50k-lipid aterial: Dr. Thomas Dayspring | Cholesterol Testing: What Matters Most?

ATLCX (Episode 29): Dr. Thomas Dayspring | Cholesterol Testing: What Matters Most? « Jimmy Moore's Livin' La Vida Low Carb Blog

In Episode 29 of “Jimmy Moore Presents: Ask The Low-Carb Experts,” we’re very excited to bring to you one of the world’s leading lipidologists and experts on just about everything you could ever want to know about cholesterol numbers named Dr. Thomas Dayspring from LecturePad.org.

He’s the Director of Cardiovascular Education at the Foundation for Health Improvement and Technology in Richmond, Virginia and is one of the most requested speakers in the United States with expertise on atherothrombosis, lipoprotein and vascular biology, advanced lipoprotein testing and more. Dr. Dayspring has given over 4000 lectures in all 50 states educating medical professionals and the lay public alike.

Many of you first heard Dr. Dayspring in Episode 585 of “The Livin’ La Vida Low-Carb Show” podcast and afterwards my listeners had lots of questions for Dr. Dayspring about cholesterol. That’s why we decided to bring him back on ATLCX to take on the topic “Cholesterol Testing: What Matters Most?” so you can speak directly with him about your burning questions on your cholesterol concerns.

This was a golden opportunity to get better clarification on any issues regarding cholesterol testing that concern you. Listen in to hear what Dr. Thomas Dayspring had to say as he took on your questions about the most important factors in cholesterol testing in EPISODE 29 on October 4, 2012.

Listen to Dr. Thomas Dayspring on “Cholesterol Testing: What Matters Most?”:

People are concerned (and confused) about cholesterol

Gary Taubes/Peter Attia turned him on to community

Atheroschlerosis “build-up of cholesterol” in arterial wall

Blood tests help doctors determine heart disease risk

People with heart disease have cholesterol levels “all over the place”

Even persons with seemingly “perfect cholesterol” can get atheroschlerosis

Tim Russert is a perfect example of this

No human has any cholesterol floating around in blood as a free molecule

Lipids must bind to protein to become soluble in water (plasma)

Lipids bound to apoproteins are lipoproteins which traffic lipids in plasma

This “illegal dump job” (lipoproteins carrying cholesterol into the artery) can lead to atherosclerosis

Thus atherogenesis is a lipoprotein-mediated disease

Atherogenic lipoproteins (lipoproteins that enter the artery wall) are the “bad guys”

The goal is to avoid lipoproteins from penetrating the artery wall

We have to have labs that measure lipoprotein concentrations, rather than lipid concentrations

This (particle concentrations) is the type of testing we all need to have done

Omega-3 and omega-6 fatty acids are within the phospholipids delivered by lipoproteins

The types of lipoproteins: VLDL, IDL, LDL and HDL

Traditional tests look at cholesterol measurements like the total cholesterol (TC)

TC is the amount of cholesterol carried within all of the lipoproteins per deciliter of plasma

HDL-cholesterol has as its surface apoprotein, apolipoprotein A-1

ApoA-I measurement serves as an HDL particle count

You can have a lot of HDL particles, but low HDL-cholesterol

Thus although apoA-I and HDL-C usually correlate, in some folks they do not (discordance)

People with low HDL-C but normal apoA-I tend not to get heart disease

Those with high HDL-cholesterol could have low Apo A-1 (low HDL particle count)

There is one apoB molecule per VLDL, IDL and LDL particle: apoB is not on HDL particles

Apo B testing measures how many VLDL, IDL and LDL exists per deciliter of plasma

Apo A-1 particle do not deposit cholesterol in the artery: they may in fact remove it.

Apo B particles after entering the artery sticks

White blood cells (macrophages) ingest apoB particle carrying cholesterol and initiate inflammation

VLDL takes lipids (mostly TG, but also cholesterol) out of the liver;

VLDL traffic TG to muscle and fat cells and as TG exit the VLDL shrinks, creating IDLs

Most IDLs are cleared at the liver but some IDL shrink and become LDLs

Liver isn’t as efficient at clearing LDL particles compared to IDLthus extending LDL plasma residence time

A normally composed LDL half-life is 2-3 days; compared to VLDL 2-6 hours or IDL 1-2 hours

Thus Apo-B test actually measures LDL-P in the blood (vast majority of apoB particles are LDLs)

Standard LDL cholesterol test may or may not help

LDL cholesterol might be low, but LDL-P could be high: normally the two tests should correlate very well: when they do they are concordant and when they do not they are discordant

Particle size has no bearing on whether LDL enters the artery wall or not

Insulin resistant Diabetics typically have the small LDL regardless of LDL-C

How you can have low LDL-cholesterol and yet high LDL-P numbers (discordance)

LDL is supposed to carry primarily cholesterol with little TG (4:1 ratio)

Increased LDL/triglyceride level occurs when LDLs are trafficking more TG than normal – in such cases they are therefore carrying less cholesterol than they should. These are therefore cholesterol-depleted LDLs.

