Why ATP-3 is B--- S---

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

Comments (8) -

  • G_Man

    8/20/2011 5:35:25 PM |

    Hi Dr. Davis.
    I’m actually both pleased and troubled with the link to Dr. Diamond’s presentation that you’ve provided.

    On the “pleased” side, Dr. Diamond’s analysis is:
    •  An excellent/very well done presentation
    •  Fact based (e.g. cites numerous studies, documented references, named experts, etc.)
    •  Spans the test of time (e.g. references from the 1800’s thru the present day)
    •  Ferrets out the major drivers of our present-day obesity epidemic & debunks other commonly held beliefs
    •  Synchs with some of the Track Your Plaque (TYP) tenants (e.g. TYP guidance on triglycerides, diet, sugars, etc.)
    •  â€œFlags” potential issues like conflict of interest which might have a tendency to creep into the science on occasion (e.g. the Keys report, the errant conclusions resulting from the NCEP report and supporting studies, etc.)

    On the “troubled” side, Dr. Diamond’s analysis seems to:
    •  Fly in the face of some of the foundational tenants of TYP
    •  His analysis/conclusions, and that of other experts he cites, is that cholesterol of any kind is NOT correlated with Coronary Heart Disease (CHD) – at least as a root cause of heart disease (see Myth #2 and Dr. Diamond’s related analysis)
    •  That LDL cholesterol – and although not stated by Dr. Diamond I’m inferring – the “sticky kind”, i.e. the small particles that actually adhere to artery walls (not the fluffy LDL particles that bounce away), are actually good!! On his “Final Issues 2” slide, and later in his related pictorial slides (entitled “What Causes Coronary Heart Disease?”), he makes reference to [LDL] cholesterol as a “Misunderstood Hero”?
    •  That small, sticky LDL particles actually help the body recover from the damage created by the real culprits… sugars that work in concert with certain bacterias to create micro-tears in our artery walls
    •  That small, sticky LDL actually results in the belt-and-suspenders, Rube-Goldberg “spackle” [which again I infer from Dr. Diamond’s presentation ultimately becomes plaque], that fixes (admittedly in a suboptimal and too-late manner) the damage already done by the artery-tearing, sugar/bacteria combo.  Plaque caused by LDL is actually the ‘finger in the dike’, last ditch effort, to fix the artery tears!  Kind of the last line of defense. [see slides on page 53 and Dr. Diamond’s related YouTube discussion.]

    As a result, just curious about your thoughts on Dr. Diamond’s hypotheses.  
    1.  Am I getting Dr. Diamond’s message(s) right?
    2.  If yes, do you concur with – or tend toward – the theory(-ies) supported by Dr. Diamond and other cited experts about the role of cholesterol in CHD?  I gather from your blog post that you sympathize with his glycation theory(-ies), but how about the rest?
    3.  If yes again, does that change some of the TYP direction?  For example, a significant part of the TYP approach is to reduce, as much as possible, small LDL particles. If LDL – and thus the resulting plaque – is indeed a suboptimal last line of defense, does reduction of LDL particles lead to a sub-optimization of the body’s last-ditch defense/“back-up plan” to deal with arterial microtears?
    4.  Also, knowing that plaque/“spackle” is admittedly a suboptimal last ditch effort, what consequence does reversing plaque ultimately have given that the real damage – the tears in the artery walls (the seemingly real CHD culprits) – has already occurred. Are we pulling the finger out of the dike… without addressing the real root cause of the problem?  â€¦and if yes, what’s the back-up plan to the body’s back-up plan? If we reduce LDL and plaque, and the arterial damage is already done due to years and years of sugar abuse, what plugs the dike then?  I’m not talking about the preventive approaches of avoiding glycation in the first place… obviously that seems to be the real, preventive answer. I’m referring to those of us – for whom preventative measures are too late because the microtears are already there – who might be already living with the consequences of years of potentially errant diet/health guidance (by Keys, NCEP, etc.) and thus “spackle” in our arteries?  If the "spackle" is removed, does the dike start leaking again?

