Crestor Raises %-Small Dense LDL (Anti-Regressive)

"It takes a wise doctor to know when to prescribe, and at times the greater skill consists in not applying remedies."

B. Gracian

The Art Of Worldly Wisdom

Definition of %-sdLDL (concentration of sdLDL)

%-sdLDL = (small dense LDL)/(Total LDL)

Total LDL = large LDL + IDL + sdLDL + Lp(a)





Over-Medication

Judicious use of medications can bring about therapeutic outcomes or can have dire consequences. In medicine, it is truly an art form to balance the two, more than a science. Science however can provide a better understanding of what ancient doctors like Hippocrates or others in the last half century have known as wisdom and deep experience showed them.





'Mindless Statinators'

(Thanks Barkeater for that phrase *WINK*) Growing evidence shows that statins have 'differential' effects on people who take them. The lower the insulin resistance, the less the small LDL particles are reduced. In fact, two studies have shown that the most potent statin Crestor/rosuvastatin in fact raises small LDL concentrations when Triglycerides (TG, Trig) are less than 120 mg/dl (see first table, above, Kostapanos MS et al. Clin Ther 2007).


Or if Trigs are less than 88 mg/dl (1.0 mmol/L)... (see below Caslake MJ et al. Atherosclerosis 2003)

Or if Trigs are less than 177 mg/dl (2.0 mmol/L)... (see below, significant data points sdLDL% increased)


WOWO.

Trigs are low in nearly all low-carb compliant TYP'ers! And definitely 100% of people on low carb PALEO.



Crestor is QUITE potent.

At 40mg daily it is THE most potent statin on the market for sledge-hammering down all the LDL particles (large v. small). Caslake et al (Table 2) found that for normotriglyceridemic individuals LDLIII (small dense) % increased from 15.3% to 21.9% (delta = +6.6% sdLDL%) after 8wks only on the maximum dose Crestor 40mg daily (see below graph with comments, the authors failed to put zero on the x-axis...wtf. So please look at how sdLDL increases as the Trigs are less than 88 mg/dl = 1.0 mmol/L and even for a great majority of data points less than 177 mg/dl = 2.0 mmol/L).


What a terrible, counterproduct, ANTI-REGRESSIVE adverse drug effect.

TYP Goal for Regression:
small LDL NEAR-ZERO or DOWNWARD TREND

The goal for combatting heart disease and to invoke regression/ reversal/ eradication of plaque is to achieve a lower concentration of small dense LDL. Surprising, regression on EBT is frequently reported even before all TYP goals are met! (Wonderful cases of late -- hillbrow, Lindybill, dcarrns!)

Like dense ignorant people, we want the least amount of density and a transformation to lighter, buoyant, more athero-protective LDL particles.

Statins can hurt people as we know (myositis, peripheral nerve effects, brain damage, depression, accidents, suicide, vision reduction, erectile dysfunction, want me to go and on...?! autoimmune disease, inflammation at the mitochondrial and cellular level, liver/kidney failure related to rhabdomyolysis, death, etc).

OK.

Statins in fact can hinder EBT regression I strongly believe and examples unfortunately exist (the REGRESSION 10yr-subanalysis is an example of higher cardiac mortality in the statin-arm in a sub-group that exhibited a phenotype/genotype for low triglyerides). When an individual temporarily stops or backs off on the dose, the large LDL re-appear and the concentration of small LDL decrease. The sdLDL may not be exceptionally great compared to sdLDL reductions promoted by low LOW carb, mod-high fat diets or ketotic diets, but they DO IMPROVE noticeably as a result from 'statin holidays'. An example of statin suppression of large LDL suppression is for instance if one had an sdLDL%=300/300=100% improve to 200/400= 50% after stopping Crestor for 1-2mos (Trigs always stay low when a TYP'er stops their statin because nearly all TYP strategies are insulin sensitizing).

That makes sense, right? You don't have to be a 20-year trained cardiologist or lipidologist to understand this data. If Trigs are less than 120 mg/dl, then small LDL concentrations are going to start growing. The graph actually shows that the lower the Trigs go, the HIGHER THE SMALL DENSE LDL CONCENTRATION BECOMES.

What is the effect over time?

What is this effect month after month after month.

What is this effect year after year after year of statin-addiction.

I can't even imagine. F*ck me...it aint regression.



EBT Calcification Progression? Y E S .

Iatrogenic, drug-induced coronary calcifications? One study with Lipitor has shown increased coronary calcifications in aortic stenosis patients compared to the placebo. Unfortunately, I see statins as well associated with coronary calcification progression on EBT when individuals continue the statin therapy after Trigs hit Dr. Davis' TYP goal of less than 60 mg/dl. To achieve EBT regression (HATS trial NEJM 2001 91% reduction in coronary mortality/ events in 3yrs NIACIN NIACIN NIACIN + simva 40/d), some reduction in sdLDL concentration is mandatory. Not... necessarily a lot.

Most individuals with severe coronary disease have ALL small dense LDL particles. In fact 100% concentration of sdLDL is not uncommon at all, at the start of the TYP program.

To reach Dr. Davis' goal of 10% concentration of sdLDL, 90% reduction in sdLDL% would help to achieve regression. It is not the end all, however. It is demonstrated over and over that perfect lipoproteins (esp LDL=60mg/dl) doesn't guarantee SH*T when it's 100% sdLDL. Regression fails to occur in those who persist in over-statinating when the Trigs are excellent less than 120 mg/dl.





Persistently Elevated sdLDL Concentrations

The signs and symptoms of over-statinating are subtle. They involve persistly high sdLDL concentrations that do not decrease with TYP strategies, low carb dieting and even the addition of fats which normally remodel sdLDL into large buoyant beautific particles (omega-3, eggs, coconut oil, krill oil, etc). In fact, sometimes (yikes!) the statin effect appears to lead to HIGHER small LDL particle counts and concentrations. Sadly these individuals (to me... IMHO) have disappointing EBT progressions of 10-25% year after year, despite all their wonderful, hard work, good intentions and optimism... Despite spectacular, dramatic reductions in Lp(a).... Unfortunately the Lp(a) is all dense, all small, all drug-related Lp(a) which may actually be accelerating progressive damage.


Would've been better to not be on a statin at all in the first place? Well, perhaps there is value in the first 1-2 wks of the TYP program, but as you can see from post-CAD patients, insulin sensitivity and Trigs are easily controlled with no starch or ketotic diets within only 6 wks (Hays JH Mayo Clinic Proc 2003).

Six weeks... 42 days. Do you have 42 days?

Those who are statin-less at TYP (Mr. 'H', Mr. 'C', Dr. 'K') on the other hand witnessed large sdLDL% reductions with each NMR or VAP lipoprotein test, perfect increases in large LDL and magnificent reductions in small LDL (even 'NONE') and consequently report EBT regression (Mr. 'C' and Dr. 'K' are pending, I have no doubt). 'Pretty lipoproteins' do not equal regression... it is how the pretty lipoproteins are achieved and the downward trends, with the minimization of iatrogenic, inflammatory drug effects.

Reduction in small dense LDL% is a very important goal to not ignore for atherosclerotic disease regression and eradication because small dense LDL reflects the internal inflammatory status.







ALL Statins Increase Small Dense LDL If Trigs Are Low

Crestor is not alone.

The other statins are NOT exempt.

Lipitor does it too.

They are certainly in fine company. The off-patent generic statins do it as well.





