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Cholesterol Question

3,340 Views | 14 Replies | Last: 4 yr ago by Deluxe
Deluxe
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AG
Article Discussing Diet, Cholesterol and Lipoproteins

I'm kind of a newb to the cholesterol game but trying to learn more since my LDL levels were a little high on my last doctor visit. My current understanding is that LDL broadly is a lipoprotein that carries cholesterol (among other things) around in the blood stream, LDL-c is the amount of cholesterol in a given LDL and LDL-p is the number of LDL particles in the blood stream.

But the following example in the article above is confusing me:

Quote:

In order to understand how LDL-c, LDL size and LDL-p are interrelated, imagine that you are going to fill a bucket with golf balls and tennis balls.

The bucket is the total amount of cholesterol contained within LDL (LDL-c). The golf balls are small LDLs, while the tennis balls are Large LDLs.

The total number of balls is the LDL particle number.

You can fill the bucket with either tennis balls, or golf balls. The bucket will be just as full, but if you use golf balls the number of balls in the bucket will be much greater.

Is this a bad example or am I missing something? Shouldn't LDL-p be the number of buckets, not the number of balls?
hph6203
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AG
Just my understanding, but I think it works better if you think of the bucket as an LDL particle, the LDL-c is the volume occupied by the balls, and the LDL-p is the number of balls, so if you have a lower LDL-p relative to the LDL-c you have larger, less dense LDL-c.

Basically from what I've heard in my limited moments of listening to podcasts is that you can have an elevated LDL number, but as long as the LDL-p number is within range you're not at increased risk. You can have a normal LDL-c number and be at increased risk if your LDL-p number is high. Basically they should be testing for LDL-p rather than calculating LDL-c, but it's more expensive so they typically don't.
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Deluxe
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AG
Ok got it. That's pretty consistent with my understanding. Thanks!
lazuras_dc
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AG
I've taken a HUGE dive into this listening to Peter Attia's "The Drive" podcasts and researching things online along with my brother who is an internist who wasn't super familiar with the sort of "up and coming" lipidology stuff.

So what it boils down to is that LDL-c is a calculated LDL level which measures the amount of cholesterol being contained in LDL particles. LDL-p is the actual count. There becomes a big difference in small dense LDL particles (bad) and "fluffy" LDL particles.



See Rhonda Patrick and Ronald Krauss:

I recently had blood work done ordered by a friend who is a dietician to measure LDL-P, Lp(a), APOb and APOe. Which Peter Attia likes to consider some of the high importance markers.

I'm also getting some inflammatory markers shown as I believe its important to know that inflammation is sort of the driver that will eventually cause these lipoprotein particles to bind as plaques which drives heart disease and atherosclerosis

Again see Rhonda Patrick:
lazuras_dc
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AG
http://sdbiomarkerssymposium.com/presentations/Taub_1.pdf

Here's a good power point I came across
Deluxe
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AG
Looks like we've been going down some of the same rabbit holes. I actually just finished part four of Peter Attia's Straight Dope On Cholesterol. Some good stuff. And totally agree about Ronda Patrick. She's been a great resource as well. Looking forward to reading through the slides you posted.

Part of my frustration in researching all this stuff is sometimes people can be lazy when they refer to LDL, cholesterol, LDL cholesterol and LDL-c (and use some of those terms synonymously). I need to have a model in my head of what's happening functionally and loose speech in this regard messes me up. The balance chart you posted helps.

I'm also with you on getting some more advanced metrics performed. The general cholesterol/lipid labs that doctors use to determine high LDL and robotically prescribe a statin just seems archaic at this point. What inflammation metrics are you looking for?

My issue (I think) is that I'm a lean mass hyper responder (which you may be familiar with if you've gone down a Dave Feldman rabbit hole). I'm a lean/active guy who recently significantly lowered my carb intake because I find fats/proteins give me more sustainable energy throughout the day. This led to a transition in my body using more fat for energy and drove my LDL-c through the roof. The interesting part is that my HDLs are way up, Triglycerides are way down and VLDL is down a bit too. I'm almost 100% certain that my LDL-p is in good shape, but going to test it to be sure.
Deluxe
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AG
Maybe you can help me with this question. But first, here are my presuppositions (which may be wrong):

LDL - a lipoprotein that carries cholesterol (among other things) around in the blood stream
LDL-c - amount of cholesterol carried inside an LDL particle
LDL-p - number of LDL particles present in a given volume of blood

When I look at my basic labs, I interpret the LDL figure as the total volume of LDL lipoproteins present in a given volume of blood (in mg/dL), but I've also heard that LDL-c is what's measured for in basic labs. I don't think those are the same thing. Which is right?
lazuras_dc
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AG
The only thing wrong is your definition of ldl-c - it's not cholesterol in one particle. But you are correct when someone gets their basic lipid panel it just says ldl but really it's ldl-c. Basically It's a computed guesstimate of how much actual cholesterol (in mg/dL) that is being carried by LDL is my understanding.

"Blood tests commonly report LDL-C: the amount of cholesterol which is estimated to be contained with LDL particles, on average, using a formula, the Friedewald equation. In clinical context, mathematically calculated estimates of LDL-C are commonly used as an estimate of how much low density lipoproteins are driving progression of atherosclerosis. The problem with this approach is that LDL-C values are commonly discordant with both direct measurements of LDL particles and actual rates of atherosclerosis progression."

