Dr. Davis has known for years that assessing and treating based on the LDL-Cholesterol alone is bunk. Just as simply visually inspecting someone's physical appearance to determine their heart status is bunk. The healthiest appearing athletes may in fact have the most profound coronary artery obstructions. Similarly an asymptomatic menopausal female with exceptionally 'high' HDLs, 'low' LDL and low Trigs may also have the highest Lp(a) and peripheral vascular obstructions in the lower extremities. Heart disease is still the #1 killer of Americans and across the globe in adults. Is it a wonder why? We are not even correctly identifying asymptomatic heart disease in moderate risk individuals ((+) family history of atherosclerosis disease (heart, kidney, peripheral, cerebral, aneurysm), Lp(a), low HDL, high Trigs, Metabolic Syndrome, high fasting or post-prandial insulin, etc).
The current protocol that physicians use to score heart disease risk is called 10-year Framingham risk scoring. Recent observational studies are elucidating the complete lack of correlation between this scoring method and detection of moderate to very severe asymptomatic subclinical disease.
Framingham scoring for low or moderate risk indivuals is bunk (Nasir et al. Int J Cardiol. 2006 Mar 22;108(1):68-75.)
Complete. Utter. BUNK.
According to Nasir et al asymptomatic Brazilian men (avg age=47) who were considered low or moderate risk according to Framingham scoring, moderate to very high risk coronary calcifications were found on an EBCT scan. "...Nearly half of individuals with CACS > or = 100 (45%) and CACS > or = 75th percentile (48%) missed eligibility..." for aggressive therapy for risk reduction. CACS = coronary artery calcium scoring.
Cardio Controversies: Dr. Harvey Hecht MD
Dr. Hecht was one of the cardiologists who has worked closely with Superko and Krauss over the last 10-20 yrs on statin trials, subfractionation of lipoproteins and more recently interventional radiology involving EBCT and MDCT. Like Callister (recall, Cardio Controversies HERE), Hecht originally saw a decline in EBTC coronary calcifications with statin monotherapy in one single study, however he could not be replicated the results at later dates. Like Krauss and Callister, he has questioned why this is the case. In a 2003 publication, he reviews the importance of many concepts that characterize our TYP program (Hecht HS. Prog Cardiovasc Dis. 2003 Sep-Oct;46(2):149-70. Free PDF HERE). Obviously, our TYP program embraces a program that is far and beyond conventional statin+niacin-centric therapy: diet, lifestyles, exercise, nutraceuticals, and no pharmaceuticals (excluding niacin and fish oil). Hecht's approach is basically mega doses of niacin niacin and more niacin (+low dose weak statin), which is quite fine but not very targeted or tolerable to most and fails to address the metabolic origins of heart disease, obesity, MetSyn, diabetes and inflammation.
LDL-Cholesterol Alone Tells Nothing
One of Dr. Hecht's first assertions is that LDL-C is completely, fully, unrelated to subclinical and clinical coronary calcifications. See above diagram, Figure 1. The R correlation quotient between LDL-C and positive coronary calcification was 0.0006 (p=0.90). To quote my favorite THINCer, Peter, 'count the ZEROES.' *ha*
Metabolic Parameters Matter
The highest correlations between overall plaque burden and measurable lipoprotein parameters were LDL peak particle diameter in angstroms, R = 0.14, P = .02 and high-density lipoprotein cholesterol, R = 0.11, P = .02). Of course these R values are not great since optimal statistically is 0.80 but this is the closest relationship determined from countless EBCT scans and patient datasets. In other words, Pattern 'A' versus Pattern 'B' makes a big difference, even a little more than how much HDL there is.
of calcium score and change in metabolic factors.
