Wednesday, September 30, 2009

Cardio Controversies: Dr. Harvey Hecht MD

Figure 1: Correlation of metabolic factors and calcium percentile
in asymptomatic patients with EBT showed calcified plaque
(Hecht HS. Prog Cardiovasc Dis. 2003 Sep-Oct;46(2):149-70.)

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*

Utterly. Unrelated.

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.

Figure 8. Correlation of annualized progression
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
before and after 14 months of statin and niacin
combination therapy in a 47-year-old man with a
baseline calcium score of 442 in the 97th percentile.

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')
--carbohydrate restriction
--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
** 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.

Not good.

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.

Superko HR. Small, dense, low-density lipoprotein and atherosclerosis. Curr Atheroscler Rep. 2000 May;2(3):226-31.

Superko HR, Hecht HS. Metabolic disorders contribute to subclinical coronary atherosclerosis in patients with coronary calcification. Am J Cardiol. 2001 Aug 1;88(3):260-4.

Hecht HS, Superko HR, Smith LK, McColgan BP. Relation of coronary artery calcium identified by electron beam tomography to serum lipoprotein levels and implications for treatment. Am J Cardiol. 2001 Feb 15;87(4):406-12.

Anand DV, Lim E, Raval U, Lipkin D, Lahiri A. Prevalence of silent myocardial ischemia in asymptomatic individuals with subclinical atherosclerosis detected by electron beam tomography. J Nucl Cardiol. 2004 Jul-Aug;11(4):450-7.

Rumberger JA. Cost effectiveness of coronary calcification scanning using electron beam tomography in intermediate and high risk asymptomatic individuals. J Cardiovasc Risk. 2000 Apr;7(2):113-9. Review.

Coylewright M, Blumenthal RS, Post W. Placing COURAGE in context: review of the recent literature on managing stable coronary artery disease. Mayo Clin Proc. 2008 Jul;83(7):799-805.

Grundy SM. Coronary calcium as a risk factor: role in global risk assessment. J Am Coll Cardiol. 2001 May;37(6):1512-5. Review.

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.

Budoff MJ, Gul KM. Expert review on coronary calcium. Vasc Health Risk Manag. 2008;4(2):315-24.


epistemocrat said...

Very nice, as always, Dr. B G!

I liked this:

"Very similar endpoints in fact can be achieved!"

And lifestyle / exercise/ nutritional bricolage is much more conservative than are drugs in terms of iatrogenesis--it's a safer modus operandi. Cheap health options abound, if we take a tablespoon of 'grace'.




Dr. B G said...

Mr. Epistemocrat,

YES! I like that M.O.! *haa*

We must heal ourselves... and not be reliant on artifices.


steve said...

you clearly are on to something! I have increased my sat fat intake- coconut oil(1tbs) in whey shake in am with ground flax(2/3tbs)Carlson fish oil and metamuceil. Today, 3 over easy eggs in butter, and 1tbs taken separately of of fish oil. Lunch(almost everyday) is salad with turkey, avocado, and various veggies with olive oil(sometimes an egg or blu cheese added. Dinner will be fish or chicken, or grass fed beef. Am due for NMR and will wait a few weeks and will be interesting to see if particles shift to large from almost all small. Diet has been pretty tight on carbs last several weeks. Still on Lipitor 10, and may reintroduce niacin(at 500/750 level) depending on the results. Think this is enough time to show results positive?

onewaypockets said...

Dr. G wrote "hardly anyone is unless they are POUNDING butter, cream, cheese, coconut oil and lard leaf."

Hi G,

You are not kidding! I thought I was practically swilling coconut oil and coconut milk, but in entering values at FitDay I was only at about 50-55% total fat. I'm not actually sure what people are actually eating that consume a 80 or more percent fat diet. Any clues? Are they drinking shot glasses of coconut oil? :-)

G, I seem to be one of the people that you write about that is very carb sensitive, even the carbs in veggies beyond a pretty small amount stall my weight loss. Unfortunately that even means no summer favorite thing about the season. :-( Excess protein also seems to make me gain, and as well I think I can see this protein reflected in my fasting glucose levels the next morning. Maybe a little Pima in me, lol, or some genetically-thrifty-northern-European-cave-creature in my long ago past. I was thinking of trying to boost the fat % at the same K cal to see about getting into ketosis and weight loss and and hopefully this would lower my fasting glucose?? Would this be a good plan? The days I tried zero carbs (no veggies at all) left me with a king sized headache and a major grouch! Hopefully that will pass...