    Although I thought I was “on the path to CHD righteousness”, I’m now confused again as a result of Dr. Diamond’s insights. Thanks for any clarifications Dr. Davis!

  • Joe Lindley

    8/21/2011 2:33:55 PM |

    Dr. Davis,
    I'm also anxious to hear what you think of the "hero" role of LDL in plaque.  I'm hoping he didn't go too far off the reservation on this point because the entire hour long presentation was so well done (comprehensive, well-explained, and credentialed) that it will be a powerful aid in spreading the word on both carbohydrates and how messed up the typical GP is with cholesterol treatment (not their fault - but the ATP-III as you say).  It was the tipping point for me.  I'm going off Lipitor now, which I"ve been on for years and will look into your TYP program to ensure I'm doing the right thing.

  • Dr. William Davis

    8/21/2011 3:27:30 PM |

    HI, Joe--

    This "hero" thing, to my knowledge, is extrapolation and supposition. It is an interesting notion. I, too, was impressed with his presentation, but I think that the "hero" thing paints LDL as an entirely innocent player and I don't believe it is. We have only to look at people with heterozygous familial hypercholesterolemia who can have heart attacks in their 30s with pure large LDL to know that there is more to LDL's behavior than a protective function.

  • Dr. William Davis

    8/21/2011 3:31:20 PM |

    Hi, G--

    By providing the link to Dr. Diamond's wonderful talk, I didn't mean to suggest that everything he says should be taken as gospel.

    Virtually everything he said up until the "spackle" I do agree with. The spackle argument is pure supposition. It makes sense, but only to a degree and ignores the quantitative (e.g., heterozygous familial hypercholesterolemia) and qualitative (small, oxidation- and glycation-prone LDL particles with unique conformations that differ from larger LDL) differences in LDL particles.

    Nonetheless, Dr. Diamond's recounting of how this mess was created was enlightening and well-presented and I still enjoyed it.

  • Brian

    8/21/2011 5:53:07 PM |

    Dr. Davis,

    I watched Dr. Diamond's presentation in its entirety.  I agree that he's done some great investigative medicine, especially looking into long-established research on carbohydrate intake, and, more recently, digging into questions of research funding and conflicts of interest.

    His presentation leaves me with a major question about the role of cholesterol.  Diamond claims that high cholesterol levels are not harmful, so long as they are below 300 mg/dL, and that cholesterol has a helpful role.  It is used by arteries to repair themselves after the arterial lining is torn, infected by bacteria, or otherwise damaged.  This is why, he says, we find cholesterol in atherosclerotic plaques, together with white blood cells and dead bacteria.  Yet, we know from your reports and others that an elevated LDL particle number *is* correlated with coronary events.

    What's going on here?  Is cholesterol itself harmful, or is high particle number just another symptom of high carbohydrate intake, which causes glycation and loss of elasticity in the arterial walls, leading to damage?

  • Brian

    8/21/2011 6:03:20 PM |

    I just read the other comments, so the above question has been answered.  Thanks for all the info!

  • Dr. William Davis

    8/23/2011 11:57:16 AM |

    Hi Brian--
    While I truly enjoyed Dr. Diamond's presentation, I think this particular path leads us down a dead end.

    I don't think cholesterol per se is harmful; I believe that the particles that contain, among many other things, cholesterol can be harmful, especially small, oxidation-prone, glycation-prone LDL particles. I believe it would be an incredible stretch to say that small LDL particles are somehow protective.

  • Joan Phillips

    7/29/2012 7:47:06 PM |

    I have inherited cholesterol and just learned from my health store guy that all the grains I have been eating are likely responsible for the high numbers of my small LDL(527) particles.  I thought oatmeal and other whole grains would squeege-mop the bad guys out of my system.  This news is also likely why I haven't  lost any weight (I eat lots of veggies and apples, fibrous fruits and protein.)  I do not use processed foods at all.  I walk a mile to work each day and I am still 10-20 # overweight (and yes it is right in my middle.)  My health guy is the one who directed me to this blog.  Any other information is most welcome.  I am trying to figure out what to fix everyday (supper/dinner) is the hardest.
    Joan phillips