No Starches, High Fat Diet in 6 Wks Decreases sdLDL By 10%

I will review this in more detail later but this VERY short trial excellently demonstrates the efficacy and safety of a ketotic diet in post-CAD-event men and women, in producing dramatic lipoprotein changes in only 6wks. By eliminating starches and restricting fruit and increasing protein and dietary cholesterol and fat, concentrations of small dense LDL reduced from 35% to 25%. These patients were on lipid-lowering medications and the average LDL was 100 mg/dl (not high whopper doses of statins apparently). During the feeding diet, Trigs diminished from 147 mg/dl to only 88 mg/dl.

Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease. Hays JH, DiSabatino A, Gorman RT, Vincent S, Stillabower ME.Mayo Clin Proc. 2003 Nov;78(11):1331-6.


References

A 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemia. (A significant increase in mean LDL particle size after rosuvastatin treatment (mean [SD], from 26.4 [0.4] to 26.9 [0.4] rim; P = 0.02) was observed only in patients with baseline TG levels greater than or =120 mg/dL.)
Kostapanos MS, Milionis HJ, Filippatos TD, Nakou ES, Bairaktari ET, Tselepis AD, Elisaf MS.
Clin Ther. 2007 Jul;29(7):1403-14.
PMID: 17825691


Phenotype-dependent and -independent actions of rosuvastatin on atherogenic lipoprotein subfractions in hyperlipidaemia.
Caslake MJ, Stewart G, Day SP, Daly E, McTaggart F, Chapman MJ, Durrington P, Laggner P, Mackness M, Pears J, Packard CJ.
Atherosclerosis. 2003 Dec;171(2):245-53.
PMID: 14644393


Comparative effects on lipid levels of combination therapy with a statin and extended-release niacin or ezetimibe versus a statin alone (the COMPELL study). (Lipitor raises sdLDL% W T F... Crestor largely does not lower sdLDL concentrations much UNLESS NIACIN IS ON BOARD; Both Crestor and Lipitor wtf raise Lp(a), the most toxic, atherosclerosis-accelerating blood component carried by 17-25% of the general population)
McKenney JM, Jones PH, Bays HE, Knopp RH, Kashyap ML, Ruoff GE, McGovern ME.
Atherosclerosis. 2007 Jun;192(2):432-7. Epub 2007 Jan 19.
PMID: 17239888


Baseline triglyceride levels and insulin sensitivity are major determinants of the increase of LDL particle size and buoyancy induced by rosuvastatin treatment in patients with primary hyperlipidemia.
Kostapanos MS, Milionis HJ, Lagos KG, Rizos CB, Tselepis AD, Elisaf MS.
Eur J Pharmacol. 2008 Aug 20;590(1-3):327-32. Epub 2008 Jun 7.
PMID: 18585701


Effects of maximal doses of atorvastatin versus rosuvastatin on small dense low-density lipoprotein cholesterol levels. (Table 3 shows Lipitor INCREASES wtf sdLDL% +10% and Crestor 40mg makes virtually no change in sdLDL% at this dose (-5%))
Ai M, Otokozawa S, Asztalos BF, Nakajima K, Stein E, Jones PH, Schaefer EJ.
Am J Cardiol. 2008 Feb 1;101(3):315-8. Epub 2007 Dec 20.
PMID: 18237592

Vitiligo: Autoimmune Silent and Overt Celiac Sign

(Picture courtesy: wikipedia)

At my children's elementary school, I'd conservatively estimate that at least 25% of the children have vitiligo the skin condition that the late Mr. Michael Jackson suffered from (or...self-induced?) that caused loss of skin pigmentation (melanocytes). Small patches of whitish areas on their tan or darker-toned faces are the tell-tale signs. I'm not a dermatologist but this is easy to diagnosis. Vitiligo is yet another autoimmune disease with high association with several HLA immune types which leads to destruction of target cells (T-cell cytotoxic lymphocyte destruction of skin melanocytes). This condition is obviously more apparent in darker-skinned individuals (like my daughter) of Asian, African, Indo-Asian and Middle Eastern descent but paler-toned individuals who have a risk of melanoma can also share the same pathology.

Common treatment is immunosuppressants which dampen the body's own immune responses. In fact we were given steroid creams to apply to the lightened spots on my daughter's face. Does these work? Perhaps for some, but in our case, none worked and we ended up just giving up. We had been on vitamin D (which cured hers and my intermittent asthma) and omega-3s for half-year but noticed no real changes on the white spots until we went gluten-free. Yes, apparently I've ruined my daughter's life since we stopped wheat and gluten (we are the 'weirdos' in her school and understandably she's horribly embarrassed).

The trade-off for ruining her life? Within 4wks of our family going gluten-free, her skin toned completely evened out and ALL the few mild white spots disappeared. Now they only re-appear to a limited extent if my babysitter tries to toxify her or if we give in to her whining for wheat.

Where did vitiligo come from?? Neither my parents or my in-laws have ever been affected by this skin condition? It's not contagious. It's inherent in the DNA.

My parents are Hakka and their ancestors grew up for hundreds of years on the Pacific-Rim island, Taiwan. They grew up eating grains like rice (which is of course non-gluten containing) and had very little wheat or flour products. With the Japanese occupation their diet in fact probably improved -- consuming more miso (fermented soy bean), varied seafood, dried small fishes, buckwheat (again not gluten), etc. Growing up we ate sashimi from a young age and rare little bread or cereal (except the little breads for succulent roasted Peking duck at restaurants). As kids we snacked on dried cuttlefish and glutinous rice balls made with Pork or Fish Sung (see picture, courtesy of wikipedia). Pemmican is a shredded, dried meat like flaked jerky eaten by native American Indians. Our Asian/Taiwanese version is Pork and Fish Sung (with a little added sugar... HHHhhhMMhh.... and lots of LARD... yum). A frequent staple was pork spareib/bone soup with seawood, mushrooms, certain Chinese berries (ginko)/nuts, and bamboo shoots. It is pretty neat imo how many ethnic foods coincide in derivations and are just mutations of the 'Paleo' diet. I don't eat much sweet potatoes but my parents love that stuff. The shape of Taiwan's geography resembles a sweet potato and it's considered one of the national foods. (I do like yam noodles which are slivery smooth and delicious and very high in protein but I think those are more Korean.) Interestingly, traditional Japanese and Taiwanese dishes are incrediblely Paleo... with the exception of the ubiquitious rice...which probably explains the extreme myopia and short stature of meat-seafood-deprived parts of Asia (btw I'm not myopic or short since I grew up here in NE, PA and Cali eating like the carnivore/omnivore that my parents raised... quite frankly, my sisters and I are Amazonian in height/size relative to all of our *wink* vertically-challenged relatives and Asian friends...some... who forbid me to wear platform high-heels near them *haa*).


FYI... Below is an excerpt from the WSJ of what modern Taiwanese eat -- many cook traditional Japanese foods like my parents.

"...much of what you find in Taiwan that's truly Japanese is a relic of sorts from its days as a colony of the empire of the sun. From 1895 to 1945, Japan occupied Taiwan and the nearby Pescadore Islands -- its spoils of victory over the Chinese in the Sino-Japanese War (1894-95). During that time, the Japanese turned an agrarian backwater into one of the most modern -- and well-educated -- societies in Asia.

