Sleep for heart health

8. June 2008 William Davis (4)
Sleep is a fascinating phenomenon.

Virtually all animals, certainly all mammals, sleep. While the form and shape of sleep can vary, sleeping is a universal phenomenon. Even fish sleep, though their eyes remain open.

Sleep disorders like sleep apnea ("apnea" = without breathing) are growing in prevalence nationwide as the country gets fatter and fatter. Our throats assume a smaller diameter, even our tongues get obese. This results in intermittent obstruction to the airway during sleep, causing snoring. It also results in sleep interruption, particularly during attempts to "descend" down to the deepest phases of sleep. Dire health and cardiac consequences can sometimes emerge, such as high blood pressure, higher blood sugar, abnormal heart rhythms, impaired heart muscle function, even sudden death.

We are all familiar with the perceptible effects of sleep deprivation: edginess, crabbiness, diminished attention span, slowed reaction time. I'm not talking about sleep apnea or sleep disorders, but just simple duration of sleep. Data are emerging that both sleep deprivation and sleep excess may trigger undesirable changes in lipids (cholesterol values):



Associations of usual sleep duration with serum lipid and lipoprotein levels.

Kaneita Y, Uchiyama M et al.

STUDY OBJECTIVES: We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level. DESIGN AND SETTING: The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan. PARTICIPANTS: The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96-2.35), and among women sleeping > or =8 h was 1.45 (95% CI, 1.00-2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29-14.94), and among women sleeping > or =8 h was 4.27 (95% CI, 1.88-9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping > or =8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications. CONCLUSIONS: Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Triglycerides go up with too little or too much sleep. Note especially the extraordinary association of low HDL cholesterol with sleeping <5 hours (nearly 6-fold increased risk) or sleeping >8 hours (more than 4-fold increased risk).

Why do these effects develop? Does sleep deprivation, for instance, trigger higher adrenaline levels, encourage carbohydrate cravings or binges, make us less likely to engage in physical activity? Cortisol is elevated; could this be a factor? I know that I am a different person when sleep-deprived: irritable, less clear-thinking, quicker to anger, more critical, and I develop carbohydrate cravings. It's curious that triglycerides increase when sleep excess is present; what might that represent?

Anyway, the data are growing: Sleep is an important facet of health, both for maintaining a bright outlook and to discourage development of low HDL and high triglycerides. Though not specifically examined in this study, we know that low HDL/high triglycerides are, as a rule, associated with the undesirable small LDL particle pattern.

As a practical matter, you may also find sleep and waking from sleep more satisfying and restful if you sleep in increments of 90 minutes, e.g., 7 1/2 hours (rather than 7 or 8 hours). This is because the full cycle of sleep, from phase 1 to REM (rapid-eye movement sleep), requires 90 minutes for completion. That doped feeling that sometimes develops when awaking will disappear if you sleep according to your sleep cycle, which is usually 90 minutes long.
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Comments (4) -

  • Anna

    6/8/2008 1:27:00 AM |

    Not to beat a dead horse, but sleep apnea is a often overlooked symptom of hypothyroidism, too.  

    One does not have to be overweight to have sleep apnea, either (& lack of  excess obesity may lead physicians to dismiss apnea as a diagnosis).  

    Untreated or undertreated hypothyroidism can result in weak muscles at the back of the throat (soft palate area) that close down during sleep.  

    For me, the sleep apnea presented as repeated violent nighttime coughing fits that would significantly disrupt my sleep (and my husband's).  Unfortunately, it was too easy to assume for too many years it was simply allergic post-nasal drip (doc was happy to Rx for that, of course, but nothing helped, nor did dusting Smile.

    A lot of weird, annoying breathing issues improved considerably once on a good dose of T4/T3 - excessive, uncontrollable yawning when reading aloud to my son (but strangely, not while talking), excessive sighing during the day (I was unaware, but my husband noticed it), etc.

  • Dr. William Davis

    6/8/2008 2:11:00 AM |

    What a fascinating insight!

    That's one I've never come across before.