My wife and I are interested in grassfed beef, we've never tried it, have you happened to try this internet supplier? Their prices seem a bit lower than anyone else, I was thinking about their sampler that includes some grassfed butter. Has anyone flipped out about a "gamey" taste at your home with grassfed beef generally? Is grassfed beef really that different tasting? I'm totally convinced about the PUFA balance difference, etc from your posts, and one look at the rendered fat color difference between grassfed and grain fed fats on some web site I had Obviously I would have to watch excessive consumption of this beef, ie: too much protein, but at least it would be healthier.

A funny/sad for big sister almost killed me. My sister is a registered dietitian, certified diabetes instructor, certified bariatric expert, even her local paper calls her for quotes as a "diet expert". She was always after me to diet, this goes back like 15-20 years, and eat more "healthy whole grains". For years on her diets I measured and weighed out tiny amounts of food, some meals were actually only whole grains and skim dairy with zero fats, etc. I felt worse and worse and always hungry and never lost an ounce. I feel all of this (and 40mg Lovastatin) led to my total hormonal decline and anemia, during while eating these extreme diets my thyroid and testosterone actually plummeted and I eventually ended up with an M.I in early 2004 despite a "wonderful" LDL in the 40's. In 2004 I ordered a whole stack of books, including the fresh off the press TYP, and the slow evolution to today. I love my sister, but we can't really talk about diet or even vitamin D. She absolutely walks and talks the party line...she's drank the Kool Aid totally. sigh. Sometimes just to mess with her I forward her emails from the Vitamin D Council attached with breezy notes "Hey Sis, check this out!" and things along that line...she flips out and tells me it will kill

Thanks for your posts G, I know they take a lot of time to put together. You always give me something to think about. :-)


Dr. B G said...


RIGHT ON... The carb elimination cannot be overstated. Some members on TYP 'think' they are low carb. These are the apo E4 folks. They cannot consume ANY carbohydates.


One lick of fruit drives the small dense LDL for these EXTREMELY carb sensitive folks. You may be one of them.

And I am truly sorry if you will miss your favorite carbs :(

Statins don't help apo E4. They have too much small LDL and the statins somehow appear to depress the HDLs after a while, which Dr. Davis has briefly discussed on the forum. HDL2b is CRITICAL for ultimate control of plaque burden.

You are on the right path. Go ketotic or to the point total net carbs are < 10-20 grams daily and you will see dramatic improvements in your next lipoprotein. Even 4wks later the results should be evident. Don't forget to read Sergad's story.

Do you notice any changes on this kind of meal plan? My patients report more mental focus, clarity, less irritability/ grouchiness. I think the world would sure be a kinder place if everyone knew the proper diet for your genetics! Food is iatrogenic. *haa*


Dr. B G said...


Thank you for your wonderful comments! I haven't heard of the grassfed ranch you menteiond but if you try it, I'd love to hear your experiences! I agree the vast differences in the fatty acids, CLA and nutrients is worth the price. Rare is good for many cuts but for the tougher ones, crock pot or pressure cooker tenderizes better than anything.

OK confesssion -- I'm an instructor and like your sister I used to be a card-holding member of the ADA, donated EVERY DARN YEAR and promoted ALL of MY DIABETES patients to join the st*pid ADA... I KNOW. For the last 10 yrs.

Can't believe??!?!

That shows the depths of my former wheat-addicted, omega-3 deficient ignorance... *haaa* Before I discovered the unveiling of these myths and fairy stories at TrackYourPlaque and Dr. Davis blog...

No. Longer.

Your poor sister. What can one do? I feel your pain.

I've had similar damage as you from the grains, fructose and n-6 fats (but being the rebel nutritionist, never gave up the eggs or saturated fats). Your story is not unlike the ones I've seen in the clinic -- complete statin failures with LDLs 50-60s, post-MI x2 or stents x2-3 or bypass x1 with residual stable angina.

