Track Your Plaque challenges

Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

Comments (31) -

  • Nigel Kinbrum BSc(Hons)Eng

    12/1/2009 5:19:32 PM |

    As LDL-c is produced by the liver (I don't know where Lp(a) is produced but I'd hazard a guess that it's the liver), could the secret lie in the liver?

    See Cirrhosis and corn oil.

    Has the effect of beef fat & MCT's on small LDL-c percentage & Lp(a) been investigated?

  • David

    12/1/2009 5:30:54 PM |

    Dr. Davis,

    Could some of the non-response be be caused by underlying food sensitivities (other than wheat), without acute allergic reactions, that contribute to underlying chronic inflammation?  I.e., a gluten like effect but specific to another food in their diet.

    -David

  • bender645

    12/1/2009 6:02:29 PM |

    Hello Dr.

    I have read elsewhere (LA Vida Low Carb, Free the Animal, Hyperlipid)that saturated animal fat intake can positively impact LPa and LDL particle size.  Particularly that of pastured-grass fed animals.  

    I am not 100% familiar with your program or dietary recommendations, but it might be worth investigating.

  • Dr. William Davis

    12/1/2009 10:30:38 PM |

    Hi, Nigel--

    To my knowledge, not beef fat specifically but various fatty acid fractions, such as stearic acid, and percent fat intake have been examined; MCTs I believe have not been investigated.

    However, the effects of adding fats to the existing strategies in the Track Your Plaque program tend to be small, since the diet is not fat restricted.

  • Dr. William Davis

    12/1/2009 10:31:34 PM |

    Hi, David--

    Don't know for certain.

    However, these are generally slender, athletic types with no bowel symptoms, arthritis, etc. So I suspect an allergic theme does not tie them together.

  • Anonymous

    12/2/2009 3:06:57 AM |

    Consider an epigenetic effect as a possible cause for the resistant patients' failure to respond.

  • Dr. William Davis

    12/2/2009 3:18:03 AM |

    Anon--

    Please elaborate.

  • Anonymous

    12/2/2009 10:02:48 AM |

    If the idea is to reduce plaque...

    http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=115645

    After one year, the group receiving the drugs, but not pomegranate showed a significant 9% increase in intima-media thickness. In contrast, the group receiving the pomegranate plus drugs showed a reduction in carotid intima-media thickness as follows:

    After three months: 13%

    After six months: 22%

    After nine months: 26%

    After one year: 35%

    Carotid artery blood flow (as measured by end diastolic velocity) improved in the pomegranate plus drugs group as follows:

    After three months: 16%

    After six months: 20%

    After nine months: 31%

    After one year: 44%

  • P

    12/2/2009 3:00:03 PM |

    hmmm, interesting.
    Such epigenetic effects have resulted in reducing diabetic moratality during famine times previously. Should be interesting if someone studied similar gene expression for your Lpa problem.

  • Scott Miller

    12/2/2009 9:56:25 PM |

    Dr. Davis, I think your diligent quest to reverse heart disease needs to embrace two important additions:

    [1] Have your patients seriously reduce inflammation-causing polyunsaturated fats (primarily, any oil with a poly content greater than 10 percent, which means olive oil barely ducks under the bar, but not many other vegetable oils do, including the oft touted as healthy canola oil).

    [2] Have them consume more saturated fat, especially coconut oil. In effect, low HDL is a symptom of saturated fat deficiency. A great source of coconut oil is cold-processed virgin coconut oil (should smell like coconuts), and full-fat coconut milk (an excellent base for sauces, and smoothies mixed with frozen berries and whey protein powder).

    The main key, IMO, is to reduce processed vegetable oils, a highly inflammatory food ingredient that has a half-life in the body of 2-4 years, so the effects of reduction may take a while to notice.

  • Peter

    12/2/2009 11:11:50 PM |

    Dr Davis,
    Since hormones have such a profound effect on lipoproteins, could there be a connection between DHT levels and resistance to treatment here?  I recently read that early baldness is a risk factor for heart disease, and that DHT opposes estrogen much more strongly than testosterone.  Since estrogen is so heart protective, is it possible that this would be another avenue of attack?  If a person had high levels of the 5 alpha reductase enzymes, testosterone normalization as a treatment avenue might be neutralized in these cases (I am assuming that all hormones have been optimized in your resistant patients).
    I was thinking about this recently as I just came across a patent application for the use of finasteride in heart disease.  You had also mentioned the use of tamoxifen in one of your earlier posts, which would obviously relate here as tomaxifin binds estrogen receptors.