C h a n g e in Plaque Burden Correlates Best With Small Dense LDL Changes
Hecht continued to examine how changes in the metabolic parameters related to change in coronary calcifications as visualized and quantitified by EBCT. The best relationship was found between percent change in Small Dense LDL (IIIa+b subfractions). Not HDL improvements (he apparently didn't look at HDL2b). Not Trig improvements. Definitely not LDL-C improvements (again, don't forget to count the zeroes,
R = 0.009, P=0.91). Not even the TC/HDL ratio improvements.
Regression or progression in coronary calcifications was highly associated with changes in sd-LDL out of ALL the parameters tested (R=0.46, p=0.71). See above. We see these correlations at TYP as well. Regression is highly associated with
--control of sd-LDL to < 10-30%
--annihilation of the 'death band' LDL-IVb from > 5% to as low as possible < 1-2 %
--solid Pattern 'A'
--increasing HDL-2b to as high as possible 60-200%
Our members do regression with DIET. LIFESTYLES. Supplements (omega-3, phosphatidylcholine, vitamin D, etc). LOW DOSE niacin 1-2 grams per day. STATIN-LESS... or on the way to statin-less.
High-Saturated Fat Diet Improves ALL Metabolic Metrics
These metabolic metrics -- sdLDL and HDL2b -- according to Krauss' research on lipoproteins are related mostly to (1) dietary saturated fatty acid intake (2) dietary carb loads.
Let's summarize Dr. Krauss' high fat study once more and then see how it compares in the context of CACS regression in an extremely high risk CAD patient whose father had an MI at age 46 (Case study #8; Figure 16). The carb intake again in Krauss' study is considered high by many standards at 39% and not as effective in lower small dense LDL or raising HDL-2b as lower carb or very low carb (VLCD) diets in insulin resistant individuals. Interesting comparisons can still be made.
Summary of Heart-Healthy Improvements with a High-Saturated Fat (18%) Diet in only Six Weeks:
(1) Increased total HDL-Cholesterol 18% (baseline 42 mg/dl)
(2) Increased Regression subspecies HDL-2 of 50%(3) Reduced Triglyercides by 30% (baseline 141 mg/dl)
(4) Increased total LDL-Cholesterol by 13% (good thing b/c LDL-diameter incr)
(4) Decreased LDL-IIIa+b from 27% to 18%(5) Decrease LDL-IV from 6.0% to 3.4%
Figure 16. Case 8. Metabolic data and EBT images
Regression Case Study in a High CAD RISK Individual:
EBCT CAC Reduction 15% Annualized
This 47 yo patient's (see above) therapy included ultra high dose niacin (equivalent to 8 tablets of OTC Slo-Niacin 500mg) which was a dose similarly used in the HATS regression trial, plus low dose weak potency statin. His CAC score put him at the highest 97-percentile of extremely high coronary risk. His father had suffered an acute myocardial infarction at age 46.
What is quite notable with this regression case is the rapid changes in multiple metabolic parameters esp Lp(a) with niacin. Niacin is one of the few therapies that successfully lowers Lp(a). In the HATS trial ~20% of men and ~30% of women had elevations of Lp(a). High dose niacin worked for this gentleman with the tremendous plaque burden. In the EBCT scan, the reduction in LAD was obvious the author stated. See above.
Recall what does niacin mimic? Niacin binds the ketone body receptors which are activated during many of the strategies employed by TrackYourPlaque members:
--intermittent fasting ('fastest way to control plaque')
--mod-high protein diet (Primal, Protein Power, phases 1-2 of South Beach)
--mod-high fat diet (TYP Diet Part 3, Primal, Protein Power, low carb high fat Paleo)
Metabolic Parameters Improved
Can we achieve similar multiple metabolic parameter improvements with diet + lifestyles alone?
Without drug or ultra high dose niacin side effects?
How would ultra high dose 15 months of Niacin 4000 mg + statin daily in a 47 yo asymptomatic male compare with 6 weeks DR. Krauss' high fat diet in n=103 healthy men (46% fat, 18% sat fat when compared with AHA-Walter-Willet-low fat 8% sat fat)? Granted it is hard to make comparisons between Krauss' healthy study participants and this asymptomatic CAD Case Study, the baseline values for lipoproteins were not that significantly dissimilar from this Case Study (Low HDL, higher TG).