The Japanese built grand public buildings, turned the harbors of Kaohsiung and Keelung into key shipping ports, and laid a railroad that stretched along the western coast of the island. In Taipei, they tore down the old city walls and built a grid pattern for the city's streets. Eventually, they extended primary education -- in Japanese, of course -- to ordinary Taiwanese, an effort to nurture literate workers."

Another article appeared highlighting restaurants that serve traditional Japanese fare in popular hot spots in Taiwan in the WSJ today.... My mouth is watering!

"After the Japanese defeat in World War II in 1945, the Chinese reclaimed the island... But the rebranding of Taiwan, which continued after the Nationalists fled the Chinese mainland in 1949, wasn’t entirely successful. There are many Japanophiles living in Taiwan, and many places offering tourists in Taipei a less-expensive alternative to a trip to Japan. The roots of Japanese culture are still on display in Taipei, in a warren of alleys that locals call “Little Tokyo,” just south of Nanjing Road.

Today, these alleys are virtually indistinguishable from Tokyo’s Kabuki-cho nightlife district, lined with brightly lit Japanese signs advertising countless tiny hostess bars hidden behind doors not quite thick enough to contain the warbling of off-key karaoke. At the bar, you’re likely to find groups of middle-aged salarymen similar to those you’d see in Tokyo, except the hostesses—sitting beside them and keeping the drinks and conversation flowing—speak Japanese with a Taiwanese accent.

The Japanese-style grilled eel at the restaurant Fei-qian-wu is far better than its bar-alley location would suggest. The smoky flavor of the eel counters the slightly sweet basting sauce, just as you’d expect in Tokyo’s finest unagi (grilled eel) restaurants.

As at most casual eateries in Japan, the menu at Fei-qian-wu hangs on plaques around the walls (laminated menus in Chinese and English are also available). Order in Japanese or Mandarin—the restaurant was founded 35 years ago by a Japanese-Taiwanese family. You won’t even find the ubiquitous Taiwan-brand beer here. Instead ale drinkers are expected to order Kirin. A regular size unajyu (grilled eel over rice served in a lacquered bento box) and a Kirin costs about $6, a small fraction of the several thousand yen you’d expect to pay at an eel restaurant in Tokyo.

It’s not just the physical manifestations of Japanese culture that survive. Taiwan is one of the few places that can successfully duplicate the tipsy camaraderie of an izakaya eatery, where Japanese kick back and relax over drinks and small dishes of food after a hard day at the office.

At Wa-ko, the specialty is fresh seafood, and it offers an excellent variety of sashimi and grilled fish, served in small portions to go with drinks. Like most izakaya joints, the restaurant has two rooms: one with tables and chairs, the other with pillows or low-benches around tables in sunken recesses—old-style Japanese. On a recent visit, the traditionally styled room was full of Taiwanese customers. Owner Asato Satoshi, 55 years old, hails from the southern Japanese islands of Okinawa, and opened Wa-ko nearly two decades ago. The most popular dish is an Okinawan xia jiu cai—tofu with small fish and lemon on top. Be sure to try the roast chicken wings and squid with tarako, a kind of fish roe.

Oden is so much a part of Japanese food culture that a steaming pot of the stuff can be found right next to the cash register in many Japanese convenience stores. A simple, lightly flavored broth with root vegetables, egg, tofu and fish paste, oden dates back hundreds of years. Besides the modern convenience-store variety, oden traditionally was consumed at sidewalk stalls, along with the requisite glass of sake or beer, as a late-night snack. Taiwan sports its own homegrown version of oden bars—called heilun in Mandarin—that date back to its occupation-era days, and it has some traditional Japanese versions as well."

Gene expression skipping between generations? What promoted the sudden gene expression of vitiligo when in previous generations it had not appeared (as far as I am aware)?

Well... I don't need to go far... I just look in the mirror. *haa* In utero wheat intoxification probably caused triggers for my poor little helpless offspring. I remember doing the prescribed Pedi progression of starches... rice meal... oats... barley meal (ding ding... GLUTEN)... then of course wheat. Like Martha Stewart, I did produce some good food processed homemade lamb stew baby food and other tasties... but at daycare she received the usual gluten/wheat drivel like goldfish crackers, hearthealthywholegrain-Cheerios, mac-n-cheese, cookies, etc. We provided our share of wheat as well. I only hope now we can make repairs and prevent damage to her children and their grandchildren... Certainly I'm in awe of the power and scope of epigenetics and yet... completely horrified.

Horrified.





I have been seeing an older 70-something year old gentleman with all 3 diabetic complications -- retinopathy, nephropathy and neuropathy. High Lp(a) and vitiligo exist as well. Lp(a) progressess ALL diabetic complications -- specific organ damage, microvascular disease as well as macrovascular disease of the coronary, peripheral and renal arteries. Tissue and cellular damage all occur faster, deeper and harder. He declined insulin (which is good b/c Lantus insulin is now associated with a 31% increased cancer risk). Therefore, at visits we hammered and hammered the diet and negotiated a few vitamins. He was already very active spending most days working around the house and helping his wife with grandchildren.

New diet:
Breakfast -- 3-6 eggs, bacon occ (nitrate free, organic), menudo (no starches, no hominy, no corn)
Lunch -- salad with protein and olive oil
Dinner -- protein, little starch (yams, few small potatoes (no corn tortillas which are all contaminated with flour/wheat; no bread)

Nutrional Deficiencies and Correction:
Magnesium 2-4 daily (all Metabolic Syndrome are depleted)
Taurine (in 3mos -- this + glycemic control resolved all diabetic neuropathic pain symptoms and lowered BGs and BPs; he stopped Neurontin, Actos and cut BP meds by half)
Omega-3: BOATLOADS of EPA DHA 6-8 g daily (for Lp(a), insulin resistance, autoimmunity, PVD, etc)
Vitamin D to achieve 25OHD 70 ng/ml
Vitamin A for skin and deficiency
Slo-niacin (vitamin B3 -- vitiligo a sign of Pellagra? Perhaps Y-E-S) 500 mg/d and gradually titrated to 1.5 g/d over sev mos


After 3-6 mos, the Creatinine (kidney measurement) improved from 1.5 to 1.2 (maybe better now -- that was 12/08), BP reduced from 160s/80s to 116/60s, HDL increased from 33-35 to 48 mg/dl (again probably better now -- 12/08 labs), he lost 4-6 inches on his large expansive belly, and his sugars were well controlled (no insulin EVAH; last a1c 6.9% from 8%). In fact, the oral medications have all had to be cut back (Prinzide, Norvasc, Glipizide); Actos and Neurontin entirely stopped. Simvastatin 20mg cut back to once weekly... yeah... the dose: a couple licks of the tablet once a week. He also conceded that he felt younger, more energetic and glad for the diet changes. We actually had some ... ummm... disagreements for the first 3 mos! He brought his daughter on two occasions to articulate his displeasure and frustration with the new meal plan. Didn't work. *evil laugh* We ended up hammering the diet with his daughter as well, much to his general disgust. Giving up food he had been eating for 70+ yrs was ahhh... let's say DIFFICULT.

Results? Standard.



Mild vitiligo on his face completely disappeared.

The extensive vitiligo on his hands and fingertips (similar to the wiki picture posted above) stabilized and did not worsen. Skin become sealed, soft, and smooth.

He attended several large family reunions and get togethers and he reported to me that many were shocked and surprised... they told him he looked so much younger. He told me that he doesn't miss eating corn, rice, bread, oatmeal or tortillas. Or upset that he has to wear suspenders to keep his pants from falling off of his tight skinny little *ss... (ok latter's my clinical assessment and physical evaluation... *ehe*).