  • Anonymous

    6/8/2008 12:06:00 PM |

    I'd like to file a complaint against the department of Mother Nature for creating excessive noise for the past 2 weeks.  This springs weather has been crazy in the mid-west with all the lightning, flooding, and tornado sirens.  Bring on the hot sticky summer weather, I'll get more sleep with it than I have with this excessively stormy spring.

    This week I was reminded that my brother in law does not sleep and that isn't an exaggeration.  The family is having a reunion this week and most are gathered at my folks house.  Instead of sleeping at night my brother in law just wonders around, gets on the computer, goes for a walk, etc.  About the only time I've seen him rest is when the TV is on.  He has what the hospital calls border line high blood pressure, 140 over something, I don't remember.  His cholesterol #s are not good also.  This is all in despite of being a marathon running, lifts weights, has little body fat.

    A month or so ago he began some parts of the TYP program.  Hopefully what he does will help.  His father had the same sleep problem and he passed away from a sudden heart attack in his mid50s.

  • Brin

    11/10/2012 3:39:52 AM |

    Hi all
    Just want to say that I am impressed by the information here. Also the friendliness of the posts. You are all working together for everyones benifits. Kudos!
    Since I was a very young child I have had insomnia, restless leg, migrains, anxiety. All of these things I have had since before starting school. All of these things, except the migrains did not have a name back then. I remember my mother coming in the morning to wake me, and i was still awake! I have also always had heart palpitations, always when I am at rest, never when I am exerting myself. Only in the last few years have "they" put names to these things. And only in the last few years have there been any information on help for same.
    A number of years ago i started Atkins, I have always been overweight. I am tall, Long fine bones, but always have had a "belly". Over time Atkins became for me Low -carb, I did not stay true to Atkins, I found low carb healthier and recipes for making delishis food is now all over the internet
    BUT always the issues of anxiety, insomnia, restless legs, migrains. I have always felt that they are all related. Of course my G.P. thinks I need to be on antidepresants .... which i was on for a number of years, then took myself off... thats a whole other story. But Because of the low carb diet a co worker lent me the wheat belly book... OMG!, then I found this blog. So now I am taking Vit. D, Magnesium, zinc, kelp,omega 3s, and about to start melitonin. Am stickin to the low carb forever, sans the wheat and grains. Am hopeing the next 57 yrs (thats how old I am ) will be healtier than the first.
    Thank you Dr. Davis, and everyone who contributes to the blog.

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A victory for SHAPE, CT heart scans, and doing what is RIGHT

A victory for SHAPE, CT heart scans, and doing what is RIGHT

24. June 2009 William Davis (7)
The efforts of Texas House of Representatives Rep. Rene Oliveira and the SHAPE Guidelines committee have paid off: The Texas legislature passed a bill that requires health insurers to cover CT heart scans.

(NOTE: Don't make the same mistake that the media often makes and confuse CT heart scans with CT coronary angiography: two different tests, two different results, two different levels of radiation exposure. The difference is discussed here.)

Track Your Plaque previously reported the release of the SHAPE Guidelines, an ambitious effort to open CT heart scanning to people who would benefit from a simple screening test for coronary disease. Rep. Rene Oliveira initially introduced the bill in 2006, after having a heart scan uncovered extensive coronary plaque that resulted in coronary bypass surgery.

The bill requires that health-benefit providers cover the cost of CT heart scans (and carotid ultrasound) in men between the ages of 45-76, women 55-76, as well as anyone with diabetes or at "intermediate-risk" or higher for coronary disease by Framingham risk score.

The usual panel of cardiology knuckleheads stepped to the media podium, expressing their incredulity that something as "unvalidated" as heart scans could gain the backing of legislative mandate. Heartwire carried this comment:

"Contacted by heartwire, Dr Amit Khera (University of Texas Southwestern Medical Center, Dallas) confirmed there are still no comprehensive, adequately powered studies showing that these screening tests lead to better outcomes. In a phone interview, Khera said he has major concerns about how physicians will use these tests, particularly primary-care physicians. "I gave a talk last week to primary-care doctors, and there were probably 250 people in the room, and when I asked how many people had ordered a calcium scan, just one person raised a hand. . . . Most people don't even know what to do with the Framingham risk score, so they're going to follow an algorithm that they don't know how to follow to order a test result that they don't know what to do with."