Btw here's an easy to read article on lp(a)
https://www.berelianimd.com/blog/lipoprotein-a
lazuras_dc
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AG
To answer your question my testing that I'm waiting on it this:
SpectraCell Lipoprotein Particle Panel: Total cholesterol, HDL, LDL, Triglycerides, Lipoprotein Particle Profile (includes: VLDL, LDL III, LDL IV, Remnant Lipoprotein, Lp(a), HDL2b, ApoB100, C-Reactive Protein, Homocysteine


If you want to do some of these test my dietician friend who's husband is an Aggie (and my former roommate) ordered the labs for me.

I also did MRT leap Food sensitivity testing (just got those results in today). And waiting on the spectracell lipid panel. On spectracells order sheet I also checked hba1c And apo E. I can keep you posted when I get results to compare with my lipid lab results I got from my PCP which was very basic at best.

https://chewsfoodwisely.com/lab-testing/
lazuras_dc
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AG
Deluxe, i had an issue with Spectracell and they rejected my submission as it was packed incorrectly by the independent lab. So I got the advanced lipid panel done by Quest instead.

Results:
MRT LEAP testing shows I have food sensitivity to cashew, broccoli, grain, wheat, buckwheat, barley, spelt , nitrates, cows milk, apples, bananas, honeydew.

Lipid Testing:
Total Chol- 192
HDL-C: 65
LDL-C: 115
Trigs: 42
LDL-p: 969 (optimal is less than 1100 nmol/L)
ApoB: 87 (optimal less than 90 nmol/L)
Lp(a): 334 (optimal less than 75 nmol/L)
HS CRP: .3 (optimal les than 1)
LP PLA2 activity: 134 (optimal under 123 nmol/min/ml)
LDL pattern: type A (opitmal)
LDL peak size: 219.9 angstroms (optimal is greater than 222)

So I think most of my figures I'm happy about other than the staggering LP(a) which is genetic. I may test again to make sure it was a fluke or test result error. But at this point not much I can do that's feasible. I know there are studies where niacin and PCSK9 inhibitors help the # but not really any adverse CV outcome.
LP PLA2 activity is inflammation in the vessel wall so that's increased.

Currently I am doing time restricted eating. If I can have a less than 8 hour eating window I am happy. I don't eat any baked good or desserts other than M&Ms in trail mix or chocolate covered almonds. But I prob eat a fair amount of processed or fast food /frozen meals and definitely pizza.
Exercise: I do one day a week stretch/mobility, 1 day a week cardio, and try and do a light kettlebell session once a week. Then throw golf or tennis on top of that once a week.

Changes: Likely will switch up diet to reduce or eliminate wheat/breads completely and reduce processed foods. and try to include more omega3's and niacin naturally rather than pharmaceutically.

Deluxe
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AG
Good stuff. Thanks for posting all that.

I actually got my Quest advanced lipid panel back yesterday and interestingly my results are almost the opposite of yours haha:

Total Chol: 249 (down from 285 a month ago)
HDL-C: 49
Trigs: 54
LDL-C: 185 (down from 219 a month ago)
LDL-P: 1,967 (higher than I was hoping for)

LDL-Small: 313
LDL-Medium: 561
HDL Large: 4,654
*All three of these were in the "high risk" range

ApoB: 130
Lp(a): 18 (pretty shocking how low this is relative to my other poor numbers across the board, but like you said, genetics play a big part)
HS CRP: 0.3 (other bit of good news)

***********

My GP still wants to put me on a statin but I'm not ready to concede that yet. At the very least, I want to continue down my current path for a longer sample size and see where it takes me. The gist of those changes that helped me lower my "headline" numbers pretty substantially in a month included incorporating more fiber into my diet (oatmeal, beans, etc), replacing roughly half my beef/poultry intake with high omega 3 fish and incorporating more cardio (mainly distance running) into my workout routine. Also been pretty obsessive about eating whole foods (except for some low cal gluten free bread with breakfast).

Part of the reason my numbers jumped a bit to begin with is because I was on a high protein/fat, low carb/fiber diet for a while and was generally just weight training instead of doing cardio. It sucks because I felt great on that lifestyle. Was burning fat for energy, keeping sugar out of my system and my muscles/joints felt great/refreshed every morning. Since incorporating more carbs/fiber, I feel a little more sore day to day, but maybe it's worth it to lower CVD risk.

Wish there were more straight forward answers on this stuff haha. Like at the end of the day, is there really a true cause/effect relationship between high "headline" cholesterol numbers and CVD? Obviously there's a historical correlation but the cause/effect relationship is inconclusive because so few variables are controlled for.

I guess what I'm learning is so much of this stuff is personal. I sent away for some Ancestry DNA data a few weeks ago and will hopefully get those results back soon. Also plan to do a diet allergy test (ie MRT LEAP) to try and gather some data points I don't currently have. We'll see how it goes.
Ronyaria
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Thanks for posting it here, I think it is really helpful and educating. I wanted to learn more about it
OasisMan
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AG
The prob with the lipid panels (hdl/ldl/tri),
If I tested them 3 days in a row I could get quite different results everyday
Deluxe
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AG
Yea the headline numbers can be variable and misleading. Which makes it crazy how cavalierly GPs prescribe statins to people based on 1-2 basic tests.

Statins can be right for some people sometimes, but I wish there was a more comprehensive diagnosis period before going that route. There's a ton of good info out there on cause/effect relationships of various lipid markers to CVD and not much of it is baked into GP standard practice. I'm fortunate to have enough time/bandwidth to research a lot of it myself. Feel bad for those who don't and end up taking statins unnecessarily for 50 years.
OasisMan
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AG
Prominent British cardiologist that is not pro-statins

Deluxe
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AG
Yep, modern wisdom on the subject seems to be trending in that direction
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