Saturday, October 31, 2009

Low Carb Paleo: Weight Loss 50 Pounds

Courtesy Shouts

A couple of acknowledgements to my uber COOL blog buddies...

Thank you NephroPal for being an amazing party-geek pal!! The above lovely SPOOKY graphics are courtesy of Dr. T.

Thank you Jimmy Moore for the recent shout-out at Livin La Vida LOCA! Jimmy, you are my HERO . . .

*evil laugh* HAAA HAA HE

Thank you Gentlereaders, today I am going scare the cr*pola out of you.

I haven't posted any 'before' vs 'after' pictures until now. I hope it might possibly inspire people to make and reach their goals. Truly NOTHING is impossible.

Transformation is about releasing what is already inside. One of the best tools that I found to motivate myself is to visualize what I want to transform myself into... like... gentle yoga-ites, wicked Angelinas, bad*ss DC comixxx superheroes.

OK so now you know my secret... mind over matter... mind over MASS... mind over the MIDDLEGUT. Feel free to share yours...

AFTER: Low Carb Paleo 19% Body P H A T

I've come a long way BABY... and I intend to stay that way. As a former fatty (yeah I can say that but you can't) like many others, you get into a mindset where you know what behaviors may trigger a so-called relapse back to former fattiness. For myself I have found through many trials and errors that certain things work. What works without fail is having good hormone control by exercising frequently (low intensity, long duration + high HIGH intensity, short short duration... yeah s*x counts unless your cardiologist told u 'no') and watching the intake of carbohydrates (fruit, ice cream, rice, potatoes, french fries MY DOWNFALL, etc). All CARBS. I indulge only if I know that I will be doing some workout later, otherwise I'll pay for it by gaining 2-5 lbs the following week. Yeah, that is just the mitochondrial biomechanics of my formerly thrashed pancreas and the intense quantity of adipose cells that I have from being 50 lbs fat.

Fat cells shrink but never go away...

BEFORE: High Carb USDA S.A.D. 38++% Body Fat

Being overweight since my teens makes me really appreciative of the transformative changes that other individuals have gone through or are currently going through. It is not easy sometimes.

Hurdles and obstacles can be like running a Navy Seal gauntlet. Holidays are even more brutal! Summers can be cake to stay active doing jogs and summer sports but I find for myself winters absolutely require strategic planning. I organize going w/friends to half-marathon events to guilt myself into not flaking on them (and me). The cold freezes my BOOTAH off. (And I live in Cali, sorry!!! *aaah*) Another deterrant for bad habits creeping back is scheduling 'rewards', for instance, going to day spas for relaxing massages. In fact, calming massages helped me to lose weight and improved athletic performance. Is everyday too much? j/k.

Diet Diet Diet

At my all-time high weight, I became committed to embrace changes when I could no longer fit into size 10 jeans... Vanity can be a great motivator. Whatever floats your boat. No I don't really care about heart disease or strokes. Just. My. JEANS.

First I started jogging again. What a cr*ppy lame*ss way to lose weight. Didn't lose more than 10 lbs per year the first three years. I had to discontinue my oral contraceptive at one point because it was giving me irregular skipped heart beats (from high insulin/ glucoses) which prevented exercising beyond a threshold.

The weight really came off when the diet came into line.

I stopped nearly all CARBS (1 carb = 15 grams high glycemic index):
--rice (2 cups daily = 6 servings carbs)
--bread, chocolate croissants, granola cereal (1-2 servings carbs)
--cranberry juice (O M G 2-3 servings carbs)
--caramel walnut sticky buns (bottomless pit)
--Peet's mochas XTRA LARGE (7 servings carbs incl HFCS)

Kept the meat, seafood and non-starchy veggies.

Low Carb Paleo Reverses Obesity

Inadvertently I went low carb Paleo though I had not even heard of Paleo back in 2005. My main grain was rice (coz I am Asian). In the beginning, it was hard to stop but when I felt lighter, stronger and less HUNGRY, it wasn't difficult.

For Asians, Pacific Rim and Indo-Asians, BMIs of 27 or greater than are considered obese (HERE). As you can see from the above 'before' pictures, no doubt about it I was obese. Metabolic syndome. Low HDL, high Triglycerides/sdLDL and blah blah blah. Back then, I would've failed any glucose or insulin tolerance test... if I didn't know how to cheat and pass (e.g. no carbs x2 days prior; I educate diabetes patients).

During pharmacy school I learned how to jog with my drinking buddies and girlfriends... but when I strained a hamstring and didn't know how to heal it, I turned to a 10 lb box of See's chocolate and regained 20 lbs. I was lucky enough that after re-injurying the same pathetic hamstring, my wonderful doctor gave me a referral to physical therapy. The skills from physical therapy changed my training and conditioning forever. I learned the benefits of stretching, strengthening and yoga, and learned that I could re-build my physical body.