It's the same criticisms hurled at heart scans over the years despite literally thousands of studies validating their application.

Studies have conclusively shown that:

--Coronary calcium scores generated by a CT heart scan outperform any other risk measure for coronary disease, including LDL cholesterol, c-reactive protein, total cholesterol, HDL cholesterol, blood pressure.
--Coronary calcium scores yield a graded, trackable index of coronary risk. Scores that increase correlate with increased risk of cardiovascular events; scores that remain unchanged correlate with much reduced risk.
--A coronary calcium score of zero--no detectable calcium--correlates with extremely low 5-year risk for cardiovascular events.
--Coronary calcium scores correlate with other measures of coronary disease. Heart scans correlate with coronary angiography, quantitative coronary angiography, carotid ultrasound (intimal-medial thickness and plaque severity), ankle-brachial index, and stress tests, including radionuclide (nuclear) perfusion imaging.

The reluctance of my colleagues to embrace heart scans stems from two issues, for the most part:

1) No study has yet been performed showing that knowing what the score is vs. not knowing what the score is changes prognosis. That's true. But it is also true of the great majority of practices in medicine. While many wrongs don't make a right, the miserable and widespread failure of other coronary risk measures, like LDL cholesterol or c-reactive protein, to readily and reliably detect hidden coronary disease creates a gaping void for improved efforts at early detection. If your LDL cholesterol is 140 mg/dl, do you or don't you have coronary disease? If your doctor's response is "Just take a statin drug anyway" you've been done a great disservice. (If and when this sort of study gets done, its huge cost--outcome studies have to be large and last many years--it will likely be a statin study. It is unlikely it will include such Track Your Plaque strategies that help reduce heart scan scores, like vitamin D and correction of small LDL particles.)

2) Fears over overuse of hospital procedures triggered by heart scans. This is a legitimate concern--if the information provided by a heart scan is misused. Heart scans should never--NEVER--lead directly to heart catheterization, stents, bypass surgery. Heart scans do not change the indications for performing revascularization (angioplasty, stents, bypass). Just because 20% of my cardiology colleagues are more concerned with profit rather than patient welfare does not invalidate the value of the test. Just because the mechanic at the local garage gouged you by replacing a carburetor for $800 when all you need was a new spark plug does not mean that we should outlaw all auto mechanics. Abuse is the fault of the abuser, not of the tool used to exercise the abuse.


All in all, while I am not a fan of legislating behavior in healthcare, the blatant and extreme ignorance of this simple tool for uncovering hidden heart disease makes the Texas action a huge success for heart disease prevention. I hope that this success will raise awareness, not just in Texas, but in other states and cities in which similar systemic neglect is the rule.

Remember: CT heart scans are tools for prevention, not to uncover "need" for procedures. They serve as a starting point to decide whether or not an intensive program of prevention is in order, and I don't mean statin vs. no statin.

Though not a multi-million dollar statin drug study, I have NEVER seen a heart attack or "need" for procedure in any person who has stopped progression or reduced their heart scan score. A small cohort from my practice was reported:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.
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Comments (7) -

  • billye

    6/24/2009 4:51:58 PM |

    Dr. Davis,

    I know how frustrated you and a few other doctors are relative to the contrariness of some of your colleges.  They hide behind the necessity for long term CYA clinical trials that never seem to take place.  I know that the road to good health and fiscal solvency of health care lies in the direction of supplementation with wild omega 3 fish oil and high dose vitamin D3 along with a low carbohydrate and high fat program.  But a study along these lines will never take place.  After all, you can't get a Patent out of such a program, therefore, pharmaceutical companies will never fund it.  
    I am a study of one for the last 9 months.  My forward thinking nephrologist,www.nephropal.blogspot.com  who follows your blog intently, put me on the above mentioned program while reassessing and stopping many of my medications.   One in particular is Staten's. I have achieved a loss of 50 pounds, my Trig/Hdl ratio is 2.73. My hbA1c diabetes type 2 score dropped from 5.9 to 4.6.  Many other health markers have greatly improved.  I tell you all of this because I can't get the notion out of my head that if the above mentioned was a national policy,  Diabetes essentially cured along with heart disease and many other metabolic syndrome diseases brought on by the western healthy diet, would not the financial difficulty plaguing universal health care be over.