I am so sorry you had to go through all that you have endured!

You are a true warrior and survivor!!

Yes... summer fruit. Not good.

Were apo E4 and other carb-sensitive folks the true warriors and survivors in harsh and barren terrains? I do believe so. The genetics are HONED TO PERFECTION TO BE SO. To survive ANYTHING. The patients I have with Lp(a) are the smartest business people, engineering geniuses and weapons deployment and designers (yeah like you know CIA, DOE all that jazz). EXQUISITE carb sensitivities abound.

Many of the PIMA and other native Americans in the U.S. are apo E4 (~double the incidence, 30%). As you are aware many of the northern Europeans are as well. With any bit of carbs, the sd-LDL fly high. With any reduction in saturated fat, guess what? The sd-LDL fly high. (Krauss had a FANTASTIC study) Combine that with Lp(a) -- boy, it's a great combo to ward off all risk of parasites, microbes, and damage from scurvy but the vasculature can sure take a hit under non-ideal circumstances.

That is interesting that you noticed wt gain with higher protein intakes (protein can convert to glucose). I'd presume your adrenals are perfect now? I believe that Dr. Broda Barnes advises a certain limit on protein otherwise it can start to affect the thyroid. Studies show protein ingestion is thermogenic b/c T3 is released after the meal. Barnes diet is very high fat and borderline ketotic. I wonder if he avoided full ketosis due to adrenal insufficiency and to prevent subsequent reactive hypoglycemia? He focused on thyroid but seemed to forget about the adrenals?

The Optimal Diet by Polish physician Dr. Kwasniewski, I believe has max protein 12-15%. Have you considered looking into it?

This is kinda similar to Jimmy Moore's diet (he told me on the phone he eats 80% fat and at least half saturated). I bet he's apo E4 (or even E4/E2).

Personally I find I kinda do better on higher protein like the trad'l Okinawans and a little carbs on days I lift wts.

For wt loss have you looked into some insulin sensitizing agents? Many of these are anti-inflammatory and improve glucoses downstream:
--whey protein (Source Naturals is great and grassfed)
--carnosine (+/- b-alanine)
--R alpha lipoic acid

Do you get enough Selenium (200mcg/d), vitamin B6 (50-100mg/d), tocotrienol + tocopherols ?

epistemocrat said...

I love this, Dr. B G:

"I think the world would sure be a kinder place if everyone knew the proper diet for your genetics! Food is iatrogenic. *haa*"

Of course, I agree completely.

Also, lean protein never made sense to me.

To hyperlipidity,


Dr. B G said...


I used to always throw away the chicken breasts... (now I learned how to brine and they turn out J-U-I-C-Y! YUM.)

Aaron Blaisdell said...

Beautiful post, G, and wonderful comments, too!

I've upped my lipids into the hyper range over the past week and have been getting deliciously deep and restorative sleep every night. I feel calmer, too. Yesterday for lunch I consumed two eggs followed by 2/3 of a tub of FAGE Total yogurt with raw cacao nibs and shredded coconut, followed by a small serving of strawberries, followed by some delicious raw-milk cheese. I was stuffed and content. This is becoming a typical lunch for me. Sometimes I'll have a can of sardines in olive oil or left-over beef from the prior dinner instead of the yogurt, but I will then eat the yogurt AND greek-milk kefir in the evening. And I don't eat fatty meat, I eat meaty fat!

To health and wellbeing!

Happy New Year!

Dr. B G said...


Happy New Year to you and ur beaut family as well!

You are in the hyper lipid ZONE dude!!! *wink*

Are we spoiled? Life is GOOD... every minute.

Ate 3-4 eggs, sauteed mushrooms (made by the hubby) and leftover miniburger patties (lamb, pork, beef from my sis' CSA -- all GRASSFED PASTURED) for breakfast w/french-pressed cafe du monde.

Just finished a nasty Xfit workout ('filthy 60') at DCF, enjoying my Peet's triple shot breve (might be the last dairy for me though for 2009 but yum... u know what they are now?), and getting ready to go SHOPPING on 4th street Berkeley w/my lil sis and our Paleo babies/kids :) (mostly window shopping but good walking *haa* as the wallet is leaner than my *ss right now!!)