#2094

What do you mean by that?

#2095

I’ve uploaded my genes to Nebula Genomics, which reported that my apoB is predicted to be very high from genetics. Higher than 100% of other people with genes related to apoB. Since apoB increases with chronological age, that might mean that it realizes over time .

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#2096

How old are you if you don’t mind answering?

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#2097

I am in my late 20’s.

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#2098

Now at least some of your (pre)occupation with blood lipids and appB seems a bit more understandable.

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#2099

How many people have uploaded their genes to this service? You’re the highest one and your apo B is around 60? I don’t think this means much at all. You’ve proven it.

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#2100

FWIW

There was a few posting on lumbrokinase and a few other enzymes on this forum last year{2022).

#2101

But this one says it stops kidney stones. Anyway the one’s made from calcium oxylate.

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#2102

I’m sorry, but I think you are overly concerned with your apoB levels.
image

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#2103

Here is the best article I have found so far addressing Lp(a) and ApoB. It is primarily addressed to clinicians and I don’t profess to understand all of the results and implications. But, your ApoB looks good to me.

From the article:

“Lp(a) is predominantly a monogenic cardiovascular risk determinant.”
“Lp(a) levels are ≈70% to ≄90% genetically determined.”

This means that it is not easy to change.

“Standard LDL-C and apoB lowering treatments have minimal Lp(a)-lowering efficacy, with some statins minimally increasing Lp(a) levels.”

My own Lp(a) levels are less than 10 nmol/L, but that does not put me at less risk if my other lipid levels are out of whack

What method is the lab using to measure your Lp(a)?
Apparently, it is more difficult to measure accurately than other lipids.

"2 major problems affecting the accuracy of Lp(a) results and their clinical interpretation. The first problem, related to the size variability of apo(a), results in under- or overestimation of Lp(a)

“The second problem is that, at present, there are 2 approaches to immunoassay calibration resulting in 2 different units for reporting Lp(a) results”

https://www.ahajournals.org/doi/full/10.1161/ATV.0000000000000147#:~:text=Lp(a)%20is%20predominantly%20a,apoB100%20and%20apolipoprotein(a).

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#2104

I have family members with LDL in 99th percentile and apoB in 80th percentile. Of course we have a difference in diet and other factors. I believe it as there is cardiovascular disease in my family too. It’s based on 5000 users of the website.

I don’t know, but it’s a reputable lab. I can test it again.
And IMO and for me it is worth lowering to 30-40 apoB or even 20-30.

#2105

What studies have you been looking at that give you that opinion?
Most of the lipid studies that are recent seem to be giving a U-shaped curve for optimal levels.
“Elevated apoB was significantly associated with an increased risk for cardiovascular mortality, while its association with all-cause mortality was non-linear correlated, with an increased risk at both low and high apoB levels.”

#2106

It’s based on RCT’s of statins and PCSK9 inhibitors showing a reduction in events to LDL levels nearing 20 mg/dl. Which means there are benefits to be had in preventing ASCVD to those low levels. The process is still active on levels above, for sure.

I don’t care about the assosciation studies. The low levels are from diseases and not from lowering it pharmaceutically.

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#2107

The genetic tests are not infallible. For instance Nebula told me I will go bald and I won’t. Not sure how that’s possible.

#2108

It’s because every measurement reported in percentiles is based on different studies.

#2109

Don’t we already see plaque reducing effects at levels below 70?

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#2110

Plaque isn’t reduced for everyone below 70 mg/dl, and the relevant part is whether plaque progresses, or not. If you could find any study showing how plague is progressing (+ - or stable) that would be good. Specifically how many have no progression (includes regression). A PCSK9 inhibitor study I read didn’t mention how many had no progression, only that more people had regression from lowering to very low levels, etc.

For regression of plaques, lower is better with 100% probability. And of course for events as mentioned earlier. Still not sure if atherosclerosis can develop at apoB or LDL at 20-30 mg/dl.