    Bravo to doctors like you that step out of the box and treat patients with the goal of cure not just a prescription and see you in 3 months.  You doctors are the unsung heroes of the medical profession.

  • Dr. William Davis

    6/24/2009 8:04:00 PM |

    Great results, Billye!

    And thanks for the kind feedback.

  • Roger

    6/25/2009 12:12:55 AM |

    What timing for your post!  I live in Texas and I am scheduled for my first CT heart scan...tomorrow.  I don't have any outward risk factors, except age and family history, but my doc thought it was a good idea.  I'm glad to know insurance is covering it!

  • stern

    6/25/2009 6:14:57 PM |

    you never seen hearth atach with hearth scan and no calcium even with lpa high?
    other dr had never seen hearth atack when magnesium hydroxide was taken routinly is it corelate each other meaning it digests the calcium?

  • Roger

    6/25/2009 11:31:32 PM |

    I posted yesterday that I was about to have my first CT heart scan...well, it was an interesting experience for reasons I coudn't possibly have anticipated.  Dr. Davis has commented in the past on the confusion in the media about the difference between a CT calcium score scan, and a CT angiography, the latter requiring a far higher dose of radiation.  I assumed this was a source of confusion only among patients and lay folks, but, lo and behold, I discovered today that doctors--or at least their helpers--can be just as confused.  

    Here's my story:

    After checking in, I asked the receptionist to see if she had any information on whether my medical insurance was covering the scan.  She called someone, and I heard her say over the phone, "he's here for a CT angiogram."  At that point my ears perked up.  I explained I wasn't here for a CT angiogram, only a regular CT scan.  "Well, do you want to call your doctor and talk about this?" she asked.  No, I said, I would like to ask one of their folks to verify exactly what test my doctor had ordered.  As luck would have it, the technician was walking by at that point.  "Is this a CT angiogram?" the receptionist asked.  "No, it's just a CT calcium score scan" was the reply.  But apparently the technician had been unclear herself, and had called my doctor just to verify.  In other words, the "default" procedure they were accustomed to doing at this august Houston vascular clinic was a CT angiogram.

    In fact, my appointment was even listed on their calendar as a "CT angiogram."  For all I know, my insurance will be billed for the same. Later, during the procedure, the technician acted surprised I wasn't doing the "full test."  I explained I had minimal risk factors (actually only one, an HDL of 34 a couple of years ago, which has since been raised to 50 partly as a result of taking advice from this site), but that my doctor was progressive (he is an MD for the Houston Astros) and thought it was a good idea since there is heart disease in my immediate family.  My doctor did indeed prescribe only a CT calcium score scan, but it seems to have been an order that this clinic, at least, wasn't all that used to seeing.

    So, I guess the message is: we have a lot of educating to do.  Had I not been a faithful reader of these pages, I certainly wouldn't have known what kind of test I was about to get, or what questions to ask!

    As for the heart scan itself, a piece of cake.  If you can hold your breath, you can take this test.  Just be sure it is the right one!

    Keep up the good work, Dr. Davis.

  • Dr. William Davis

    6/26/2009 3:18:54 AM |

    Thanks, Roger. And thanks for telling about your near-miss with a CT coronary angiogram!

    Your comment is so helpful that I'd like to use your story as the focus for a Heart Scan Blog post.

  • buy jeans

    11/3/2010 10:29:04 PM |

    All in all, while I am not a fan of legislating behavior in healthcare, the blatant and extreme ignorance of this simple tool for uncovering hidden heart disease makes the Texas action a huge success for heart disease prevention. I hope that this success will raise awareness, not just in Texas, but in other states and cities in which similar systemic neglect is the rule.

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The two kinds of small LDL

The two kinds of small LDL

27. December 2010 William Davis (17)
You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.
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Comments (17) -

  • Tommy

    12/27/2010 3:37:38 PM |

    "But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, but reducing fat in the diet)"

    Just to be clear about the above quote. You say "it is made worse, in fact, but reducing fat." Did you mean "by" reducing fat?