Rebuild my brain? Gluten, omega-6 and obesity are toxic to the brain. Diet, yoga and fish oil rebuilt my brain.

Saturated Fat Grew My B**BIES Back

Like any anal retentive pharmacist, you go to the nth degree. I chronically ran a lot (really hard, really far) because I thought it was 'healthy'. My lowest weight was too low (lost lean mass, sarcopenia). My diet was too low saturated fat... though back then I 'thought' it was sufficient and actually high.

The result was I got really sick. In 2004, I developed asthma and coughing spells for 6-8wk durations annually. The birth control contributed (raised insulin, decreased B12, lowered estrogen and testosterone which maintain healthy bronchodilation and lung immunity). I was a stupid pharmacist; I didn't know. A couple of courses of antibiotics likely j*cked up the inflammation further by imbalancing the gut flora and biofilms. Later I was fortunate to discover vitamin D in 2007 (via the heartscanblog) and cured myself and my kids. We are now all off inhalers, antibiotics, steroid tapers, albuterol breathing treatments and same-day urgent care visits. THANK GOD for the stellar Dr. Davis, his healing strategies and opening my eyes to the lies behind the fairy stories. When my daughters were on steroid inhalers, I noticed that they stopped growing for 3 months. I always wonder if my oldest is permanently stunted from the effects of antibiotics and steroids. Now... the only steroid we do is vitamin D!

When I lost 50 lbs of weight by 2007, I also lost some feminine A S S E T S . My BMI at the time was 18.2-18.6 and weight 108-110 lbs (lifetime low). Took 5 years to lose 50 pounds. And the t&a. Bra size: (---) A ! (normal: D). When I started blogging February 2008 for Dr. Davis, the timing coincided with the beginning of my personal trial with Crossfit and high saturated fat diets for the purpose of attaining and regaining health benefits. Petro turned me on to Hyperlipidemia.

It worked.

My muscles and mammaries all grew (back). I started Crossfit shortly afterwards in March 2008 after reading Volek, Drs. Eades and Robb Wolf. At my DiabloCrossfit affiliate I met several others who had also lost 50+ lbs in only 1-2 yrs (not 5). Our family went gluten-free July 2008 and threw our first Paleo princess bday party (albeit high carb) in August for our daughter. Got Xfit nutrition certified in October 2008. Got more sat fat in and did some more Xfit, gained some muscles... some gluts... more mammaries... good stuff. What a rollercoaster of the best times of my life!

Muscles and mammaries net GAIN: 11 lbs ! Boo !

Prior Posts:
--What To Do After You've Lost 50#
--Get Into My Genes

Pubmed Reference (THANK YOU nocarb! Will try out ur COOL handy dandy TOOL):
Prevalence of overweight and obesity and their association with hypertension and diabetes mellitus in an Indo-Asian population. Jafar TH, Chaturvedi N, Pappas G. CMAJ. 2006 Oct 24;175(9):1071-7.

Friday, October 16, 2009

Body Fat Loss: Saturated Fat Kicks the Cr*pola Out Of Olive Oil

Loren Cordain Is Getting Into Coconut Oil

Yes. It is true.


C O U R S E . . .

From Robb, "Cordain likes coconut oil, just as a mix to a standards paleo approach. " (adrenal post) Robb cracks me up.

Recall Dr. Cordain's recent publication with the history-making conclusion: 'In general, experimental evidence do not support a robust link between SFA [saturated fatty acid] intake and CHD [coronary heart disease] risk.' PDF click HERE Curr Treat Options Cardiovasc Med; 2009;11:289-301. I just had to repeat that. It's like... *haa* the SOUND OF MUSIC... [the hills are alive... *big winky*]

The Thing About Fat...

Let me quote another expert, Jeff Volek (see his testosterone study at end), "The Fate of Fat: You are not what you eat; you are what you do with what you eat. Eat fat with carbs you get fat, but eat fat with low-carbs and you get LEAN — and insulin is the switch that controls the fate of fat.

— Jeff Volek, The New Low-Carb Guru

This is true if you are eating olive oil, monounsaturated fats, omega-3 oil, canola oil, coconut oil or MCT oil. Cut out carbs. Esp GRAINS, LEGUMES and FRUCTOSE. FRUC F*CTOSE, the nastiest carb of them all. (If you are gonna have limited carbs... yams, sweet potatoes, red potatoes, and wild berries (higher in oils, lower in sugar) are slightly more acceptable.).
This holds especially true for those who are insulin resistant (HYPOTHYROID (e.g. FT4 and FT3 s*ck), lacking other major steroid hormones (adrenals, testosterone, estrogen, progesterone, adiponectin, vitamin D, and the previously or currently overweight/obese... like me, I used to be 50 lbs fatter *wink*).