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#2111

I found a meta-analysis looking at plaque reduction at certain LDL levels. Not sure how well done it was but I’ll post it anyway for others to pick apart.

To explore the target level of LDL for plaque regression, the included studies were divided into five groups according to the levels of LDL at follow-up: < 70, 70–80, 80–90, 90–100, > 100 mg/dL. The subgroup analysis of TAV data showed significant plaque regression in the LDL < 70 mg/dL group (SMD: 0.195 mm3; 95% CI 0.086, 0.304; P < 0.001) (I2 = 59.0%, P = 0.001, Fig. 1A) and the 70–80 mg/dL group (SMD: 0.078 mm3; 95% CI 0.003, 0.153; P = 0.042) (I2 = 0.0%, P = 0.752, Fig. 1A) at follow-up. The subgroup analysis of PAV data showed significant plaque regression in the LDL < 70 mg/dL group (SMD: 0.152%; 95% CI 0.001, 0.303; P = 0.049) (I2 = 78.9%, P < 0.001, Fig. 1B), 70–80 mg/dL group (SMD: 0.079%; 95% CI 0.003, 0.155; P = 0.042) (I2 = 0.0%, P = 0.97, Fig. 1B) and LDL 80–90 mg/dL group (SMD: 0.423%; 95% CI 0.196, 0.651; P < 0.001) (I2 = 45.1%, P = 0.141, Fig. 1B) at follow-up. The total effect was statistically significant.

There was a significant plaque regression in the LDL < 80 mg/dL and HDL > 45 mg/dL group (SMD: 0.163 mm3; 95% CI 0.092, 0.234; P < 0.001) (I2 = 29.5%, P = 0.088, Fig. 3A) in the subgroup analysis of TAV, and there was a significant plaque regression in the LDL < 90 mg/dL and HDL > 45 mg/dL group (SMD: 0.186%; 95% CI 0.081, 0.291; P = 0.001) (I2 = 71.3%, P < 0.001, Fig. 3B) in the subgroup analysis of PAV. The total effect was statistically significant.

According to the latest guideline for the management of blood cholesterol and dyslipidemias, experts recommended that patients with a very high risk of arteriosclerotic cardiovascular disease (ASCVD) reduce LDL levels to below 70 mg/dL, which can delay the progress of risk factors and reduce the incidence of adverse events8. Our subgroup analysis showed that TAV was significantly reduced when the LDL levels were less than 80 mg/dL at follow-up, and PAV showed a significant decrease when the LDL levels were less than 90 mg/dL at follow-up.

Our analysis suggests that patients with CHD require an LDL level below 80 mg/dL and HDL above 45 mg/dL at follow-up for regression of coronary plaques to occur.

The effects of lipid-lowering therapy on coronary plaque regression: a systematic review and meta-analysis | Scientific Reports (nature.com)

This study implies even reducing your levels well below 100 could be enough for some plaque reduction and below 70 you get significant plaque reduction.

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#2112

Glad to hear that.

I was only pointing out the U-shaped curve.

I am in the “Dr. Lipid” camp that your LDL can’t be too low if you are healthy.

I am attempting to reach that goal without a statin. A few weeks ago I added ezetimibe to the mix. My latest lab

That was with an atorvastatin 40 mg tablet in the evening and 600 mg of Pantethine in the morning. In the last two weeks before the test, I added 10 mg of ezetimibe in the morning along with the pantethine.

For my next experiment, I will have been on 10 ezetimibe and 600 mg of pantethine in the morning and 10 ezetimibe in the evening for about 6 weeks before my test. I have dropped the atorvastatin and switched to a carnivorous diet. Not, too scientific but I don’t have time to continually test one variable at a time.

I have felt zero side effects from both the ezetimibe and the Pantethine.

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#2113

I’m very interested in your journey to lower your apoB and LDL with natural supplements since those could be used as adjunctives to my current rosuvastatin/zetia therapy. To 100 and beyond!

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