It takes 40-70% more cholesterol-depleted particles to traffic a given amount of cholesterol

In such cases we need a therapy to remove triglycerides from LDL

High triglycerides/low HDL-cholesterol ratio (> 3.0) is very indicative “insulin resistance”

You can’t guess particle levels by looking at TG or cholesterol values provided in traditional test

Triglycerides should be well under 100, even below 70 to be physiologic

What if you have large LDL particles and normal Apo B (i.e. normal LDL particle count or LDL-P)

Total cholesterol minus HDL is called non-HDL cholesterol: it reveals how much cholesterol is in the apoB particles and thus serves as a better measure of atherogenic apoB particles than does LDL-C

However, even Non-HDL cholesterol misses 30% of persons with high apoB (LDL-P) at-risk cases

Just get an Apo B and/or LDL particle test and know exactly if atherogenic particles are present

It’ll be the best money you’ll ever spend on health

You can get Apo B test run in any lab in America

Why the NMR Lipoprofile test (LDL-P) is the one to get run (nuclear magnetic resonance spectroscopy)

LipoScience is the only lab that runs this test now

FDA just approved smaller versions of their analyzer for other labs to purchase

Two other technologies exist that measure LDL-P, but those methods are “unproven” in clinical trials

Everyone needs to know their LDL particle number (LDL-P or apoB)

When you order LDL particle test, they also report standard lipid concentrations

Even kids should have a LDL-P test if there is a family history of heart disease, high cholesterol or diabetes or if the kids are obese

Severely elevated LDL-P disorder can and should be treated early in life

But almost nobody is screening these children at all

LDL cholesterol levels under 100 mg/dL has long been the standard

LDL-P of 1600 nmol/L is in the 80th percentile

A desirable LDL-P of 1000 is the 20th percentile population cut point: 80% of the populations has a higher level

LDL-P under 700 is in the 5th percentile population cut point: 5% of folks are less and 95% are higher

If particle counts are high, nutritional therapy first and then maybe drugs

The most common cause of why LDL-P becomes high: insulin resistance

You gotta take carbs out of your die to combat IR or take drugs or both

Insulin resistance is at the heart of high LDL-P

Why NCEP guidelines don’t say anything about LDL-P: Actually 5 US specialty Society guidelines do advise apoB or LDL-P testing

Apo B is in the European guidelines, but not LDL-P (LDL-P by NMR is not available in Europe)

Guidelines are never meant to take be cutting edge

LDL particle tests are more expensive than regular lipid concentrations

LDL-P by NMR in a patient without insurance coverage is four times more costly than traditional tests

The majority of doctors don’t know understand or know of Apo B and LDL-P

If these tests are done, because so many with fine cholesterol levels will have high apoB, drug use will quadruple and third party payers and govenrment does not want that

Drugs are almost always necessary unless you start eating low-carb ASAP

The low-fat diet (without carb restriction) is the “worst thing you can do” in a person with IR and high LDL-P

The specialty societies (ADA, ACC, AACC, ACE, NLA) are on board with new tests

Individual patients often have “discordance” between cholesterol measurements and apoB (LDL-P)

I convinced my own doctor to start doing NMR testing

Dr. Dayspring’s story about personal lipid revelation:

Dr. Jim Otvos inventor of NMR LipoProfile in reality likely saved his life: Dr D had a perfect lipid profile, but a very high LDL-P that never would have been discovered without doing the NMR LipoProfile

His 2012 study of diabetics looking at LDL particles (American Journal of Cardiology Sept 2012)

Check out information on why LDL particle tests good

Once LDL is 190 mg/dl, that’s familial hypercholesterolemia

Definitely get an Apo B and LDL-P immediately to see the extent of apoB elevation

Normal cholesterol and high LDL-P suggests IR and calls for low-carb diet

Some low-carbers have “paradoxical” rise in both LDL particles and LDL-C

These people might require aggressive use of drugs

The drug therapies that are needed for people with FH

Most FH take up to 4 medications to control LDL-P

Several new drugs are “in the pipeline” coming soon

I’ve personally seen my LDL-cholesterol and LDL-P go way up

That shouldn’t happen under normal circumstances

These people are “enigmas” with potential yet to be discovered genetic abnormalities

This doesn’t mean you should stop your low-carb diet

If you’re insulin resistant, you need low-carb

My current high-fat, low-carb n=1 experiment

Apo B is a worldwide standard for lipid/lipoprotein health

If patient is stable, it’s not unreasonable to stop statin and test again (no more than 4 weeks later)

Statins (can) have downsides, so take off if possible: in general for folk with high apoB the benefit of statins is vastly superior to any downside)

Lipoproteins can change drastically in 2-3 weeks with lifestyle and drugs

Retest again after one month to see how it goes off statins

Any studies looking at low-carb and decreased LDL-P

This is the type of thing modern researchers will be doing

There’s support for this, but mainly from Atkins diet studies

Lifestyle and/or meds reduce risks of high LDL-P

Risk of sterols in the development of arterial plaque

Watch Part 1 of Dr. Dayspring’s lecture on sterols

Cholesterol, a zoosterol, is one sterol; plants also produce sterols called phytosterols

