Saúde Cardiovascular

[adssx]

@Yoo

Any evidence that LDL-Tryg is superior to tryclicerides or apoB as a biomarker of cardiovascular disease?

The paper says:

Using a large general population cohort (N = 40,202), we examined the relationship between the different test results from the standard lipid panel with LDL-TG concentrations, as measured by BQ reference method (BQLDL-TG) (Figure 1). Both non-high-density lipoprotein-cholesterol (nonHDL-C) (Figure 1A) and TG (Figure 1B) were positively correlated with BQLDL-TG, but there was a closer correlation to TG. In contrast, high-density-lipoprotein-cholesterol (HDL-C) was inversely related to BQLDL-TG (Figure 1C). Apolipoprotein B (apoB) also had a weak positive association with LDL-TG (Supplementary Figure 1), but because it is currently not often used in routine clinical care and not part of the standard lipid panel, it was not further utilized.
we chose the 80th percentile (eLDL-TG ≥ 44.6 mg/dl; 0.50 mmol/L) as the cut-point.
Notably, eLDL-TG was more strongly associated with ASCVD events than Rem-C, sdLDL-C and apoB.
Unexpectedely, we also observed in the UKB cohort that eLDL-TG was superior to measured apoB or estimated sdLDL-C as a risk marker for ASCVD. We also show that eLDL-TG appears to increase ASCVD risk even above and beyond LDL-C > 190 mg/dl.

I guess that’s one more good reason to test omega 3 and supplement with EPA in if it’s low: Omega 3 makes me depressed: why? - #17 by adssx

Here’s the equation in SI units (mmol/L) for Europeans (Supplementary Figure 3):

[mccoy]

@adssx

Here’s the equation in SI units (mmol/L) for Europeans (Supplementary Figure 3):

I wonder which are the Europeans countries where mmol/L is the preferred unit. In my place, Italy, I’ve always seen the mg/dL unit used in lipid panels

[adssx]

Yes, it’s not really Europe vs US: the UK, Australia and Canada use mmol/L, I think. Many European countries as well (Germany?). France uses a bit of both depending on the lab.

[adssx]

I find this new biomarker useless because you still need to look at its components to take action: Do you have a non-optimal eLDL-TG because of high TG (and then you should take EPA)? High non-HDL-C (take ezetimibe, statin, etc.)? Low HDL-C (take obicetrapib?)?

I prefer Sam Tsimikas’ unproven “rule of 50” (in mg/dL, although Lp(a) should always be in nmol/L…):

I would add hsCRP < 0.7 mg/L to that list.

[mccoy]

@adssx

I find this new biomarker useless because you still need to look at its components to take action: Do you have a non-optimal eLDL-TG because of high TG (and then you should take EPA)? High non-HDL-C (take ezetimibe, statin, etc.)? Low HDL-C (take obicetrapib?)?

Your objection is sensible but, since eLDL-TG is a joined risk factor, the equation seems to be, per se, a useful biomarker as far as the optimization of ASCVD is concerned.

It is also possible, once you have your lipid panel and the eLDL-TG estimate, to simulate the interventions to be carried out on TG or on LDL (or on both) to take the eLDL-TG into a low-risk domain.

You may choose a target, for example take nonLDL-C down 30% and see what happens to the eLDL-TG. Or take TG down 30% if you want to use EPA instead of statins. Or to do both.

The safety domain though has not been well elucidated in the article.

However, my main objection remains, that the authors used a single relationship for ‘regular’ values and for huge values of TG and nonHDL-C. From the graphs, it appears clear that these subgroups follow different mathematical relationships.

Also, we’ll have to wait if their theoretical relationship will be validated by actual measurements since it appears that there is already a test for this biomarker.

Take take-home message to me is that it appears to be a useful marker but work is still in progress.

[AnUser]

ApoB Levels and Heart Disease: What You Need to Know | Daniel Soffer | The Proof Podcast EP #339

Simplified from where video starts.

→ Lower LDL/apoB is better.
→ 70 mg/dl or higher can still progress with atherosclerosis. Residual risk at this level.
→ Enhance outcomes with target 30-50 mg/dl, physiologic levels.
→ Only possible side effect is from the drug, not the reduction in LDL.
→ PCSK9 inhibitors pretty much side effect free to our physiology, only minor ones.
→ Statins primarily used because of data and cost. Athletes at higher level might want lower dose or other drug if they have muscle side effects etc.
→ Statin are magical because of abundance of clinical trial evidence in different populations, compared to PCSK9 inhibitors / Ezetimibe / Bempedoic acid, not pleiotropic effects.
→ Ezetimibe can for example be used after reaching maximally tolerable statin or if keeping statin dose lower for whatever reason.

Current disease additional therapies:
→ + Aspirin good if someone has plaque. Risk for bleeding higher with increasing age. CAC >100 and low risk of bleeding, for example.
→ + CAC >300 or >1000 (?), additional therapy with PCSK9i.
→ + Semaglutide good if someone is overweight.
→ + Colchicine, especially if they have inflammation.

[AnUser]

EmpowerDX in Europe (Only France it seems), but the cholesterol (including production / absorption test is not here):

empowerDX EU | Tests de santé à domicile - Livraison gratuite

In Ireland the one exists:

At home health testing and screening - empowerDx

Here’s the standard US one:

empowerDX - Self-collected health tests | Free shipping

We don’t like to see absolute concentrations of desmosterol below 0.8 mg/L in our patients. We also treat patients with one or two copies of the APOE e4 alleles or a family history of dementia with kid gloves and make sure they have a desmosterol level greater than 1.0 mg/L.