    Also, if that is the case, is that because of the fat itself or because less fat means replacing it with carbs?

  • Jonathan Byron

    12/27/2010 4:50:45 PM |

    In addition to CETP inhibition, some other benefits of red/blue/purple foods (that also include polyphenols other than the anthocyanins - elligitanins, etc) include:

    1) inhibition of amylase - less of a blood sugar spike after eating starchy foods, less aberrant glycation and AGEs.
    http://www.ncbi.nlm.nih.gov/pubmed/15796622

    2) Estrogenic activity - anthocyanin stimulates the beta-estrogen receptors in blood vessels and bone, not much activity in the alpha receptors in breast, uterus.
    http://www.ncbi.nlm.nih.gov/pubmed/20049322

    3) Phosphodiesterase inhibition!
    http://www.ncbi.nlm.nih.gov/pubmed/15769121

  • Peter

    12/27/2010 5:09:05 PM |

    I was surprised that Ron Krauss, who did a lot of research on small particle LDL and recently published a mega-study supposedly showing saturated fat is unrelated to heart disease, made these comments in a recent interview:

    People should limit saturated fat to 10% of their diet, though some can get away with more.

    Optimal carbs intake: 35 to 40%.

    People used to get heart disease from high cholesterol, but now its mainly high carbs.

    The interview is here, and those ideas are toward the end:

    http://www.meandmydiabetes.com/2010/03/26/ldl-cholesterol-ron-krauss-md/

    I would love to know if you have any comment.

  • Geoffrey Levens

    12/27/2010 5:20:51 PM |

    This is worth knowing about! Low cost (relatively) lab tests without needing a doc visit/prescription

    https://summitcountymedicalsociety.prepaidlab.com/

    All tests performed by LabCorp

  • steve

    12/27/2010 9:35:35 PM |

    sometimes it comes down to our health being all about our genetics. As a result of the recomendations of this blog with regard to wheat and sugar elimination, normalizing vitamin D i have taken down my LDL from 1810, all small to 609 of which 346 are small; i can only lower my particles with statins- diet alone will not do it.  My understanding of the research is that at low levels, size does not matter. I will note that when my particles were sky high i thought i was follwoing a very healthy low fat, grain oriented diet.  Now, i eat now grains and have a fair amount of mono fats from avocado and olive oil, some sat fat from lean meats, poultry and eggs, and hope i have minimized the progression of artery plaque that shocked me when i found out i had it when i followed healthy heart diet, exercise and maintained a very lean body weight.  Gentics are tough to overcome, but the risks can be minimzed via diet and meds.

  • Might-o'chondri-AL

    12/28/2010 6:12:34 AM |

    Different segments of the same carotid artery can apparently be affected by a different gene. Each segment is itself susceptable to different pathological processes, like shear rate of the near inner arterial wall. Artherosclerosis at different arterial segments seem to predict if pathological event will be ischemic stroke or myocardial infarction.

    The North Manhattan Study tried to tweak 145 genes modulated by 702 single nucleotide polymorphisms. That study and the San Antonio, Erasmo Rucphen and Framingham have led to opinions that 30% to 60% of the thickness of the carotid artery's intima-media is geneticly inherited. Then for carotid plaque +/- 28% is passed on geneticly.

    Sex of the individual and racial ethnicity are other genetic variables. Doc Davis' clinical observation is telling us something equally important about small LDL's genetic variation.

  • Ryan

    12/28/2010 2:47:00 PM |

    Is small LDL the "VLDL" on blood results?

  • Dr. William Davis

    12/28/2010 2:55:38 PM |

    Hi, Tommy--

    Yes, indeed. Just a typo.

    Probably both.

  • Dr. William Davis

    12/28/2010 2:57:59 PM |

    Hi, Jonathan--

    Excellent! Yes, the conversation surrounding anthocyanins is becoming increasingly interesting.



