HDL Not Useful Anymore? Maybe the Whole Lipid Profile is Useless

So the New York Times dropped a stunner to the world this week with an article that called into question how useful HDL really is. Lots of TheFatNurse’s fellow peers were shocked by it. Is this really new tho? Or has the community just been looking at HDL cholesterol in the wrong manner? Indeed, just earlier in the month another study showed HDL being harmful depending on whether the HDL has a apoC-III protein on it. In a manner similar to the discovery of Dr. Krauss that not all LDLs are alike, not all HDLs are alike either.

Dr. Thomas Dayspring, a lipidologist, has been saying all along that the standard LipidProfile test that you get done at the doctor’s office is outdated and may not accurately predict atherogenic risk. I know I know this is probably your reaction:

Just hear TheFatNurse out!

However, with the exception of Non-HDL (Total cholesterol- HDL cholesterol) and triglyerides/HDL to get a “poor man’s insulin resistance” (ratio of 3 or above = likely insulin resistance)” the other values on the standard lipid profile may not be as useful. Yes even the LDL cholesterol (insert another GTFO pic!). Instead, getting a test to see the size and number of particles in LDL may be a better predictor of atherogenic risk.

What is this particle nonsense you say? It’s the view that risk is not dependent on total LDL cholesterol but the way LDL cholesterol is carried through the number and size of LDL particles (Some evidence is showing that the size is of lesser importance than previously believed and it’s the number of LDL particles themselves that are important). The more particles the higher the risk (driven by insulin resistance). Dayspring believes a number below 1000 nmol/L would be ideal and a number above 1600 nmol/L is the start of high risk. If you find this intriguing, the video below features Dr. Dayspring talking about all of this along with a case study to follow along with:

The Bottom Line: The New York Times article is a good starting point for people to reevaluate and redefine what cholesterol is. Much of the cholesterol knowledge that is taught in schools and to the public is outdated and there have been newer theories and tests developed that are much better than the traditional “HDL = good LDL = bad” advice. Are these newer theories right? Maybe, maybe not, but they should certainly be discussed more often than the same old archaic advice which is often treated as medical fact rather than theory.

12 thoughts on “HDL Not Useful Anymore? Maybe the Whole Lipid Profile is Useless

  1. OK I’m trying to get people on board with my framework here. Not sure if an expert maybe would find reasons to disagree but I think I must be close enough.This way we can save a lot of trouble and say, “South Beach Agatston, he’s a 3G guy; Protein Power took the 2G view” etc. Here’s the progression of our understanding of cholesterol:

    1G: Total cholesterol is measurable. Higher = bad. Interventions should aim at lowering cholesterol (1st generation theory, or 1G).

    2G: Turns out cholesterol consists primarily of two types: HDL and LDL. HDL is good and protective, the higher the number, the better. LDL is the bad cholesterol; the lower the number the better. Interventions should be aimed at raising HDL and/or lowering LDL.

    3G: Actually not ALL LDL is bad. It’s really only the small, dense variant of LDL particle that is bad. Larger, buoyant, “puffy” LDL particles are OK. So what matters most is the pattern of small vs. large LDL. HDL meanwhile is still protective. Aim of intervention should be to get HDL higher and to shift LDL pattern from largely small dense particles to mostly large fluffy particles.

    4G: OK, the only thing that REALLY matters is total quantity of LDL particles, LDL-P. Big or small particle size makes no statistically significant difference. Any other metric that MIGHT seem significant (HDL, various ratios) is only significant inasmuch as it correlates to LDL-P, but such metrics are unreliable at that. Far better to get direct count of LDL by an NMR test.

    • Kevin – that is a beautiful rendition of the evolving history. Thank you! Just goes to show people that lots of things in healthcare are evolving theories (why it’s called a practice!) and not always solid full proof facts.

    • Point one is ture, cholesterol is measurable but is not the perfect predictor of CV events we have all been lead to believe

      Point 2 is fiction: There is only one cholesterol molecule – it does not exist in any other form so the terms good and bad are nonsensical, thought up decades ago help explain the epidemiological fact that low HDL-C is often associated with CV risk. 50% of the cholesterol caried by LDLs (LDL-C) originates in HDLs — it is then transfered over (using a lipid transfer protein called CETP) — so does the “good cholesterol” suddenly become bad? Not if the LDL returns it to the liver – but yes if the LDL invades the arterial wall. Good and bad cholesterol are dumb terms, used by people clueless with lipid and lipoprotein physiology that we must all stop using.

      3 is totally wrong: Patientswith the rather lethal disease called familial hypercholesterolemia (FH) get CHD in childhood (thehomozygites) or early adulthood (the heterozygotes) – they have 100% giant, fluffy-buffy LDLs that are horrifically atherogenic. Diabetics with small LDL get events in their 50s and 60s (not childhood or early adulthood). All LDLs are atherogenic if they exist in increased numbers, none are if they do not. It is particle numer (LDL-P or apoB) that matters not particle cholesterol counts (LDL-C and HDL-C). Once adjusted for LDL-P or apoB, LDL size has no statistically significant relatiionship to clinical events (please see the recent biomarker statement issued by the Naitonal Lipid Association)

      Statement 4 is right on

      Thomas Dayspring MD, FACP, FNLA aka Dr Lipid

      • Thanks for the feedback Dr. Dayspring! Happily I’ve been led to your work by following Peter Attia.

      • Always happy to have your input here Dr. Dayspring! Been following your work, and your explanations on cholesterol and particles have been very enlightening.

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  3. Is CAD reversal possible or progression stopable? How low do particle levels of LDL have to be for this if at all possible?

  4. Steve,

    In nursing school CAD was taught as a mostly progressive disease that needed aggressive attention to modifiable life factors such as quitting smoking, decreasing salt, decreasing LDL-C, increasing HDL-C, decreasing saturated fat/cholesterol intake, decreasing alcohol and relieving stress. Medications usually involve statins and BP meds as well. Surgery is another option involving stents and CABGs – Very traditional management of CAD right?

    See the dilemma there? If saturated fat, HDL-C and LDL-C cholesterol may not be as significant as previously thought, how effective are some of these traditional dietary factors in slowing progression? You may be interested in Dr. William Davis: http://blog.trackyourplaque.com/ from my Dispatch link. He is a cardiologist with some clinical observations and anecdotal evidence on plaque reduction and LDL particles: http://www.trackyourplaque.com/success.aspx who is well received in the LCHF crowd.

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