I am unfamiliar with this stuff. Is there a primer on the primer for the discussion? Is there any discussion of the mechanism by which particle count/LDL particle cholesterol desaturation occurs? Any tie-in to inflammatory processes?
There have been many threads about cholesterol. As most of us know the basic lipid analysis (total, LDL-C, HDL-C, trigs) that most doctors will have people undergo is largely useless.
However, advanced lipoprofiles (VAP/NMR) that include PARTICLE numbers and size, along with CHOLESTEROL counts tends to give us much better information (much higher correlations to cvd events) than the basic testing. Brief primer below.
Example from "LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study - Implications for LDL Management".
Has anyone had this testing done? Any of the docs have opinions on the matter?
I just got my test results back and they were quite disturbing in terms of particle numbers (I'm probably going to die soon), but pretty solid in terms of particle size and type (doesn't correlate to good health or CVD events as well as particle NUMBER, but much better than cholesterol numbers).
I wanted to start this thread so hopefully we can have a thread with some quality information about cholesterol without all the noise.
I am unfamiliar with this stuff. Is there a primer on the primer for the discussion? Is there any discussion of the mechanism by which particle count/LDL particle cholesterol desaturation occurs? Any tie-in to inflammatory processes?
Does anyone know if we took drugs to make our particles just the right size would it change anything as far as health and longevity?
This is where I started. The article includes links to various studies.
This is the company that performed the NMR test
In case link is removed.
I'm sure Sully and Jordan have more insight into this.The NMR LipoProfileŽ test is an advanced cardiovascular diagnostic test that uses nuclear magnetic resonance (NMR) spectroscopy to uniquely provide rapid, simultaneous and direct measurement of LDL particle number and size of LDL particles, as well as direct measurement of HDL and VLDL subclasses. This detailed lipoprotein particle information allows clinicians to make more effective individualized treatment decisions than previously possible based on standard lipid panel testing. The atherosclerotic culprit is LDL particle number, not LDL cholesterol.
Seems particle SIZE has far less to do with a cvd free existence than particle COUNTS. I'd like to have more information on that, though.
This quebec study seems to be the go to study on the topic
My Dr is providing the same types of tests and my last report was 6 pages long. He also is more concerned about my particle numbers and size rather than total cholesterol numbers. I had a lengthy conversation with Sully last Saturday night at our coaches conference about this very subject, but since we were drinking whisky, I don't remember much other than he not worried about it as much and that statin drugs pose risks of their own. Maybe he will weight in on this thread and remind me what he already told me.
When controlling for LDL-P, particle size doesn't seem to matter wrt risk of atherosclerosis. The initial confusion was that, at a given LDL-C, type A LDL (bigger, fluffier) implies a smaller LDL-P, and the converse for type B (higher LDL-P). So in that sense, type A is "better," all else constant. Sometimes, however, all else isn't constant, as there are a whole lot of people with type A who still have LDL-P, which would still logic out to be potentially atherogenic.
If you directly know your particle number, you can skip that information. In your case, that's high. Is it a potential health problem? Quite possibly.
To be totally honest, going through the history of what we "know" about heart disease and its relationship to LDL/cholesterol is extensive, and when people depend exclusively on low-carb authors (Taubes, the paleo guys, etc.), it's also extremely tiring. What we "know" on the subject is a combination of epidemiology, controlled trials using animal models (including primate models), metabolic ward trials of the differential impacts of different food items on cholesterol, investigation into genetic abnormalities related to LDL (including the very high, i.e. familial hypercholesterolemia, and the very low, which they're still identifying), research into the LDL receptor and the impact saturated fat/cholesterol have on this (related to familial hypercholesterolemia), drug research, RCT's attempting to use interventions to alter people's biomarkers and mortality with some combination of lifestyle + drugs, and all sorts of stuff in between. It is is not a particularly light subject that you can hope to grasp by reading a few diet books, and probably takes access to higher level academics to really begin to get the scope of it all.
I will say that I had low carb/paleo leanings myself at one point, but after having cholesterol issues that I managed to clear up by taking the vector opposite advice (a large increase in carbohydrate intake in the form of oats, fruit, and sweet potatoes with a simultaneously large decrease in sources of saturated fat and cholesterol), I attempted to explore that research better. What I found was that depending on low carb and paleo types for a comprehensive understanding of cholesterol issues was a very large mistake.
In terms of how to lower it, that also depends. There is a large genetic component to variability in dietary responses (e.g. the apolipoprotein E alleles and their differential impact on saturated fat and cholesterol metabolism), so it's hard to know what will work for you minus good old-fashioned trial and error. As a rule, any diet which causes weight/fat loss will tend to move biomarkers in the right direction, LDL-P included. That isn't always the case, however.
Easy things to try to help lower LDL-P
* A sustainable diet that results in weight (fat) loss that has a shitload of fruits/vegetables.
* Lowering saturated fat and cholesterol, depending on genetic susceptibility.
* Removing junky carbs, particularly dense sources of fructose/HFCS (e.g. sodas and other sugary drinks).
Parasitic infection also seems to have a positive impact on cholesterol, but I'd probably avoid that one.
Note: references available on demand.
Here's a good start. First part of Dr. Peter Attia's 9-part series. Seems NMR is a better test than VAP, and counts matter more than size, and we don't really entirely know why. http://eatingacademy.com/nutrition/t...esterol-part-i
I lost ~20 lbs: 178 to 158, and it had ZERO effect on my basic lipid profile. Total was 2 pts different. LDL was exactly the same. HDL was about 2 pts different. Trigs were 3-5 pts different. I took a blood test at the end of novice bulk and my total jumped ~60 pts (255 to 314) and after losing all the weight over the last 2-3 months, there was no change. Granted I have no idea if/how the particle numbers changed, since I never took that test before now.
For reference what I eat is pretty constant.
BREAKFAST
nada
LUNCH
3-4 ounces of chicken or turkey
2-3 cups of steamed veggies
SNACK
1/2 cup oatmeal
1 cup plain greek yogurt
PW
10g BCAAs
DINNER
9 ounces 85/15 grass fed beef
Whole wheat hamburger bun
2 cups of red cabbage
or
10-12 ounces of free range chicken breast
1 cup of sweet potatoes
2-3 cups of broccoli
(some variant of these 6 things: no cooking fats at all)
SNACK
1 scoop Whey protein.
All liquids are coffee, tea, diet coke, and water. Nothing else.
I eat this every single day except on Saturday when I have a cheat meal: usually 3-4 slices of Pizza and some ice cream or something.
Apparently, my genes are shit.