    Hi, Peter--

    I don't personally know Ron Krauss, but I too have been puzzled by the fact that his public comments don't seem to reflect his research findings. If he were to echo the important findings of his research, he would indeed be a low-carb, high-fat advocate.

  • Dr. William Davis

    12/28/2010 2:59:31 PM |

    Steve--

    Wonderful results! The diet approach works, no doubt about it.


    Hi, Ryan--

    No, two different things.

  • Anonymous

    12/29/2010 5:50:28 AM |

    Hello Dr.Davis,
    Your comments sound very similar to Dr Ray Strand...do you read his work? If not, I think you would enjoy his thoughts. His website is www.drraystrand.com
    Cheers,
    Sue in BC Canada

  • Brent

    12/29/2010 4:02:25 PM |

    Question for all you Small Particle techies out there.  Always had "Good" lipid panels, even though overweight and borderline type 2 under control with a low carb diet.

    Numbers usually average:
    Total Cholesterol 125
    LDL  65
    HDL  45
    Tri  90  

    Just got first particle size test done, results in VAP format:  

    LDL-1Innocent 3
    LDL-2Innocent 0
    LDL-3(B) 36
    LDL-4(B) 34

    I know particle size goes down as the LDL- number goes up, but how do these numbers translate to the NMR numbers Dr. Davis listed as a target for those of us genetically pre-disposed to pattern B LDL?

  • Anonymous

    12/29/2010 9:22:31 PM |

    ^I'm interested in the same thing

  • David

    12/30/2010 8:30:59 PM |

    Brent,

    Your small LDL makes up 96% of your total LDL particles. This is a severe pattern.

    Also, your HDL is too low and your triglycerides are a tad too high. Dr. Davis' Track Your Plaque goal of 60-60-60 is a good rule of thumb. LDL down to 60, HDL up to 60, trigs down to 60.

    If you're currently following a low-carb diet and still have all of this small LDL, your small LDL pattern is probably the genetic type that Dr. Davis talks about here.

    David

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    7/10/2011 3:29:30 AM |

    ThatÂ’s not just logic. ThatÂ’s ralley sensible.

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    7/10/2011 9:56:07 PM |

    IJWTS wow! Why can't I think of thnigs like that?

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No need to re-invent the wheel

No need to re-invent the wheel

2. May 2007 William Davis (0)
I seem to be repeating myself lately, but I think this does bear repeating:

There's no need to re-invent the wheel when it comes to gaining control over your heart scan score.

The Track Your Plaque program is the most powerful approach known to help you gain control over your coronary atherosclerotic plaque and CT heart scan score, bar none. While 100% of people do not drop their score, more and more people every week are doing so. (One of the admitted weaknesses of the Track Your Plaque website is our failure to list more success stories; we're working on it.)

The basic program is quite simple:

--The Rule of 60 for lipids (LDL 60 mg/dl; HDL 60 mg/dl or greater; triglycerides 60 mg/dl or less)

--Identify hidden causes of plaque, esp. small LDL, Lp(a), and IDL, followed by specific corrective action

--Fish oil--minimum 1200 mg per day of EPA + DHA

--Normal vitamin D3 blood levels (We aim for 25-OH-vitamin D3 of 50-60 ng/ml)

--Normal blood sugar (<100 mg/dl)

--Normal blood pressure (<130/80)

--An optimistic attitude



Much of the other stuff--vitamin K, matrix metalloproteinase reducing strategies, flavonoid strategies, exercise-induced hypertension, etc.--are, for the majority, fluff. Their real role is in people who may have failed in stopping the rise of their heart scan score just doing the basics of the program.

If you neglect the basics, hoping to find some magic potion, I'm afraid the overwhelming likelihood is that you will fail. I've seen it happen time and again. Someone will come to my office with an extraordinary list of supplements--hawthorne, dozens of anti-oxidants, EDTA, concentrated flavonoid preparations, and on and on. Not only is it shockingly expensive to do this, it's also unnecessary and foolhardy. This kind of unfocused, hocus-pocus in the hopes of getting it right fail time after time.

The Track Your Plaque program, while not foolproof, is the best I know of. Stick to the basics and wander off when the basics fail. But there's extraordinary power in just achieving the basics.
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