References:

Genetic variation of promoter sequence modulates XBP1 expression and genetic risk for vitiligo.
Ren Y, Yang S, Xu S, Gao M, Huang W, Gao T, Fang Q, Quan C, Zhang C, Sun L, Liang Y, Han J, Wang Z, Zhang F, Zhou Y, Liu J, Zhang X.
PLoS Genet. 2009 Jun;5(6):e1000523. Epub 2009 Jun 19.

Vitiligo and melanoma-associated hypopigmentation (MAH): shared and discriminative features.
Hartmann A, Bedenk C, Keikavoussi P, Becker JC, Hamm H, Bröcker EB.
J Dtsch Dermatol Ges. 2008 Dec;6(12):1053-9.

Autoimmune etiology of generalized vitiligo.
Le Poole IC, Luiten RM.
Curr Dir Autoimmun. 2008;10:227-43. Review.

Recognition and management of the cutaneous manifestations of celiac disease: a guide for dermatologists.
Collin P, Reunala T.
Am J Clin Dermatol. 2003;4(1):13-20. Review.

Lack of functionally active Melan-A(26-35)-specific T cells in the blood of HLA-A2+ vitiligo patients.
Adams S, Lowes MA, O'Neill DW, Schachterle S, Romero P, Bhardwaj N.
J Invest Dermatol. 2008 Aug;128(8):1977-80. Epub 2008 Mar 13.

[ssociation of HLA class I and II alleles with generalized vitiligo in Chinese Hans in north China]
Wang J, Zhao YM, Wang Y, Xiao Y, Wang YK, Chen HD.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Apr;24(2):221-3. Chinese.

Association of HLA loci alleles and antigens in Saudi patients with vitiligo.
Abanmi A, Al Harthi F, Al Baqami R, Al Assaf S, Zouman A, Arfin M, Tariq M.
Arch Dermatol Res. 2006 Dec;298(7):347-52. Epub 2006 Sep 22.

Linkage and association of HLA class II genes with vitiligo in a Dutch population.
Zamani M, Spaepen M, Sghar SS, Huang C, Westerhof W, Nieuweboer-Krobotova L, Cassiman JJ.
Br J Dermatol. 2001 Jul;145(1):90-4.

HLA class II haplotype DRB1*04-DQB1*0301 contributes to risk of familial generalized vitiligo and early disease onset.
Fain PR, Babu SR, Bennett DC, Spritz RA.
Pigment Cell Res. 2006 Feb;19(1):51-7.

Autoimmune diseases in vitiligo: do anti-nuclear antibodies decrease thyroid volume?
Zettinig G, Tanew A, Fischer G, Mayr W, Dudczak R, Weissel M.
Clin Exp Immunol. 2003 Feb;131(2):347-54.

Possible transfer of vitiligo by allogeneic bone marrow transplantation: A case report.
Mellouli F, Ksouri H, Dhouib N, Torjmen L, Abdelkefi A, Ladeb S, Othman TB, Hmida S, Hassen AB, Béjaoui M.
Pediatr Transplant. 2008 Nov 18.

Benefits of High-Saturated Fat Diets In Heart Patients (Part IV)

Few studies review the benefits of high-saturated fat diets in actual heart disease patients. Perhaps, researchers worry about... M A L P R A C T I C E . . . ?

Like urban myths, do such studies exist?

Indeed studies of high saturated fat diets in heart disease patients IN FACT do EXIST.

LA...la la la... I feel on top of the world... (LMFAO)


The diagram exemplifies a normal coronary artery, with a large.. wide diameter... spacious... flexible.. lumen (Courtesy: medicinenet.org). The diameter of the artery can be measured accurately down to fractions of a millimeter via angiography.

It was observed that in post-menopausal women with documented heart disease from the Estrogen Replacement and Atherosclerosis (ERA) trial, a multicenter clinical trial evaluating the effects of hormone replacement therapy on atherosclerotic progression, in the group consuming the highest-saturated dietary fat diet (12.0% Sat Fat), an enlargement in coronary diameter of 0.01 mm and a 0.1% regression in coronary artery stenosis.

Quoted to Men's Health, "In the nutrition field, it's very difficult to get something published that goes against established dogma," said Dr. Dariush Mozaffarian MD MPH, assistant professor, Harvard. "The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence." Mozaffarian says he believes it's critical that scientists remain open minded. "Our finding was surprising to us. And when there's a discovery that goes against what's established, it shouldn't be suppressed but rather disseminated and explored as much as possible."

In a year during my pharmacy student training at Stanford, I worked with Dariush on an internal med rotation for 4wks. I think I learned more about drugs and how to use them than some of my preceptors combined. His teaching approaches were usually articulate, concise and patiently provided. Gosh, can I say, I've had serendipity with many mentors in my little drug journey so far. *haa*

• Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. PDF click HERE. Mozaffarian D, Rimm EB, Herrington DM. Am J Clin Nutr. 2004 Nov;80(5):1175-84. EDITORIAL. Figure 1 below.
  

Dividing the saturated fat intake into quartiles, the individuals at the highest quartile (dietary saturated fat intake: 12.0%) demonstrated the least progression on angiogram of coronary diameter. In fact, this was the only group that exhibited REGRESSION.

This group was also characterized as having the:
--least medications, including lipid-lowering medications
--the least medications and the higher the saturated fat, the more coronary artery widening in coronary artery diameter
--highest LDL (low density lipoprotein) measurements
--highest HDL (high density lipoprotein 'good cholesterol)
--highest HDL2 (the regressive particle)
--lowest Trigs
--MOST PAST AND CURRENT SMOKERS
--highest dietary fat intake (32%)
--highest monounsaturated fat intake
--lowest dietary carbohydrate intake (47.1% v. (!!) 69%)



Improved Anti-Atherogenic Lipoproteins
"A higher saturated fat intake was associated with a more favorable lipoprotein profile, including higher HDL,HDL2, and HDL3 cholesterol; higher apoprotein A-I; lower triacylglycerolc oncentrations; and a lower ratio of total cholesterol(TC) to HDL cholesterol (TC:HDL cholesterol). Women who consumed more saturated fat consumed less carbohydrate and dietary fiber and more total fat, protein, cholesterol, polyunsaturated fat, trans fatty acids, and monounsaturated fat."



Lipid-Lowering Drugs: The Less, The More Regression
The researchers astutely noticed that "among the women not taking lipid-lowering medication at baseline or during follow-up, there was 0.22 mm less progression for each 5% greater energy intake from saturated fat, compared with 0.09 mm less progression for each 5% greater energy intake from saturated fat among women taking lipid-lowering medication (P = for interaction 0.008)."


Omega-6 PUFAs: Highly Associated with Progression
After the Lyon-Diet Heart trial was completed and showed a dramatic reduction in all-cause mortality, cardiac death and events with simple reductions in omega-6 PUFAs and increase omega-3 from fish and ALA sources like olive oil, I think this trial hits it home again that any increase in dietary PUFAs are extremely pro-inflammatory leading to progression of coronary artery diameter reductions. The lowest quartile consumed less than 3.9% PUFA which was positively (see above) associated with less of a decline of average minimal coronary artery diameter (P for trend =0.04) compared with other quartiles. Clearly, a dietary PUFA concentration greater than 3.9% was highly statistically correlated to angiogram progression. The highest quartile that consumed 7.5% PUFA in the diet this was shown to produce the second highest amount of artery diameter constriction in this trial.

