Conversion factor for ApoB units?

(BuckRimfire) #1

Lab test results for ApoB in my care system are reported in mg/dL, but in publications they’re often in molarity (e.g. nanomoles per liter). Anyone know the conversion factor?

I could just look up the molecular weight of an ApoB protein and do it directly from that value, but I’m wondering if there is something about the measurement/reporting method that would confound that.

In fact, I tried doing that from my ApoB test result (which was near the middle of the “normal” range), and got 23 microM (23,000 nanoM), which is ridiculous! And 2300 nM would be extremely high, while 230 nM would be impossibly low, so I doubt I’ve made an order-of-magnitude error.

(Bob M) #2

This might work:

http://unitslab.com/node/35

(Bob M) #3

My last value was 83mg/dL:

image
image.png834×398 14.2 KB

Note that a mere 3 days before this my ApoB was 116. So, it went from 116 to 83, in three days. The 116 was after 4.5 days fasting, and the 83 was after eating 3 days of high fat, high calorie, and 12 hours fasting.

(Bob M) #4

The changes wrought in three days of high fat, high calorie, from 6/14 to 6/17:

image
image.jpg1305×654 206 KB

(BuckRimfire) #5

Jeez, that calculator says I was at 2.3 µM. I guess I did make a factor-of-ten error. Gotta try that calculation again.

That’s very high in the MESA data range but not terribly high in the “standard range” quoted by my lab. Not sure I understand that yet. But the MESA and range shown in your figure would be more concordant…

(Bob M) #6

I personally don’t believe that LDL or ApoB or Lp(a) cause heart disease. The root cause is something else. At most, if the root cause is causing damage, higher values of these MIGHT be more problematic, though I’m not sure about that.

I think the root cause is damage to the endothelium/glycocalyx/vasa vasorum. That root cause may be many factors: stress; poor diet; smoking; etc.

(Bacon is a many-splendoured thing) #7

There is a paper by Ravnskov and Diamond, in which they posit that damage is continually occurring to the arteries, but as long as the repair mechanisms can keep up, atherosclerotic plaque does not accumulate. However, dietary factors (such as excessive carbohydrate intake) can accelerate the rate of damage, which causes an accumulation of plaque, eventually leading to calcification. The risk of death, stroke, or myocardial infarction then arises from factors (such as glycation of the haemoglobin; again, resulting from excessive carbohydrate intake) that cause the blood to be likelier to clot as it passes through the narrowed, stiffened arteries.

They may not be altogether correct, but it’s a plausible mechanism, and they do have some supporting evidence.

(Bob M) #8

It’s really the only thing that makes sense. Anyone who wants to read more can go to Dr. Malcolm Kendrick’s blog and read his 50+ posts about what he think causes heart disease, which agrees with what we both just said.

Like many low carb gurus, though, you might take his covid analysis with a grain of salt. Or just ignore it, as I think his heart disease theory is a good one.