Ok so med induced, that makes sense, a different context.
I got a lot of my inspiration from Ivor. Here he goes over the Kraft curves and how they can tell you how well you are doing. I suppose it is expensive to do it this way, but why use something cheap if it doesnāt work?
Ivor is greatā¦metabolic syndrome = CVD.
Just commenting on the study right now re progression of coronary calcium scores and CAD. I hadnāt seen that study and it was very interesting. As an aside, one of the authors is Roger Blumenthal, a very respected preventive cardiologist at Hopkins.
So, if you have a baseline CAC of zero and then progress by 5 units a year, your risk increases , but itās still low on an absolute scale.
If your score is non- zero and you progress at 100 or more points/ year, thatās a significant risk. If the progression is 300 or more then thatās a very high risk of both cardiovascular and even total mortality.
This would be a good way to alert your doctor to be more aggressive in your management.
The scan is fairly low radiation risk these days and affordable as well.
Thanks for that study.
Yes that is an amazing reference CAC risk study. Keeping progression < 15%/yr is key.
I think interventions even younger, maybe in the 20ās , would also be beneficial especially in regards to the rapid increase in obesity. Monitoring for visceral fat in the young could be very important.
1 Like
Thanks for the paper, thatās interesting (& hopeful) info.
This group out of Brazil demonstrated in a prior study that the ratio of triglycerides to HDL was the most powerful predictor of CAD when over 4.
In this study they show via the gold standard of coronary angiography that the same ratio was also the most powerful indicator of extensive coronary artery disease. These triglyceride rich VLDL particles lead to the very dangerous small density subgroups of LDL.
It would have been interesting if they had looked at ApoB.
Your TG crossing over 150 is clinically hyper TG, but as rivasp12 asks, ādo we treatā?
Clearly, Rapamycin appears to have dysregulated your lipids, but youāre otherwise feeling good/ābetterā?!
Your TG/HDL is 2.5 and remnant cholesterol (TC-LDL-HDL) is 23, both of which would suggest a more atherogenic profile? But you donāt fit the profile of classic metabolic syndrome. I assume normal BP.
Have you had a CAC?
Are you looking deeper into your lipids? Sub particles apoB, sdLDL, etc.
Whatās your level of CVD concern? Do you consider taking a statin a medical blockade to your lipids?
The study on the relationship of HbA1c and heart failure doesnāt impress me that much. It looks scary on the graph of relative risk, but the absolute risk between 5.4 and 5.6 is very small per 1000 people. Even at the level of 6.5 the absolute risk seems to be about 1% per the graph and thatās not even considering that the increase in glucose secondary to rapamycin may be entirely benevolent.
at what age should one do a baseline coronary calcium CT ? I have a high lp(a) and ldl (which has been lowered by statin use), but im 24 and i asked my doctor about it and he told me he wouldnt recommend it since I am so young and also my other biomarkers are good along with low CRP.
1 Like
Yes, I have been taking Atorvastatin 40mg once daily.
My BP is very good for my age typically < 115/65
My BMI is ~22.3
Well, youāve got some discordant markersā¦so what is your āactualā current CVD risk given your lipid dysregulation taking Rapamycin, yet good overall health profile?
Iād do a CAC and look under the hood to see where you are.
This ratio is a well known atherogenic marker, a very good one. Thatās way too high TG/HDL near to 4. For anyone with say HDL at 55, even someone with a TG/HDL of 2.72 would be clinically hypertriglyceridemia (TG > 150).
My own personal targets are TG/HDL <1, with remnant cholesterol < 10. My last 4 lab panels hit both metrics.
Your risk metrics are way more generous than mine!
Prediabetes is 5.7%-6.4%, and diabetes 6.5%+.
It is without debate a prediabetic, and especially full on diabetic metabolic profile, is very high risk for CVD. Different risk if rapamycin induced? One major issue is the translation model: most all the data is in mice, and mice donāt die of CVD.
Dr B makes many arguments for benevolent glucose on Rapamycinā¦yet he includes a conditional caveat:
āNo hyperglycemic effects of rapamycin/everolimus have been detected in healthy people. For antiaging purposes, rapamycin/everolimus can be administrated intermittently (e.g., once a week) in combination with intermittent carbohydrate restriction, physical exercise, AND metformin.ā
I missed that little add on until now. Why these glucose blunting interventions?
Itās interesting in a recent study that treating pre diabetes reduced the incidence of diabetes but not of cardiovascular events.
Yeah, Blagosklonny is very much into very low carb and high protein diets right now. Not certain that heās still an advocate of metformin, but one thing is for sure, heās frequently referred to hyperglycemia secondary to rapamycin as benevolent.
Agreed , take a look
Yes because the glycolax, kidney, pancreas and vasculature is already permanently impaired!
Big pharma to the rescueā¦let us reduce your glucose, thank you.
Always a difference between ideal numbers and high risk numbers. Not having ideal numbers must be then seen in context of other risks, but high risk numbers would be seen as independent and interventions would be appropriate.
Heās extrapolating wild type mice and chronic cancer patients re ābenovolenceā. He asserts NO ONE healthy taking intermittent rapamycin will achieve hyperglycemia, and by extension, elevate all cause mortality risk? (central thesis is Rapamycin will extend lifespan in humans too.)
Missing is the other major part of the metabolomeā¦lipids.
So what about LIPIDS Mikhail?
Mice cannot talk, and cancer patients, well, CVD is far down their list of concerns.
1 Like