FIGURE 1 (divided, above, below). Mean (SE) change in minimal coronary artery diameter according to intake of different nutrients, with adjustments as in Table 2 (see footnote 1), except that total fat was not adjusted for carbohydrate, and carbohydrate and protein were also adjusted for polyunsaturated fat. These models estimate the effect of saturated fat replacing other fats (monounsaturated or polyunsaturated),monounsaturated fat replacing other fats (saturated or polyunsaturated), polyunsaturated fat replacing other fats (saturated or monounsaturated), total fat replacing carbohydrate, carbohydrate replacing saturated or monounsaturated fat, and protein replacingsaturated or monounsaturated fat.

Median intakes(% of energy) for quartiles 1–4 were as follows:
saturated fat*** (6.1, 7.8, 9.5, and 12.0),
monounsaturated fat (6.9, 8.6, 10.7, and 13.0),
polyunsaturated fat** (3.9, 5.2, 6.1, and 7.5),

total fat (17.6, 21.7, 27.0, and 31.9),
carbohydrate* (47.1, 55.6, 60.5, and 68.9)
protein (12.7, 15.8, 18.0, and 21.2).

P for trend = 0.001 (**saturated fat), 0.40(monounsaturated fat), 0.04 (**polyunsaturated fat), 0.48 (total fat), 0.20 (protein), and 0.001 (*carbohydrate).

High Carbohydrate Intake: Associated with Coronary Plaque Progression
The authors also found that "Carbohydrate intake (see above) was strongly positively associated with progression, with a 19-mm greater decline in mean minimal coronary artery diameter in a comparisonof extreme quartiles of intake (P for trend = 0.001)."


Overview
The design of this particular study was novel in examining multiple dietary components against a validated heart disease marker for progression. Obviously, prospective RCTs utilizing high-saturated fat, low carb, low PUFA diets would constitute the best scenarios to show unequivocal heart disease reversal. Am I going to hold my breath?



R e g r e s s i o n
With a high-saturated fat diet in documented heart disease patients... coronary artery stenosis regression occurred shockingly in individuals who took less lipid-lower drugs, smoked more, and basically were hedonistic beyond a conventional cardiologist's belief. Should we live life a little dangerously... disobey the 'rules'?

Living Dangerously...Like Vin Diesel

When I need liquid c-r-a-c-k, I do a Vin Diesel at Peet's or here Cole's (awesome CRACK, triple espresso).

What is it about the XXX movie series and Mr. Diesel?!? My kids LOVE his babysitting movie!


Y e a h . . . *haa aha* I live real dangerously. Ok oh yeah.

Actually what gets me REALLY going are all the stories I inevitably hear.

Transformations are like DAY AND NIGHT (Kid Cudi).

Mental cognitive function and peak physical function return from a vegetative-state to the prime human animal form that we were all meant to lead.

Of course sometimes the excessive feedback is overload for me but I get full gory details anyway. Like... an older-generic-Type-1-DM gentleman who came to me to discuss reactive hypoglycemia -- excessively low glucoses despite perfect HgbA1Cs of 6.5% on insulin and diet. We examined his diet. He is a lean handsome dude who has escaped the B-below the knee amputations that affected one brother so far.

He's concerned he is losing his mind. His kids are complaining that his forgetfulness is worsening and demanding that he obtain a dementia workup. I say... 'no'... Is it diet-induced stupidity? Whole-grains-based-brain damage? Transient? Correctable?

I dunno.

But I also suspect a vast fatty acid deficiency.

Diet
B: coffee, 2 toast or sometimes cereal, milk, 1-2 pieces fruit
Walk: 3 miles or wt lift
L: sandwich
D: meat, potatoes or rice, veggies

Where's the fat?
Where's the protein?


For 6-weeks he argues with me (standard with all the most diligent Paleo warrior-patients) and says he can't do it. We end up adjusting the insulin to a fraction of the dose. The hypoglycemia episodes stop. The 300-350s mg/dl of blood glucoses (BG) post-prandially after fruit and toast get wiped out.

For 6-weeks he attempts:
--no grains
--no milk
--minimal beans (he loves BEANS)
--omega-3 free range eggs, some bacon (organic nitrate-free), pot roasts, etc
--more non-starchy veggies, occ potatoes or yams
--almonds
--occ berries (no apples bananas oranges grapes)
--stop cooking with cheap olive oil (hidden omega-6 LA source) and switch to coconut oil
--vitamin D 5000 IU, fish oil, slo-niacin 500mg every other day


Prognosis perfect. His memory and faculties return. In fact... his male functions return! I try to cover my ears (in reality this is part of my therapeutic assessments, asking about ur boner). Yes indeedy. Function this boy hasn't seen for 2 decades has returned.

He reported to me how... ecstatic... his girlfriend is noticing these... ummm... changes. He makes a request for Viagra (hey?!? do I look like the local Viagra-dispensing machine..thought I was Viagra... j/k).

"I feel wonderful! I have so much more energy now. My kids say my memory is good again. I think this plan is working -- I think I'm going to stay on it. I'm living... dangerously..."

Watch out world.

Accidentally he was referred to a S.A.D. dietician (eg, nutri idiot) who asked him to add 2 servings of whole grains to every meal and more fruit. Later he informed me, he told her 'no'. Or no *$%#@$ way, I don't recall now.

• Effects of High Saturated Fat, No Starch Diet on Reactive Hypoglycemia (Hays JH et al. Mayo Clin Proc. 2003 Nov;78(11):1331-6. PDF)
• Effects of Hunter-Gatherer Paleo Diet on Blood Glucoses, BP, LDL reductions, TG reductions (Frasetto LA et al. Eur J Clin Nutr. 2009 Feb 11. Abstract)
• Erectile Dysfunction animal pharm post (caution: NSFW)

Show Me Your Lipids!

If you have great HDLs please let me know your HDLs and lipid panel!

If you have an LDL particle size and count, as Robb Wolf suggests getting at his Crossfit Nutrition certifications (yes, I am certified . . . be scared), that would be bangin as well...

Benefits of High-Saturated Fat Diets (Part III): My Paleo Peeps With High HDLs

Wanna know what impresses?

Gambling...? Gawwds, no...got no pokerface... (Lady Gaga)


Tell me your labs. (Or show me ur abs...j/k)

You'll get a reaction.

Yeah, you thought... I was... e a s y. *ahhhaa*

I'm not.


This is what we do on the TYP forum... the reaction can vary: wonderful!! v. consider doing x, y, z for regression/ stabilization/ optimum-vitality. Of course others who carry more weight provide their feedback too. Renaissance man, resident NMR/TYP expert, Jeg Esq ROCKS.)


When I hear an HDL cholesterol is off the charts, like triple-digit-over-100 mg/dl... you my dear have my full attention.



HDL Cholesterol: The Higher, The HOTTER

HAWT HDLs.

The TYP goal for HDL-cholesterol is 60 mg/dl or higher. Studies like the Four Prospective American Studies by Castelli WP et al found "A 1-mg/dl increment in HDL-C was associated with a significant coronary heart disease risk decrement of 2% in men (Framingham/FHS, CPPT, and MRFIT) and 3% in women (FHS)."

According to master cardiologist Dr. Castelli (who has successfully escaped premature family hx of CAD), if one's baseline HDLs are 30's and one increases this to 80's, this may represent a 100% reduction in relative risk for a coronary event. For girls, if one increases from HDLs 50's to 80's, then also a 100% coronary risk reduction could be relied upon.