  • Anonymous

    12/3/2009 3:50:01 AM |

    It's so funny that Cheerios has targeted your site for its google ads.

    Cheerios® Cereal
    Improve Your Heart's Health With Cheerios® Cereal Today
    www.Cheerios.com

  • Nigel Kinbrum BSc(Hons)Eng

    12/3/2009 4:05:09 AM |

    Dr William Davis said "However, the effects of adding fats to the existing strategies in the Track Your Plaque program tend to be small, since the diet is not fat restricted."

    I was thinking more along the lines of substituting MCTs for omega-6 fats rather than adding fats.

  • Francis

    12/3/2009 5:22:29 AM |

    I may be wrong but there seems to be an emphasis on treating potentially benign lab values in your post.

    What do the heart scan scores show for the patients you mention? Isn't reversing their plaque the ultimate heart-goal of the program? If their plaque is reversing, so what if some lab values aren't perfect?

    The interesting question is what happens to the risk of having a heart attack or a stroke when plaque is under control, but small LDL or Lp(a) are not.

  • András

    12/3/2009 10:59:53 AM |

    Dr Davis,

    What about Pauling's old protocol for Lp(a) that involves Vitamin C and Lysine? Is it good?

  • Dr. William Davis

    12/3/2009 1:45:48 PM |

    Andras--

    I WISH the Pauling/Rath protocol worked.

    We've tried it and I've had a number of patients try it on their own. I have never witnessed any effect whatsoever on Lp(a), though diarrhea is a predictable result (from the high-dose vitamin C).

  • Kent

    12/3/2009 6:48:29 PM |

    In January of 09 I started out with LP(a) of 198 nmol/L. After finding Dr Davis and reading his book, I started applying his principles by bumping my Niacin from 1500mg to 2000mg, fish oil dosage of 7200mg to 9600mg combined EPA and DHA, Coq10, flaxseed, oatbran, little to no wheat diet, etc.

    However, with Dr Davis suggestions, I also followed the Pauling Therapy of 6g of Vitamin C and L-Lysine along with 2g of l-proline daily. In 3 months my LP(a) went from 198nmol/L to 105nmol/L. In 9 months my LP(a) was down to 45nmol/L, A 77% reduction from January! If you look on Dr Mercola's site, he also states that kind of documented results from the Pauling Therapy.

    I give credit to both Dr Davis and Linus Pauling, but most of all my Lord and Saviour Jesus Christ for answered prayer.

  • Anonymous

    12/3/2009 11:34:16 PM |

    Dr. Davis,

    thats interesting. How long did you try?

    As I understood him, he didn't recommend vitamin C and L-Lysin in isolation, but together with a Multivitamin, additional vit A, Bs, D, E, K, amino-acids arginine, carnitine, taurine, magnesium,..

    I myself started Pauling's protocol against a PAD - and within a half year my walking distance doubled from below a km.

    Short before this improvement I also got to experience the 'predictable' result of diarrhea, due to increasing from the usual 6 grams of vit C daily by titrating up to bowel tolerance (which, with 50 grams, proved quite high).

    Beside that, I experienced some other unexpected effects:

    # a rush on my back I had for a year healed right away
    # my seasonal strong hay fever ceased
    # a strong chest pain, for which I've been to hospital for one week 3 years ago without any diagnosis or treatment - particularly painful in physical or mental stressful situation - is gone now too.

    So already these 'minor' side-effects make me very grateful. Not to talk how glad I am about being able to walk faster than a snail again..
    However, in this respect there's still much improvement potential for me.

    Therefore, any clarifications - why it could have failed in your case - would be highly appreciated.

    Kind regards..

  • Dr. William Davis

    12/3/2009 11:53:19 PM |

    Hi, Kent--

    I'm glad it worked for you. Perhaps there are subsets of Lp(a) that respond, as Lp(a) is subject to great individual variation in behavior.

    It's also possible that it's the high-dose fish oil. We've seen such delayed responses to high-doses of EPA + DHA that take over a year to develop.

  • Dr. William Davis

    12/3/2009 11:55:44 PM |

    Hi, Anon--

    The experiences have been scattered, but all involved only C, lysine, and proline, though everyone here takes fish oil and vitamin D. Many also take magnesium. Most tried for about 6 months.

