but I feel like it shows that it works? Unless we believe CR to not work in humans, thus we can’t determine how valid his method is based on it. I might be confusing myself here, though.
I thing the answers to this might be yes - check out the the different Nature journal paper after the Yale Calorie Trial and all the CRONy stuff.
@CronosTempi can probably help with examples from the top of his mind
For anyone interested in CR studies in humans and the associated research, you should look at the work of professor Luigi Fontana. He’s the primary investigator behind the CALERIE trial. He’s done a ton of CR work in humans over the decades, and if you google around you’ll find his work everywhere.
Here’s a taste - an interview from 2018:
Thanks @CronosTempi
@A_User and any anyone else interested in this topic (@adssx what is your latest thinking), here is one thread that also references several other recents ones
2 years of mild caloric restriction significantly reduces biological age?
Having an accurate method of evaluating strategies is way more valuable in my view than any intervention. The latter has often undue weight and leads to a lot of waste in supplements and lifestyle changes that don’t work.
@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?
@A_User Not an expert but think at too high degree of CR the bodies uses up not just some of your normal (skeletal) muscle, but also some of your heart muscle - which does not seem to be a good thing
You might be right about GLP-a meds as a way to achieve meaningful CR at less hunger hassle. It may or may it be better than not being on CR (@AlexKChen might have thought and experimented with that).
At the same time it may not be as good as achieving the same amount of CR without the GLP-a meds (given eg the potential increase in insulin levels).
Still if the actual choice a person faces is less/no CR without GLPa and more CR (to a reasonable degree) with GLPa, then perhaps that is still better
Introduction to Biological Age Testing
Importance of Frequent Testing
Tracking Year-to-Year Changes
Understanding Biological Age Variability
Focus on Mean Corpuscular Volume (MCV)
Optimal MCV Levels and Trends
Dietary Influence on MCV
Iterative Process for Improvement
Muscle Mass and Aging
Study Overview
Biochemical Analysis
Personal Biochemical Tracking
Metabolite Analysis and Trends
Longevity Interventions
Metabolomic Data and Triglycerides
Human Data on Triglycerides and Longevity
Tracking Triglycerides
Dietary Influences on Triglycerides
Outlier Analysis and Future Testing
Introduction to Biomarkers
Optimal Ranges for Heart Rate Metrics
Personal Data Overview
Trends in Resting Heart Rate
Factors Influencing Heart Rate Metrics
Impact of Body Weight
Role of Physical Activity
Collective Influence of Identified Factors
Biological Age and Blood Tests
Interventions for Biomarker Optimization
Optimal Levels and Biomarker Tracking
Food Correlations and Dietary Adjustments
Impact of Dietary Changes on Cistatin C
Additional Experiments and Biomarker Monitoring
Cheat Meals and Dietary Philosophy
Dietary Composition and Macronutrient Breakdown
Micronutrient Intake and Optimization
Sodium Intake and Future Testing Plans
He doesn’t mention whether the Niacin he took was IR. Since it was 350 mg one time thing, probably was not IR. That would burn. IR does not cause the problem with 2PY, 4PY which is where this stuff comes from.
Oops, I just looked it up and actually got that one backwards. IR is bad for 2py 4py. Slow release is good for those, but bad for your liver. I may quit the Niacin.
I would be very cautious supplementing with niacin in any form, unless you are frankly deficient. It’s a very double edged vitamin.