Very similar endpoints in fact can be achieved V E R Y rapidly!
The primary parameters to compare are:
High Fat x 1.5 months:
** Increased Regression subspecies HDL-2 of 50%
** Decreased LDL-IIIa+b from 27% to 18%
** Pattern 'A' to 'A+++' (LDL diameter from 25.9 to 26.5nm)
Pharmacotherapy x 15 months:
** Increased Regression subspecies HDL-2b of 71%** Decreased LDL-IIIa+b from 34.1% to 18.6%
** Pattern 'B' to 'A+++' (LDL diameter from 24.9 to 26.6nm)
Lp(a) Reduced By Saturated Fatty Acids and Raised by Low-Sat-Fat Diets
Benefits of Krauss high-saturated fat diet cannot be overstated. Saturated fats control CETP and thus control the amount of Lp(a) individuals produce. In fact, when an experiment group was put on a low fat, high veggie diet, Lp(a) increased significantly by as much as 9% (Silaste ML et al Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):498-503. Free PDF HERE .)
Additionally, the low fat diet produced HIGHER oxidized LDL (OxLDL) by 27%. Recall the small dense LDL are less resistant to oxidation than buoyant large LDL and transform to OxLDL rapidly.
For. Plaque. Burden.
OxLDL causes fatty/calcified organs: arteries (atherosclerosis); endothelium (hypertension); liver (NASH); pancreas (diabetes, MetSyn); thyroid (Hashimoto's), visceral fat (obesity); etc.
Saturated fat lowers and controls Lp(a) and coconut oil is one great example (Muller H et al . J Nutr. 2003 Nov;133(11):3422-7. Free PDF HERE). In this study by Muller et al women with elevated Lp(a) in the 30s mg/dl were provided a coconut oil-rich diet (22.7% sat fat; 3.9% PUFA) was compared with a high PUFA-diet (15.6% PUFA !!yikes). Lp(a) was reduced 5.1% compared to baseline habitual diets with the high saturated fat diet whereas in the high PUFA diet, Lp(a) increased a whooping 7.5%. The difference between Lp(a) on the high sat fat compared to the high PUFA diet was 13.3%.
[Coconut oil is great unless one is allergic. I am aware of a friend allergic to both olives + oil and coconuts + oil. Dr. Hyman discusses food allergies and how to determine what they are via an elimination diet HERE to control inflammation and reduce autoimmunity.]
Hecht HS, Superko HR. Electron beam tomography and National Cholesterol Education Program guidelines in asymptomatic women. J Am Coll Cardiol. 2001 May;37(6):1506-11.
Nasir K, Santos RD, Roguin A, Carvalho JA, Meneghello R, Blumenthal RS. Relationship of subclinical coronary atherosclerosis and National Cholesterol Education Panel guidelines in asymptomatic Brazilian men. Int J Cardiol. 2006 Mar 22;108(1):68-75.
Santos RD, Nasir K, Tufail K, Meneghelo RS, Carvalho JA, Blumenthal RS. Metabolic syndrome is associated with coronary artery calcium in asymptomatic white Brazilian men considered low-risk by Framingham risk score. Prev Cardiol. 2007 Summer;10(3):141-6.
Campbell CY, Nasir K, Carvalho JA, Blumenthal RS, Santos RD. The metabolic syndrome adds incremental value to the Framingham risk score in identifying asymptomatic individuals with higher degrees of inflammation. J Cardiometab Syndr. 2008 Winter;3(1):7-11.
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Hoff JA, Daviglus ML, Chomka EV, Krainik AJ, Sevrukov A, Kondos GT. Conventional coronary artery disease risk factors and coronary artery calcium detected by electron beam tomography in 30,908 healthy individuals. Ann Epidemiol. 2003 Mar;13(3):163-9.
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