Sounds excellent to me!

It is not difficult to raise HDLs.

This is observed at TYP and in clinical practice ALL THE TIME.

Eliminating wheat/d*mn-dirty-GRAINS/carbs, adding some vitamin D, omega-3s, Taurine, and Slo-Niacin 1-2 grams/day. Throwing away the Mazola and any packaged food items. Oh yeah, and add some fat. Individuals may continue their EVO (but not too much b/c it cranks up hepatic lipase, see HERE) but they increase eggs 2-6 daily, add some (organic nitrate-free preferably) bacon and some coconut oil.

And...reduce their statin (if even taking).

I know, s a c r i l e g e . . .

Consider the value of not over-statinating.

Over-statinating stagnates the formation of large particles. wtf. This is observed on the TYP forum as well -- easily corrected. The statin or fibrate is withheld or severely dose-reduced (TYPically, I advise 'licking the tablet' yeah that is a clinical term *haaa*). See below medscape cases as well.

Yes, statins and fibrates LOWER HDLs ('good chol') for many individuals.

Esp those Paleo and fully engaged in TYP.

Esp additionally if you are an apo E2 carrier (you have lower TC LDL HDLs compared to the general pop). Or... if you eat low fat, low cholesterol, low saturated fatty acids. The interaction is hypothesized to be related to a statin-and/or-fibrate-related apo A1 reduction in activity (and because you are chol/fatty-acid-deficient).

Please, Ladies and Gents... what nicely raises apo A1 and cardioprotective HDLs and lowers TOXIC small LDL?

Saturated fat and C H O L E S T E R O L.


Yeah, even if you are moderately high carb, smoke, and had an event already. We'll go over some post-CAD event trials in the near future to describe yet again some interesting paradoxes. Eat fat to lower body fat. Eat fat to lower bad fat, sd LDL. Eat fat to raise 'happy' good HDL cholesterol. Hhhhmmm... provocative? Our Paleo/TYP experiences and the medical literature will tell us.

Paradoxical Decrease in HDL-Cholesterol With Statin and Fenofibrate Combo: S E V E N Case Reports (medscape.com)

Castelli WP, et al. High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am J Med. 1977 May;62(5):707–714.

Castelli WP, et al. High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation. 1989 Jan;79(1):8-15.

If you'd like to amuse yourself and see how cardio-stat-idiots attempt to debate themselves out of the above clinical findings, read THIS. "We found no significant association of change in HDL cholesterol with the log risk ratio in any model after adjustment for changes in LDL cholesterol." wtf? Note their funding... 'unrestricted grant from... Pfizer.'




Paleo Maximizes/Magnifies HDLs

Below are my Paleo peeps who have ROCKIN' ghetto-FAB lipoproteins with Paleo (or semi-Paleo) (units are mg/dl):


Mr. Richard Nikoley, the King:
TC 223 (6/2008: 219)
TG (57)
HDL 133 (106)
Real LDL 66
Calc LDL (104)


Mr. Stephan Guyenet (almost-Paleo)
TC 252
TG 49
HDL 111
Real LDL (n/a)
Calc LDL 131 (wrong, but who cares)


Mr. Scott Miller (BF 9% -- nukem, dude, awesome! Lives the ultimate Paleo expanded lifespan plan...lots of coconut oil/70% dark chocolate, some HIIT 3 min/wk that mimics evo-behavior/hunting...zen-like martial arts. He smokes out his friends on 3hr-vigorous mountain bike rides w/minimal effort.)
TC 223
TG 51
HDL 98 (baseline: 38-ish and BF 26%)
Real LDL (n/a)
Calc LDL 125
Lp(a) 2


Mrs. Anna (Against the Grain GRRRLL! )
TC 230 (2007, still transitioning to sat fat/grain-free)
TG 59
HDL 72 (from 60's)
Calc LDL 146


Ms. Anne (Paleo and grain-free)
TC 255
TG 36
HDL 93
Real LDL (n/a)
Calc LDL 154


Mr. Jimmy Moore
Diet: La-Vida-low carb/70%-high-fat
Small-LDL: nearly big PHAT zero on NMR
Large-LDL: ALL per interview with Dr. Davis
Family hx of premature CAD: YES
EBT score: wish I knew... wanna wager 'zero'? Bummer, said I didn't gamble... right? *ha*



My Labs:

6/2009 (on coconut oil, Paleo, [25OHD]=50 ng/ml)
TC 249
TG 68
HDL 105
Real LDL 125
Calc LDL 130 (wrong by 4% but, again, who's counting)
Lp(a) 2


12/2008 (Paleo/Xfit+15#muscle, [25OHD]=60 ng/ml)
TC 229
TG 82
HDL 89
Calc LDL 124

2/2008 ([25OHD]=80 ng/ml; started X-fit)
TC 190
TG 37
HDL 84
Calc LDL 99

10/2007 (vit D deficient [25OHD]=20 ng/ml)
TC 170
TG 51
HDL 71
Calc LDL 90




TYP Hall Of Fame (Statins Optional)

Many others have HDLs to provoke tremendous envy at the TYP forum:

Mr. 'O' (brilliant brain who understands HORMONES, like the powerful hormonal effects of Sat Fat w/the line 'the AHA low fat diet...will kill your HDL...and eventually kill you as well!' *haa* HDL 65 w/niacin IR 1g/d, 6g/d EPA DHA and small amounts of coconut oil)

Mr. 'D' (EBT regression 5% w/in only 8mos by adding 1-3 Tbs virgin coconut oil, 4 cage-free eggs/d, niacin 1g/day; Large-HDL tripled from 3.2 to 9 umol/L)

Mr. 'LindyBill' (EBT regression 33.6% in one year and 21% HDL increase from 38 to 46 mg/dl with major weight loss of several inches off the abdomen which accounts for 5-7% Body Fat recomposition (eg, utilization of stored 25-30# Sat Fat) via walking/ball-rm-dancing/ swimming daily and low carb diet; stopped simva 20/d a while ago due to aches but no updated labs)

Mr. 'H' in the UK (EBT regression 30.2% in one year by walking 1hr per day fast, 3 g/d EPA DHA, niacin 1.5/d, vitamin D, burning 2.5 stone (=5 kgs or 10#) *saturated fatty acids* off the body, Wt Watchers but unlimited (high fat) treats on holiday, high dose vitamin 'O' and... btw... no hint of statins)

Dr. 'K' (HDL 68 Feb but probably higher now; reduction in 100% sd-LDL to only 11% by eating COCONUTS and freq fat, eg eggs-n-butter, steak, krill-omelets, gamey duck; 9.0 g/d EPA+DHA doesn't hurt for 100% sucky-sd-LDL-baselines...statin-free!!)

