Eddy Edson
Well-Known Member
- Relationship to Diabetes
- Type 2
Poster from current American Heart Association 2022 scientific sessions:
This study really encapsulates what I take to be the latest thinking amongst lipid experts:
- ApoB particle count is the causal thing for atherosclerosis.
(This correlates with non-HDL cholesterol levels, because every non-HDL particle has one apoB particle. But there can be discordance: eg with metabolic syndrome and T2D you can get smaller LDL particles, so for the same non-HDL cholesterol level you get more LDL particles and hence more apoB particles. So apoB is the best measure, and it's also easy to do, but until that makes it's way into clinical practice, stuck with non-HDL-C measurement as a proxy.
Anyway, better than total cholesterol and much better than "ratios" like total cholesterol/HDL-C and trigs/HDL-C, which these days are generally recognised as clinically irrelevant and not valid treatment targets.)
- What matters is not the snapshot of apoB levels but the total exposure over time. It's like with smoking; the important thing is "pack-years", ie how much & for how long.
- Along with that, the standard 10 year risk assesment is inadequate; what matters is lifetime risk, which is generally a lot higher, and the accumulation of risk starts young.
- So the standard "don't worry until you're over 40" advice you see is misguided.
- In fact, the advice should be, "As low as possible for as long as possible, starting from a young age".
- The study summarised by this poster looked at how total apoB & other particle-count exposures during the ages 19-40 years correlated with new-onset cardiovascular disease after the age of 40.
For every standard deviation increase in total apoB exposure during younger years, the CVD risk in middle age is about 50% higher.
- There appears to be a threshold effect, with an average daily apoB exposure of approx 80mg/dl = 0.8 g/l being the point at which long-term risk increases.
The reference ranges you see are usually something like 0.5 g/l - 1.5 g/l, but at least some NHS trusts, for example, do recognise 0.8 g/l as a risk threshold: https://www.nbt.nhs.uk/severn-pathology/requesting/test-information/apolipoprotein-b
- How that compares with the things you see on a standard lipid panel currently is not exact, but there are empirical models which give estimates which seem to work reasonably well, except when they don't, if you know what I mean.
Eg: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0051607
That's in American units, giving apoB in mg/dl = g/l X 100. Different equations depending on whether trigs greater or less than 270 mg/dl = about 3.0 mmol/l.
Multiply TC (total cholesterol) and HDL by 38.7 and trigs (TG) by 88.6 to convert from mmol/l to mg/dl.
I have TC = 2.5 mmol/l, HDL = 1.3 mmol/l and trigs = 0.5 mmol/l and the model estimates my apoB at 34 mg/dl Other similar models estimate it in the range 34 mg/dl - 38 mg/dl.
That's good, but too late to stop me from developing PAD! Curse my misspent youth etc etc.
As another example: Take somebody with LDL = 2.5 mmol/l, HDL = 1.5 mmol/l, trigs = 1.0 mmol/l. Total cholesterol would be 4.5 mmol/l. Few practitioners would see this profile as a problem for an under 40 year old, I think. Also, the "ratios" are good, for those who don't think they are completely irrelevant: TC/HDL = 3.0, trigs/HDL = 0.7. Lots of low carbers would see these as "excellent", I think.
But the models estimate an apoB level for this profile of 81+ mg/dl - 90 mg/dl. So it is likely that a young persion with this profile is slowly accumulating CV risk which may materialise in middle age, and it would be good to jump on it now.
This study really encapsulates what I take to be the latest thinking amongst lipid experts:
- ApoB particle count is the causal thing for atherosclerosis.
(This correlates with non-HDL cholesterol levels, because every non-HDL particle has one apoB particle. But there can be discordance: eg with metabolic syndrome and T2D you can get smaller LDL particles, so for the same non-HDL cholesterol level you get more LDL particles and hence more apoB particles. So apoB is the best measure, and it's also easy to do, but until that makes it's way into clinical practice, stuck with non-HDL-C measurement as a proxy.
Anyway, better than total cholesterol and much better than "ratios" like total cholesterol/HDL-C and trigs/HDL-C, which these days are generally recognised as clinically irrelevant and not valid treatment targets.)
- What matters is not the snapshot of apoB levels but the total exposure over time. It's like with smoking; the important thing is "pack-years", ie how much & for how long.
- Along with that, the standard 10 year risk assesment is inadequate; what matters is lifetime risk, which is generally a lot higher, and the accumulation of risk starts young.
- So the standard "don't worry until you're over 40" advice you see is misguided.
- In fact, the advice should be, "As low as possible for as long as possible, starting from a young age".
- The study summarised by this poster looked at how total apoB & other particle-count exposures during the ages 19-40 years correlated with new-onset cardiovascular disease after the age of 40.
For every standard deviation increase in total apoB exposure during younger years, the CVD risk in middle age is about 50% higher.
- There appears to be a threshold effect, with an average daily apoB exposure of approx 80mg/dl = 0.8 g/l being the point at which long-term risk increases.
The reference ranges you see are usually something like 0.5 g/l - 1.5 g/l, but at least some NHS trusts, for example, do recognise 0.8 g/l as a risk threshold: https://www.nbt.nhs.uk/severn-pathology/requesting/test-information/apolipoprotein-b
- How that compares with the things you see on a standard lipid panel currently is not exact, but there are empirical models which give estimates which seem to work reasonably well, except when they don't, if you know what I mean.
Eg: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0051607
That's in American units, giving apoB in mg/dl = g/l X 100. Different equations depending on whether trigs greater or less than 270 mg/dl = about 3.0 mmol/l.
Multiply TC (total cholesterol) and HDL by 38.7 and trigs (TG) by 88.6 to convert from mmol/l to mg/dl.
I have TC = 2.5 mmol/l, HDL = 1.3 mmol/l and trigs = 0.5 mmol/l and the model estimates my apoB at 34 mg/dl Other similar models estimate it in the range 34 mg/dl - 38 mg/dl.
That's good, but too late to stop me from developing PAD! Curse my misspent youth etc etc.
As another example: Take somebody with LDL = 2.5 mmol/l, HDL = 1.5 mmol/l, trigs = 1.0 mmol/l. Total cholesterol would be 4.5 mmol/l. Few practitioners would see this profile as a problem for an under 40 year old, I think. Also, the "ratios" are good, for those who don't think they are completely irrelevant: TC/HDL = 3.0, trigs/HDL = 0.7. Lots of low carbers would see these as "excellent", I think.
But the models estimate an apoB level for this profile of 81+ mg/dl - 90 mg/dl. So it is likely that a young persion with this profile is slowly accumulating CV risk which may materialise in middle age, and it would be good to jump on it now.
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