    So it's hardly a systematic study. But any hint of an effect would have been encouraging, but I have yet to see it.

  • David

    12/4/2009 2:24:47 AM |

    Hi Dr. Davis,

    What about exercise-induced hypertension? Do you still find that to be a persistent problem when all other biomarkers are optimal?

    Thanks,
    David

  • David

    12/4/2009 2:27:26 AM |

    Also, is there a way to know one has exercise-induced hypertension? Would one get headaches?

  • Dr. William Davis

    12/4/2009 3:14:39 AM |

    Hi, David--

    Yes and no. Following all the components of the program will reduce blood pressure. However, some people just don't respond as readily and hypertension with exercise and emotional stress persists. A simple stress test remains the best way to assess this.

  • Kent

    12/4/2009 6:20:49 PM |

    Dr. Davis,

    I've thought about that concerning the high dose of fish oil. I'm wondering possibly if it's a synergizing effect of all the supplements, including the C, Lysine and Proline.

    I also wanted to mention that I split the doses up throughout the day. I've been informed that Vit C and L-Lysine only stay in the system for a short time, therefore, if you take it only once or twice a day, it's not going to have near the effect as splitting it up. I take 2g of the proline, lysine and C in the morning, then take the remaining amounts of C and Lysine throughout the day every 2 hours or so at 1g each, with my last dose at 5:00pm. I try to take my last dose a couple of hours before taking my Niacin, as I've heard the C can sometimes have a negative effect on the Niacin.

    My brother has high LP(a) as well, without seeing it go down. He was taking pretty much everything I was, with the exception of proline and only 4-5g of fish oil. And he was only taking the lysine and C twice a day. He has altered it to match more of what I'm doing, so we're anxious to see what his next blood test reveal.

    By the way, thanks to applying the principles you laid out in the book and here on your site, my other blood levels have been improved drastically. For that I am extremely greatful!

  • Anonymous

    12/4/2009 11:30:22 PM |

    Dr. Davis,

    thanks for your clarification. I appreciate that you remain open to possibly more positive results with Pauling's protocol in the future..


    Hi Kent,

    what is the negative effect of vit C to Niacin you heard of? I'm aren't aware of any, though I too take the biggest part of vit C separate from meals, during which I use the Niacin.

    thanks..

  • StephenB

    12/6/2009 5:11:30 AM |

    For non-responders doing everything correctly but still holding on to lots of small LDL, what's happening to their heart scan scores?

    I was wondering if there were any possibility that small LDL is more associative of heart disease than causative.

  • Kent

    12/7/2009 4:11:09 PM |

    Hi Anon..

    The negative effects I've heard about Vit C to Niacin are spotty. What I've heard is that there is a possibility of any anti-oxident to diminish some possitive effects of Niacin, such as reducing it's HDL raising ability a bit. I don't know anyone personally that has experienced this, I just try not to the two together if possible.

  • Anonymous

    12/8/2009 3:08:01 AM |

    I try to filter out the "faith" based claims and stick with scientifically backed information.  Niacin improved my very low HDL by 30% but complete elimination of the exercise induced angina I had suffered disappeared for me when I subjected myself to high dose K2 for 6 months.  Nothing I have tried (including wheat elimination) enables me to stay off reasonably high dose statins

  • Anonymous

    12/8/2009 11:33:01 AM |

    Thanks for the reply, Kent. Though my HDL did raise about 18% within one year of 1.5 gram Niacin use, at 33 now it's still much too low.

    On your suggestion I'll try to take them more separated, beside raising the dose of Niacin. Which I think is advisable in my case due to Lp(a) anyway (57).

    What is the advised upper limit of the daily dose of Niacin at TYP?

  • Kent

    12/9/2009 6:17:13 PM |

    Anon..

    I really noticed a huge jump in my HDL, when I bumped Niacin from 1.5g to 2g, introduced high intake of fish oil, at least 7200mg to 9600mg, got vitamin D levels up, and alomost eleminated wheat. I went from HDL's of 40's/50's to 86.

    I believe the upper limit of Niacin depends on the type, wheter it be immediate, sustained, or slow release. Perhaps Dr. Davis could address that.

  • buy jeans

    11/3/2010 3:42:21 PM |

    We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

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

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

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