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Is Low LDL Bad For The Epigenetic Pace of Aging?


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I really appreciate the longer video here Michael. It is a bit wild to think that no foods/nutrients are significantly correlated with DunedinPACE. Nice work getting to 11th or 12th on the Rejuvenation Olympics leaderboard (even if that isn't your overall goal). How many names have been submitted? I heard it's about 4000 at this point, which would make your results pretty impressive!

I don't understand why a higher LDL would result in slower aging. Intuitively this just doesn't make sense to me and it doesn't square up with the Ornish/Esselstyn studies that have reversed heart disease and had patients with very low LDL's. I know that this is obviously different than aging and all-cause, mortality, I'm just trying to square this up in my basic brain. I'll be curious to see how this shakes out with more tests. Are calories associated with DunedinPACE in your data?

I commend you for your detailed testing of SFA, LDL, and Dunedin pace without "blowing up the system" as you put it. 

 

 

Edited by drewab
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Thanks drewab. I'm not sure about the why, but it looks like this effect may not be specific to me: 

"After adjusting for age, race/ethnicity, sex, fasting status, and lipid-lowering medication use, greater epigenetic age acceleration was associated with lower TC, HDL-C, and LDL-C, and higher TG (p < 0.05)."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10925395/

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You really should differentiate sdLDL vs the other types. sdLDL is uniquely bad, other types are barely different from HDL. It's easy to get lipid subfractions, the technology is not that expensive, and all LDL measurements are confounded by fraction that's "good" vs "bad" LDL. Your results might be especially good, but we don't know until we see your lipid subfractions

https://www.questdiagnostics.com/our-company/actions-insights/2017/ldl-subfractionation-testing-can-help-id-patient-risk

If your LDL is of the unusually good subtype, good for you, but potentially misleading for others.

Edited by InquilineKea
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7 hours ago, InquilineKea said:

You really should differentiate sdLDL vs the other types. sdLDL is uniquely bad, other types are barely different from HDL.

Not necessarily. It's a rapidly fading theory. Dense LDL particles are associated with those with more severe CVD, but by themselves do not appear to have predictive value.

Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic (oup.com)

 

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IMHO the situation with abnormally low LDLs originates from the approach of contextless data sciencing and creates unwanted confusion due to this.

For myself I use this model to understand it (or "understand", for obvious reasons of complexity).

There is a flux of materia into a sophisticated transforming machinery called liver. There is a processing capacity with optimal range of operation let's say 40-90% of approximated saturation point. With such a flux the size of exported cargoes will be determined by many factors but most of them will fluctuate close to mean values observable in the population. If we will artificially increase the flux at the input then the system will leak the extra to some other paths (if they exist and to the extent of their saturation) or will start to export lower sized cargoes, just to get rid of overload because there is no housing for it (yes, there is some and fatty liver is a sign of saturation of this backup mechanism). So actually it is pretty imaginable within the queing theory used in engineering.

There is a rare exceptional share for small abnormal cargoes - genetically determined, these people will produce abnormal particles within a normal flux values but my intuitive feeling is that they account for minuscule shares of a percent.

In other words - for most of the people the start of production of smaller particles is a redflag about unwanted input overload that itself is a sign that a lot of problems will come in other areas - the network of queues goes deoptimized and no one could predict where the things will start to break. No magic pill or any kind of mimicking or biohacking will help, there is no way to mimic normal traffic in a congested network, there should be incoming rate limit implemented until it will become too late and parts of the mechanism will be deformed.

From this perspective it does not make a big difference if smaller particles are more atherogenous themselves, this adds to the bad prognosys but should be of concern especially for those with rare unfortunate genetics, 99.9% of other people should rethink their energy balances.

Br,

Igor

 

Edited by IgorF
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