Mr.&Mrs. 'A' (dramatic reductions in Lp(a) by 38%, raising Large-HDL 11 to 22.4 umol/L, raising HDL 63 to 78 mg/dl, and lowering sd-LDL... statin-free)

Mr. 'C' (Italian Ferrari w/HDL incr from 50 to 79 and now 'zero' Small-LDL (on VAP; on NMR 3.7% LDL-IVb)! Regressive HDL2b from 10 to 43% or 34 mg/dl... yeah btw no statin but SloNiacin 1g/d, 8 g/d EPA+DHA, krill oil, kelp...low carb, mod Sat Fat, unlimited vegetables, unlimited EVOO, eggs (organic free range plus omega 3), cheese, avocados, red wine, coconut milk (for smoothie), no or limited fruit, cinnamon,unsweetened natural alkaline free cocoa powder; meditation; IF irregular/ unpredictable cycle; lost 20# BF13%)

Mrs. 'M' (HDL=92 mg/dl and teaches me much about omega-3, bless ur heart...statin-free? undoubtedly!!! on virgin coconut oil + niacin 500mg/d which also dropped sd-LDL)

Mr. 'P' petroleum engineer ('Unrestricted fats', low carb, Lp(a) reduction of 80% from 70 to 14 mg/dl; niacin 1.5g/am, dhea, 3 g/d EPA DHA, Pauling protocol (L P C), and low dose Crestor/pm)

Mr. 'PBG' (HDL 71 mg/dl, Lp(a) reduced 76% from 83 to 20 mg/dl; sd-LDL reduced to 23% from 56%; statin-free of course!!!)

Mr. 'J' (27# wt loss! on low carb; HDL 61 from 43 mg/dl in a few mos! 42% HDL increase after being statin-free several wks prior to lab testing)

Mr. 'N' (semi-off-not-really-wheat/ carbs, 'mod Sat Fat/pufa' diet; semi-fasts 'perpetually hungry' long 15-20 days every 2mos; 66# wt loss; Lp(a) dropped 85% from 123 to 18 mg/dl; HDL 49 mg/dl who admits when he takes 'lipitor-10mg/d-free holidays' his energy/ mood/ brain brighten)

Dr. 'R' for regression (young endurance triathlete; HDL incr from undetectable b/c TGs 400s to HDL 64 mg/dl; with a low carb TYP/Paleo diet with 6kg wt loss and imminst.org antioxidants; simva reduced from 40mg/d to 20mg/d w/the plan to stop after 3mos d/t leg heaviness; I hypothesize astronomical improvements in Lp(a) and EBT but no baselines to report)

Mr. 'R' (elite athlete stud HDL2b 35% and HDLs 115 mg/dl (95 on VAP) 200% increase from 60's wow with low carb etc...mmmm... no further comments at this time counsel *haa*)

Mr. 'CP' (you ROCK!! HDL 71 from 57 mg/dl and definitely statin-less; 33% sd-LDL% after remarkable 67% drop previous baseline after only 3 mos...how? 'more butter, more eggs, more meat...' despite a lotta back pain)

Mr. 'H' (my favorite hunter/tracker in PA -- 200% increase to HDL 76 from lipitor-low-31 to 40 mg/dl with a Paleo, low carb diet; HEEYYGGE 94.9% sdLDL reduction to nothing 3.4% for sdLDL% that resembles centenarian phenotypes consume ...statin-free? yes but low dose and no longer LDL-suppression from effects lipitor 10-20/d or previous low fat diet as evidenced by how the LDLs bounced up from 48 to now. . . PHAT fluffy . . . 90)

And...many others my ADHD memory fails to recall!





Diet?

They all eat a TYP-Diet/Paleo, semi-Paleo, or Paleo+dairy (eg, Protein Power) or some version of these.

With no fear of fats.

Esp some Sat Fats and Cholesterol (egg yolks).

And oh by the way mainly statin-free.

Esp in the cases with the grossest, most spectacular lipoprotein outcomes (high HDL, low sd-LDL%, lower Lp(a)).




@The Heart of Darkness Dot Org

At a cardiologist forum where I pimp-TYP/lurk (when I'm thoroughly bored and want to entertain myself with the latest, greatest thoughts of cardio-geniuses), some silly physicians attempted to persuade Mr. Carey (see below) to give up Paleo/ meat/ no-grains/ no-legumes and adopt the heart-healthy whole-grains WHOLE-DISEASE Mediterrean diet and... reconsider re-statinating himself . . . *wicked laugh*:

"Mediterranean diet was not enough for me. As an FH with a TC of 340, I followed the Mediterranean diet approach (high fiber vegan + salmon +sardines) for over 12 years, while I was on 40mg Pravastatin (TC= 220, HDL = 35, LDL = 130), but after severe plantar fasciitis and muscle wasting set in from the Prav. (even on a dosage reduction to 2mg from 40mg), I stopped rx and tested all the other statins and more without success.

The Paleo diet has changed my ability to metabolize fats, reduced my blood glucose levels, and dramatically increased my HDLs (84). On the same daily running and biking regimen, my body fat % dropped from 15.5% to 8% during the last 6 months. I eat huge quantities of non-cereal, non-grain foods all day and continue to lose weight while feeling far more energetic. As an added benefit, at the age of 44, I recently ran a road race at a pace I have not been able to match since I was on the high school track team.

I loved to eat legumes and healthy grains, but I have seen such a dramatic improvement that I will never go back."


His lipoprotein results with Paleo:

"Paleo diet + exercise + psyllium TRIPLED my HDL to 84. I am a slim FH patient who tried and failed to raise my HDL levels above 40 using a low-fat vegetarian, high exercise lifestyle (My LDL was 240). I could not tolerate ANY statin or Welchol. Now, I eat only lean meat, vegetables, fruits and raw nuts while avoiding all sugar, cereals, grains and legumes. With my unchanged intense exercise regimen, I have lost 10 pounds over 6 months, yet grown stronger and faster. I have reduced my LDLs to 202, while raising my HDLs to 84 from as low as 35.

At 44, I feel like I have turned the clock back st least a decade. "

A M E N brother!

Benefits of High-Saturated Fat Diets (Part II): Centenarians, CETP, TYP Diet Part 3

We've been talking a lot of about increasing dietary saturated fatty acids (SFAs) at TYP. The Part 3 Track Your Plaque Diet was published approximately half a year ago and I've been remiss in not promoting it more sooner.

The NEW Track Your Plaque Diet:
Part 3 Special Issues
-- Lp(a)
-- Apo E
-- Diabetes
-- Pre-diabetes
-- Metabolic Syndrome (MetSyn)

Key Summary from Dr. Davis:
--Liberal fat intake of some saturated fats from eggs, meats (non-cured and processed), dairy; monounsaturated; fish oil
--Completely avoid hydrogenated, “trans,” fats
--Wheat and cornstarch reduction or elimination

The Track Your Plaque Basic Diet Principles

Diet Principle #1: Eliminate wheat and cornstarch, limited dairy
Diet Principle #2: Don’t limit fats, but choose the right fats
Diet Principle #3: Unlimited vegetables, some fruits
Diet Principle #4: Unlimited raw nuts and seeds
Diet Principle #5: Unlimited healthy oils
Diet Principle #6: Foods should be unprocessed

Regression or Stabilization

Pioneering the field of cardiovascular research, regression and plaque tracking, Dr. Davis has been promoting (the below) seven TYP goals for Y E A R S . . . light years ahead of the common conventionalist/ interventionalist. New recent observations made by both researchers investigating atherogenic dyslipidemias and by those conducting long-lived healthy centenarian research are, in fact, aligned with several of these seven TYP goals. Maximixation of plaque control and regression have been observed when these seven goals are optimized (TYP 2.0).

For carotid arteries, achievement of any of the below factors will likely induce entire resolution of atherosclerotic plaque. However for the coronary arteries, regression is slightly tougher for a variety of reasons and achievement of all or nearly all seven will support dramatic coronary calcification regression.

Coronary arteries are thinner and more affected by systemic inflammation and the shearing forces secondary to high blood pressure (whether during physical exertion or at rest).