Intestines usually push out plant sterols; not always

Some make into lipoproteins and penetrate arteries

Measuring phytosterols is probably a good idea: they serve as a biomarker of intestinal sterol absorption

Physicians are starting to measure this more and more

Cholesterol-absorption blockers can reduce intestinal hyperabsorption of sterols

Phytosterols sold in stores may be more harmful than good if taken by a person who is a hyperabsorber

Humans with normal sterol absorption would not be harmed by phytosterols

A hyperabsorber taking phytosterols might lower LDL cholesterol, but raise phytosterols

Without assaying sterol absorption These products may not be “heart-healthy” at all, just “hocus pocus”

The phytostanol, sitostanol, (Benecol) reduce cholesterol absorption and stanols are not absorbed, so this canbe an excellent functional food that safely lowers LDL-C and LDL-P

LDL cholesterol levels may or may not be associated with LDL particle concentrations

20 years ago, in assaying LDL we’d were “extolling” LDL-cholesterol tests

Changing things in medicine is a slow, hard road

Patients must educate yourself and get what you need done

Don’t assume doctors are “genius” on all health matters, especially cardiovascular biomarkers

How the various cholesterol numbers are calculated

Calculated LDL-cholesterol is an imprecise equation

If your trigs are under 100, divide by 5 for VLDL-cholesterol determination: Once you have VLDL-C, you can calculate LDL-C using the equation LDL-C = TC minus HDL-C – VLDL-C

Triglycerides is a key marker that few health care professionals truly, understand

Trigs over 70 in an IR adult, LDL-P needs checking

Large VLDL’s and high total and small LDL-P are markers of insulin resistance

Kids need to “get off the damn carbs” and substitute fat and protein instead

Whether it’s possible to have “too low” cholesterol

You don’t need cholesterol in blood, but in the cells and all cells in the body manufacture it

a href=http://en.wikipedia.org/wiki/Hypobetalipoproteinemia>Hypobetalipoproteinemia have low LDL-P (apoB) and very low cholesterol levels

These people tend to live a very long life and suffer no cholesterol deficiency issues

What Apo E genotype issues you should be aware of

Apo E4 is a marker of elevated risk of heart disease”

ApoE2 is usually desirable but Apo E2 with high triglycerides is a high risk lipoprotein abnormality with normal LDL-P: they have too many VLDLs and IDLKs, but not LDLs.

Apo E4 is also associated with Alzheimer’s disease

A ketogenic diet might ward off Alzheimer’s longer

“Drown yourself in omega-3 fatty acids” if Apo E4

ApoE genotyping just a one-time genetic test you run

Whether an Apo E4 needs to lower their fat intake is truly not known at present

Are they REALLY over-absorbing fat–maybe, maybe not

If your lifestyle controls Apo B, no need to worry

What one test gives most info on heart disease risk: ApoB and LDL-P

No matter what Apo B is, other tests such as inflammatory markers can also tell about CV risk

The totality of tests help doctors treat you better

Triglycerides and Apo B/LDL-P gets most info needed to start

Christine had 300 trigs, dropped to 130 in 6 weeks

Can’t change LDL-P by eating carbs day before test (LDL half life is typically 3 days)

Takes trigs a few days to alter lipoprotein metabolism and jack up your LDL-P

If Apo B and LDL-P come back one high, one normal – discordance is present

It happens in 10-12% of people; repeat test again

If LDL-P is high and Apo B is normal, there is no consensus on what to do

LDL-P tends to “outperform” Apo B as a key marker

Why HDL cholesterol decreases on autoimmune issues

Endothelial lipase expressed with such diseases increases HDL catabolism

Women with anorexia tend to have transient high cholesterol as adipocytes are a cholesterol storage tissue

Wait one month after weight loss and then test again with high LDL-C and LDL-P

Thus weight loss can make transiently make your LDL cholesterol seem higher

What he thinks about having a heart scan conducted

His concern over having a CT scan of your chest: too much radiation

Why do I care about this if LDL-P and Apo B is high: the image result would not change therapy

Whether LDL-P and Apo B are impacted by non-fasted: NO

LDL particles are present in plasma on average 3 days and are is a steady state and thus levels are stable over several days

Liposcience does not offer apoB testing: they provide LDL-P by NMR. If you have LDL-P you do not need apoB

The VAP test offers a calculated Apo B–BOGUS!

You have to insist on a MEASURED Apo B test (using a protein immuno assay)

Chris Masterjohn says major deviations in cholesterol

You’re “playing with fire” with traditional testing

It’s time to say goodbye to these kinds of tests

You gotta move on when newer biomarkers come along

We must abandon traditional cholesterol testing

Get the new tests in there as the standard bearer

It’s a “total joke” when heart disease is #1 killer

Doctors often think someone advocating particle testing is “some quack”

Never be afraid to change doctors if necessary

Publisher asked me to write layman’s cholesterol book

Peter Attia’s “Straight Dope On Cholesterol” series

Your doctor better know Apo B and LDL-P or fire him

Dr. Dayspring on Twitter: @DrLipid

Dr. Dayspring on Twitter: @DrLipid TRY THIS NEW LOW-CARB SNACK OPTION FROM NICK’S STICKS:

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