Does low cholesterol cause cognitive impairment? Part II - Peter Attia

I’m wondering it the European EmpowerDX will have the cholesterol test as well to measure desmosterol, among other things.

[DeStrider]

Interesting list of blood tests that are highly corollated to heart disease. Really interesting.

The factor with the highest corollation is HBA1C!

And instead of measuring ApoB, you should be measuring Oxidized ApoB.

Tests for Assessing Cardiovascular Risk

[John_Hemming]

I think the issue with glucose is that high levels of glucose cause more ROS in the mitochondria.

Perhaps HbA1c is one of the reasons why alcohol consumption is pleiotropic.

[Barnabas]

Is elevated HbA1c a canary in the coal mine (indicates that blood glucose has been too high on average) or is it itself a problem? I.e. does high HbA1c mediate problems caused by high blood glucose or just indicate it?

[John_Hemming]

Its the glucose that is the problem. Actually probably the peaks over 8 mmol/l

[Barnabas]

That’s what I would expect.

[Hire]

I’ve been in a similar boat with managing CVD risk and trying to stay proactive. I started statins a while ago after resisting them, and luckily, I haven’t had any side effects. Cutting back on saturated fat was a big shift for me, too, and I’ve found that exercise and managing stress have been just as important as the diet changes. I’ve heard good things about PCSK9 inhibitors and how they can lower LDL and help with plaque reduction, so I’m definitely curious to see where that goes, but like you, I’m waiting on more solid data before jumping in. It’s definitely a balancing act, but I think taking an active approach is key.

[desertshores]

I was pointed to this “Research ArticleVolume 419132698January 15, 2025” reference by a talking head on YouTube, whom I will not mention because he constantly promotes supplements that he profits from. I don’t mind a little of this, but the frequent interruptions of his YouTube videos for promotion are excessive. IMO
In any case, the article is fine.

Is this the bottom line?
The tests that count in determining your coronary atherosclerosis risk are:

Total triglycerides

HDL particle size
“Increasing circulating levels of small HDL associated with diabetes with an OR of 1.37 and 95 %CI of (1.15–1.63). Among the HDL lipid components, phospholipids in small HDL associated with diabetes. On the contrary, lipid rich large (triglyceride) and extra-large (free cholesterol, phospholipids, and cholesterol esters) HDL associated with a lower risk of diabetes”

A1C

CRP

Many studies and social media doctors claim that there is no real correlation between LDL cholesterol and coronary atherosclerosis.

I previously thought that LDL particle size was a significant factor, when in fact, the HDL particle may be more predictive.

A Quest test from Ulta Lab that measures the particle size of HDL, LDL, etc.

https://www.internationaljournalofcardiology.com/article/S0167-5273(24)01320-2/fulltext

[DeStrider]

My mother was prescribed 80 mg of Atorvastatin after her heart attack and stents. Unfortunately, she is suffering from muscle weakness in her thighs and we believe it could be statin-related.

After researching the data here:
https://www.ahajournals.org/doi/10.1161/01.cir.0000068312.21969.c8

It seems that Atorvastatin 80 mg is just as effective at LDL reduction as 10 mg + Ezetemibe. The Ezetemibe + 10 mg increases HDL as a bonus. I’m going to ask the doctor to switch her to 10 mg of Atorvastatin and Ezetemibe.

Anything I’m overlooking here?

[tj_long]

I would look into studies where secondary prevention is the focus of the research. The effect of statins in reducing heart attacks in individuals who already have heart disease is likely due to mechanisms other than lowering LDL-C levels (e.g., anti-inflammatory effects and plaque-stabilizing effects). Of course, LDL-C still plays a significant role over the long term.

However, as I understand it, even a small dose of statins provides the greatest benefits, for example, in reducing inflammation. Regarding the stabilizing effect, I’m not sure.

Personally, in that situation, I would probably ask for Atorvastatin 20 mg + Ezetimibe 5–10 mg

[sol]

Possibly related, my relative switched to pitavastatin for similar challenges, and found no deleterious side effects.

Also inexpensive when purchased from India. (Compared to it not being covered at all, which the insurance co decided to do as of 2025.)

[CronosTempi]

FWIW, I’ve switched from atorvastatin 10mg/day, to pitavastatin 4mg/day. I tolerated atorvastatin extremely well - basically no side effects and zero effects on any liver, kidney, glucose or other blood markes. However, atorvastatin started losing effectiveness as far as lowering LDL after a few years, and so I wanted to try pitavastatin. I picked pitavastatin for a variety of reasons, especially effectiveness against MACE and general CVD benefits. My PCP only offered to boost the dose of atorvastatin to control my LDL, and I thought this not effective. I therefore had to buy pitavastatin from Indian pharmacies, and the prices seemed very reasonable to me. I got Pivasta 4 from Zydus for $111 for 300 tablets.

I’ve stopped atorvastatin on Oct. 29/2024 and initiated the pitavastatin 4mg on November 1. So, it hasn’t been a month yet. I have so far not felt any effects whatsoever. I intend to get a lipid panel at the start of January 2025.

Before I decided on pitavastatin I’ve done a fair amount of research, and FWIW, there does seem to be less glucose perturbances, muscle pain, drug interactions and generally side effects with pitavastatin compared to atorvastatin, so that might be a consideration for some users. Meanwhile at least for CVD outcomes pitavastatin appears pretty stellar compared to most other statins.

[AnUser]

“High cholesterol is healthy!” (Myth finally explained)

[RapAdmin]

Source (and video) Here: x.com

Full interview here:

Dr. Benjamin Levine: How Exercise Prevents & Reverses Heart Aging