On the other hand, for stabilization and complete elimination of coronary events (angioplasty, stent, MI, bypass or death), gaining control of only three out seven is right on the money... imo.

We define stabilization as EBT CAC score progression of less than 10-20% annual increase.

The average American increase is 30-60% annually (of course faster in Lp(a), apo E4, diabetes and MetSyn).

Wouldn't you like your investment portfolio to grow as fast as American plaque?



So...Easy. To gain control.

Choose any 3.



1) Small-Dense-LDL < 10% of total LDL particles (imo irregardless of total LDL on NMR or VAP) (Dr. Davis' TYP Goal)

2) HDL > 60 mg/dl (Dr. Davis' TYP Goal)

3) HDL2 (Large-HDL) > 50% of total HDL particles (Dr. Davis' TYP Goal)

4) Large-LDL > 60% total LDL particles (soft goal)

5) vitamin D = 60-80 ng/ml (Dr. Davis' TYP Goal)


6) Sufficient omega-3 ALA and EPA DHA (fatty acid profile, AA:EPA ratio of 1.5-2.0:1; if we flip the ratio around to EPA:AA, in other words omega-3 to omega-6 ratio of 1:1.5, then we're talking 60% of our RBC/cellular membranes being enriched with omega-3 PUFAs content versus omega-6 PUFAs. We really like 60% for some reason at TYP...go figure.)

7) control of inflammation (unfortunately few 'markers' to TRACK):

• dietary (avoidance of gluten, food allergens, casein, etc; adequate ADE K1 K2 MK4-9 vit C B-vits the right ones and minerals Iodine Mg Zn Se, fiber (if tolerated), saturated fatty acids, CLA, GLA, cholesterol, CoQ10/quinones, plant sterols (esp stigmasterol), etc)
• environmental (stay away from plastics/bisphenols/ heavy metal exposure/ pollution/ pesticides, etc)
• mental /psychosocial (stress, excessive physical training, etc)
• hormonal (optimization of thyroid, vit ADEK1K2, omega-3, SFAs, E T P DHEA preg, insulin, cortisol, melatonin, etc)
• pharmaceutical/xenobiotic (adequate intake of antioxidants/ omega-3/ phytochemicals/ FOOD to thwart toxins; avoidance of synthetic hormones, certain drugs (excessive statins), synthetic vitamins (eg, Lurotin, D2/Ergocalciferol, etc), omega-6-PUFA seed/legume oils, etc))
  

Original TYP Goals for Regression: 60-60-60

HDL = 60 mg/dl or higher
TG = 60 mg/dl or lower (#9)
Vitamin D [25OHD] = 60 ng/ml or higher

Am I a *haa* h e r e t i c . . . ?

(LDL = 60 mg/dl is #8 and IMO optional -- this is the easiest with synthetic drugs but unfortunately it prevents #1-4 for some low chol/low fat folks)




VLCD + Cholesterol + SFAs Support 'Super-TYP' Goals #1 through 4

Dr.Volek has published numerous articles on nutrition and metabolism in regards to the benefits of VLCD (very low carb diets) and ketogenic diets in controlling insulin and other hormones. He has shown in various studies how very low carb diets shift small dense LDL particles (atherogenic) to large, fluffy, buoyant LDL particles (regressive). Cholesterol and SFAs (saturated fatty acids) from eggs were demonstrated by Volek to be particularly effective at promoting larger HDL particles, the 'good' cholesterol associated with plaque regression, longevity and cancer protection.

Below is a diagram illustrating the proposal how low carb diets reduce insulin and how high fat/cholesterol diets increase Large-HDL (HDL-2) particles and increase LDL-receptors on adipose cells (and presumably the 'cholesterol core' of atherosclerotic plaque in diseased coronary, carotid, renal and peripheral arteries).

Again, obtaining the lowest proportion of small dense LDL is the holy grail of plaque victims (eg, anyone with a positive (+) EBT coronary calcification score).

Modification of lipoproteins by very low-carbohydrate diets.
Volek JS, Sharman MJ, Forsythe CE.
J Nutr. 2005 Jun;135(6):1339-42. PDF here.

Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. Mutungi G, Volek JS, et al. J Nutr Biochem. 2009 Apr 13.

Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet. Mutungi G, Volek JS, et al. J Nutr. 2008 Feb;138(2):272-6.








Healthy Centenarians Attain ~4 of 7 TYP Goals

Long-lived centenarians, also known as probands, had lipoprotein analyses performed via NMR. Of the markers tracked, four out of seven TYP goals were achieved. Interestingly, centenarian data shows that they still display vitamin D deficiency like the rest of us.

See picture (top)

Figure 2 displaying the Percentage of Large and Small HDL and LDL Particle Sizes in Long-Lived Probands, Offspring, and Ashkenazi and Framingham Controls HDL indicates high-density lipoprotein; LDL, low-density lipoprotein. *P less than .001 for probands vs Ashkenazi and Framingham controls and P less than .001 for offspring vs Ashkenazi and Framingham controls for both large and small HDL and LDL particle sizes.

1) Small-Dense-LDL < 10% of total LDL particles (irregardless of total LDL on NMR or VAP) (TYP Goal)

2) HDL ~ 60 mg/dl (Table 1: women HDL=56 (SD 15); men HDL=50 (SD 17)) (TYP Goal)

3) HDL2 (Large-HDL) > 50% of total HDL particles (TYP Goal)

4) Large-LDL > 60% total LDL particles (soft goal)


Barzilai N et al. JAMA 2003. Oct 15;290(15):2030-40. Unique lipoprotein phenotype and genotype associated with exceptional longevity.


Apparently this sub-population of Ashkenazi Jewish have a genotype variation on the CETP gene which regulates and controls HDL-particle sizes. HDL-cholesterol is an antioxidant and they have the genetic ability to upregulate Large-HDL particles more than the rest of us. Their offspring may have version as well. The offspring (and controls, who were the spouse of the offspring) who were free of any chronic conditions (no hypertension, no metabolic syndrome, no cardiovascular disease) incidentally displayed similar high HDL particle counts, large HDL and LDL particle sizing and buoyancy, and reached the TYP goals of greater 60% Large-LDL and greater than 50% Large-HDL. Their counterparts with chronic conditions failed to meet these goals.



Polymorphism in CETP Gene and Phenotype of Exceptional Longevity

Can we exert control on our gene expression? We already know by altering omega-3 and vitamin D blood levels, we can alter gene expression of the various components of our immunity and cardiovascular health (Weaver KL J. Biol. Chem 284: 15400-15407; Biocarta; DeLuca HF PNAS 1993 90(20):9257-9260).

Volek et al have demonstrated how one can achieve control of small dense LDL via inhibition of CETP activity by a very low carb diet/HIGH-FAT DIET with additions of dietary eggs/cholesterol/SFAs.

Can we obtain similar sd-LDL < 10% lipoprotein profiles as long-lived heart-disease-free, cancer-free centenarians? We may not have the genetic programming/genotype but I certainly believe with our current understanding and technology, achievement of the centenarian phenotype is a definable undertaking.


Previous animal pharm posts:

• Saturated Fats as Potent Anti-Atherogenic Drugs: Lauric Acid Diets Decrease CETP, Increase PLTP
• Lauric Acid Diets (Sat Fat) Reduce Small Dense LDL (atherogenic) MORE THAN Oleic Acid Diets (Olive Oil)