cthalupa

25 ms·

361.
by cthalupa 1y ago
We have all sorts of RCTs, blinded studies, placebo controlled studies, MR studies that look at genetics, meta-analysis, etc. etc. etc. that all support the causal link of cholesterol... I've linked literally dozens of these in the com
362.
by cthalupa 1y ago
> 1. Lowest mortality is with ldl of 140, not lower/. https://www.bmj.com/content/371/bmj.m4266 I guess we're on repeat here. U and J shaped curves in observational studies are notorious for being con
363.
by cthalupa 1y ago
The cholesterol hypothesis certainly leaves room on the table for multiple causal factors, and from very early on we knew that inflammation was key to plaque actually being deposited on arterial walls. The cholesterol hypothesis has always
364.
by cthalupa 1y ago
Experts can be wrong, even in mass consensus. But you have to separate the fallacy from it being supportive evidence of other data. There is a difference from saying X must be true because Y person said it and they're an expert on Z. B
365.
by cthalupa 1y ago
Trig/HDL and LDL/HDL ratios are outdated science that have been superseded by our better understanding of the causative factors and our ability to drive LDL way lower than we could in the past. MR studies have shown very little ev
366.
by cthalupa 1y ago
> Heart disease progresses over decades <...> You don't want to wait til you're 18 months out from a heart attack to do anything. I don't think this is good advice Correct. The idea is commonly referred to as "L
367.
by cthalupa 1y ago
Please stop spreading misinformation about life-saving medication. This is simply untrue. https://www.lipidjournal.com/article/S1933-2874(25)00317-4/f... > Based on the Cholesterol Treatment Trialists Collabora
368.
by cthalupa 1y ago
MR studies rule out the idea that inflammation is the sole causal factor, and we have a lot of them. We have MVMR studies that look at multiple variables https://journals.plos.org/plosmedicine/article%3Fid%3D10.137...
369.
by cthalupa 1y ago
No, it really isn't. Why in the world can't there be multiple causative factors? We have a mountain of evidence that LDL-C/Lp(a) are causal regardless of hsCRP levels, both from medications that don't lower hsCRP, LDL-C&
370.
by cthalupa 1y ago
PCSK9 inhibitors do not universally lower hsCRP but still reduce cardiovascular events. https://pmc.ncbi.nlm.nih.gov/articles/PMC4876179/ https://pubmed.ncbi.nlm.nih.gov/36779348/ MR studies
371.
by cthalupa 1y ago
LDL and BMI's u and j shaped curves on all cause mortality disappear when you start controlling for other factors like a variety of diseases. Cancer, kidney disease, AIDS, etc. Lots of people end up with very poor nutrition when close
372.
by cthalupa 1y ago
PCSK9 inhibitors don't universally lower hsCRP ( https://pmc.ncbi.nlm.nih.gov/articles/PMC4876179/ ) but do lower adverse cardiovascular events https://pubmed.ncbi.nlm.nih.gov/36779348/
373.
by cthalupa 1y ago
PCSK9 inhibitor trials have shown significant benefit for reduction in CVD events independent of whether or not the inhibitors lowered hsCRP. Ezetimibe makes an impact on events without reducing hsCRP when administered on it's own. (Bu
374.
by cthalupa 1y ago
Calcium scores only reflect calcified plaque - not soft plaque. CTTA is what you need for that. Particularly for people below ~45 with significant plaque buildup, calcium scores are often 0 or very low, because all of the plaque is soft. Th
375.
by cthalupa 1y ago
Calcium scores only show calcified plaque - not soft. You need a CTTA for that. https://pmc.ncbi.nlm.nih.gov/articles/PMC10920137
376.
by cthalupa 1y ago
>If one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. This is such a silly statement I'm not sure where to begin. Plenty of people smoke and drink and don't die of iss
377.
by cthalupa 1y ago
High LDL or Lp(a) on its own causes enough localized inflammation to continue plaque deposition. We can’t drive down every cause on inflammation to 0 to the point that there is zero plaque deposition at all in the presence of high LDL, ther
378.
by cthalupa 1y ago
No, I mean the positive impact of lowering LDL. Statins of course show positive impact, and yes, including from also lowering inflammation. But so do other drugs that lower LDL through other mechanisms, including ezetimibe, bempedoic acid,
379.
by cthalupa 1y ago
LDL levels at admittance do not tell us what their lifetime LDL levels were. But even your own link is arguing for lowering the the number at which we consider LDL levels risky. PCSK9 inhibitors when coupled with statin therapy have gotte
380.
by cthalupa 1y ago
LDL has always been both a worthwhile measure and target. It's not perfect as a measure - it doesn't account for Lp(a), for example, and why ApoB is a better indicator for the atherogenic particles portion of the equation - but we
381.
by cthalupa 1y ago
Localized foam cell activation and cytokine signaling does not necessarily raise hsCRP yet allows for continue plaque deposition. This is a very well understood mechanism. No one knowledgeable here is saying that inflammation isn't wor
382.
by cthalupa 1y ago
This just isn't true. Modern statins have extremely good efficacy to side effect ratios. These are some of the most studied medicines in human existence. They're not perfect and there are some people that do not tolerate them for
383.
by cthalupa 1y ago
Comments like these just aren't based in reality. LDL levels are not a proxy or a wet streets cause rain. We even have a strong understanding of the mechanisms in which cholesterol causes things like heart attacks, strokes, peripheral
384.
by cthalupa 1y ago
> Statins in trials show benefits for secondary events, but for primary protection statins don't actually work that well. This just simply isn't true and we have massive quantities of data pointing towards protection against ma
385.
by cthalupa 1y ago
Anecdotal data does not disprove the millions of data points from well controlled well structured RCTs that have been poured over by the brightest minds in the field. The positive impact of lowering LDL is some of the strongest science we h
386.
by cthalupa 1y ago
Other methods do. https://pmc.ncbi.nlm.nih.gov/articles/PMC6661243/
387.
by cthalupa 1y ago
The body can produce needed cholesterol locally just fine. The PCKS9 inhibitor trials show that having basically no serum LDL is not harmful. People that have the genetic mutation that results in no PCKS9 have extremely low rates of CVD
388.
by cthalupa 1y ago
Most of this is reputation is based on early generation statins. The side effect profile is incredibly slimmed down on statins like rosuvastatin.
389.
by cthalupa 1y ago
The guidance has been changing significantly over the past few years. The consensus from expert organizations is now that we should be lowering it far earlier. https://www.lipidjournal.com/article/S1933-2874%2825%290031
390.
by cthalupa 1y ago
No. They’re saying that damage is cumulative over a lifetime - plaque deposition - so that a point in time snapshot of LDL says little about lifetime exposure. If I live my life with high LDL and only get on statins at 65 I might have low L

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