#162

Here it is. This one is particularly interesting because it has CVD and all cause mortalities.
It is consistent with all the similar studies:

  • High TC is only bad below 60 and good after 60.
  • High APOB is bad below 60 and don’t care after 60.
  • Very high APOB is very bad below 60 and slightly bad after 60.
  • Very low TC and APOB are always bad or trending bad.
  • High TG is always bad.
  • Low APOA1 (HDL) is always bad.

image
image1290×1508 196 KB

From The association of apolipoproteins with later‐life all‐cause and cardiovascular mortality: a population‐based study stratified by age

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#163

However if we expect to have longer lifespans than regular folks, we may want to keep ApoB and TG lower for longer.

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#164

it’s not what the plots show.
Very low TC is always bad for all cause mortality for all age groups.
Very low TC is trending bad for CVD mortality for all age groups though not statistically significant.
So if you have a too low TC you die sooner.

For APOB there is no significant effect for very low, low or medium levels.
Very low APOB is trending bad though not statistically significant.
High and very high APOB is bad.
So keep your APOB low of medium. Extremes are bad.

In all cases TG is bad and low HDL (APOA1) is bad.

#165

I think we can only say that very low TC is associated with por all cause mortality. It may or may not be bad.

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#166

Yes, that’s correct! These do not imply causality.

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#167

Sorry, I made a typo. I meant TG not TC. I agree with both of you.

#168

Actually your debates with youthful assertiveness (:grinning:) were pretty educational for me. I learnt a lot. So, keep debating!

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#169

Thanks.

But people with low ApoB probably have low TC as well?

Could it be that you want to minimize ApoB while maximizing some “good” cholesterol (that is probably more complex than just “HDL”).

As I said earlier what I’d love to see is a two dimensional chart with ApoB and TC (or HDL or some HDL subtypes as it seems that quality matter).

Could be done in 3D like this:

image

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#170

I believe that what matters most is the process of reverse cholesterol transport. It’s not just about the composition of HDL-C or quantity of apoA-1 particles, but rather the effectiveness of removing cholesterol from tissues. Unfortunately, this process cannot be easily measured and is not fully understood yet. Once we find a medical intervention to address this issue, then we can consider the end of ASCVD IMO.

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#171

What makes you believe this?

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#172

People are working on it

https://www.jlr.org/article/S0022-2275(20)33852-9/fulltext

https://vascularstrategy.com

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#173

2016 paper with 0 recent citations: is there more recent progress in this field? (I don’t know anything about this topic)

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#174

While researching CETP inhibition, I came to listen to John Kastelein’s interview with Petter Attia and he talks about this. And it makes sense since studies show poor correlation between LDL-C and ASCVD, meaning you can get ASCVD at both high and low levels and avoid it at high levels. So yes, there are all other risk factors, but still sometimes does not male sense. In some people there must be another protective mechanism that protects them from getting ASCVD and reverse cholesterol transport makes perfect sense to look at as lowering of LDL-C has just as much power as we know from RTCs. Even drastic lowering reduces absolute ASCVD mortality only marginally and data from prevention trials on healthy people is even more puzzling.

#175

Regarding your side note: same. So far I have muted a total of one. I wonder how many have muted me? Probably more.

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#176

The death from any cause graphic (bottom right) sure doesn’t look particularly compelling. And I say this as a person who is currently taking Rosuvastatin.

#177

Really! Who’d you mute?..just a test…to see if he hears me.

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#178

You ( (ng0rge) , Vlasko, and Thorin have muted the same individual.

My USD$50 goes to a charity of your choice if I am mistaken.

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#179

Cholesterol Lowering, Cardiovascular Diseases, and the Rosuvastatin-JUPITER ControversyA Critical Reappraisal

Michel de Lorgeril, MD; Patricia Salen, BSc; John Abramson, MD; Sylvie Dodin, MD; Tomohito Hamazaki, PhD; Willy Kostucki, MD; Harumi Okuyama, PhD; Bruno Pavy, MD; Mikael Rabaeus, MD

Author Affiliations Article Information

Author Affiliations: Laboratoire Cœur and Nutrition, Faculty of Medicine, Université Joseph Fourier and Centre National de la Recherche Scientifique, Grenoble, France (Dr de Lorgeril and Ms Salen); Harvard Medical School, Boston, Massachusetts (Dr Abramson); Department of Obstetrics and Gynaecology, Laval University, Quebec City, Quebec, Canada (Dr Dodin); Department of Clinical Sciences, Institute of Natural Medicine, University of Toyama, Japan (Dr Hamazaki); Cardiology Department, Clinique Antoine Depage, Brussels, Belgium (Dr Kostucki); Open Research Center for Lipid Nutrition, Kinjo Gakuin University, Nagoya, Japan (Dr Okuyama); Réadaptation Cardiovasculaire, Centre Hospitalier de Machecoul, Machecoul, France (Dr Pavy); and Cardiology Department, Clinique de Genolier, Genolier, Switzerland (Dr Rabaeus).

#180

Who me? (what me worry?) I wouldn’t mute anybody…I rejoice in the whole spectrum of human idiosyncrasies. (and believe me you see 'em all here…not you, of course!)
P.S. I am just starting a charity tho.

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#181

Okay. My mistake. Name your charity. I was serious about the USD$50.