Medium Chain Sat Fats and Coconut Oil

Coconut oil is ~100% saturated fatty acids.

No industrial toxic omega-6. No industrial trans-fats.

There are civilizations which consume high, ULTRA-high saturated fat diets (40-56%) of coconut oil with no elevated associations of cancer, heart disease, dental disease or chronic conditions (Tokelau, Sri Lanka).

Coconut oil and MCT Oil are thermogenic and produce ketones despite consuming carbohydrates.

Coconut oil is predominantly medium-chain triglycerides (only 28-30% long-chain). Coconut oil is 1:1:6 (C8:C10:C12). MCT Oil is ~1:1 (NOW brand) or 2:1 (MCT Gold); no lauric acid, C12.

Butter is ~1:2:2. (70% saturated, 20% monounsaturated)

Medium Chain Sat Fats and Breastmilk

Human breastmilk is 40+% saturated fatty acids and high in cholesterol. The role of medium chain saturated fatty acids in the early survival of babies cannot be overstated. Medium chain sat fats are anti-microbial and anti-fungal and promote ketosis which is anti-inflammatory. Lauric acid (C12) exhibits POTENT PROTECTIVE properties. I discussed earlier here (californication post). Colostrum medium-chain ratios are 1:10:60; HEEEYYYYGE GINORMOUS quantities of protective lauric acid. Mature breastmilk, as well, 1:10:40 (Gibson RA et al Am. J. Clin. Nutr. 34: 252-257, 1981.). Baby infant formulae contain negligible lauric acid (C12), omega-3 fatty acids or cholesterol (Giovanni et al Acta Pæd 83(s402):59 - 62). F*Q. Does that explain anything healthwise? Was not 'in fashion' to breastfeed in the 1970s (at least not in Nebraska). Commercial infant formulae actually contain a lot of TOXIC omega-6 LA (Oveisi et al Acta Medica Iranica, 44(4): 225-229; 2006.) The omega-6 LA is soybean and/or peanut oil (WTF?) (p.97, Natural toxicants in food By David H. Watson).


How does Slo-Niacin (vitamin B3) work?

It hits the ketone receptors which is anti-inflammatory and subsequently leads to lower sdLDL, annihilation of the 'death band' LDL-IVb (the most dense and lethal), and raises the HDLs OUT OF THE ROOF.

Again, how do we produce ketones?
--low low low carb diet
--low low carb diet
--low carb diet
--physical low-moderate intensity activity > 1-2 hours (max HR 50-60%)
--fasting > 5-6 hours
--intermittent fasting 12-36 hour fasts (we all do this in the Paleo blogosphere, Crossfit, evolutionary lifestyles)
--drink human breastmilk (just kidding)
--eat a lot of medium chain SATURATED fatty acids (coconut oil, coconut butter, MCT oil, coconut milk/meat, grassfed goat cheese/milk, grassfed butter oil (, grassfed butter/ghee/cream, etc)

Apparently eating saturated fats 12% in the form of MCT Oil can double the body fat loss compared with equal portions of olive oil in near-obese (BMI ~29) men and women on a muffin diet. (Yes, high carb muffin diet.) These studmuffins still somehow lost body fat -- visceral and subcutaneous.

P H A T ! ! !

Saturated Fatty Acids Bind PPAR-Receptors

Saturated fatty acids are hormonal in action. They bind the potent PPAR series of steroidal nuclear hormone receptors (that drugs bind like Actos for diabetes and Tricor for low HDLs, high TGs). Food is our medicine. Recall saturated fats bind PPAR: prior post Lp(a) Dangerous At Any Level. Dietary carbohydates, on the other hand, degrade the PPAR receptors and raise Lp(a), inflammation, insulin and plaque progression.
Remember... medium chain saturated fatty acids are anti-aging (because they bind and activate PPAR and promote anti-inflammatory ketones)... it is a frequent component of the diets of many centenarian and long-living communities (Okinawan, Sardinian, Cretan, Belgium -- from goat milk and dairy products). Check this out again: Kaunitz. Medium chain triglycerides (MCT) in aging and arteriosclerosis. J Environ Pathol Toxicol Oncol. 1986 Mar-Apr;6(3-4):115-21.

In upcoming posts, my buddy NephroPal Dr. T will be reviewing the PPAR receptors. WOOO y-e-a-h !!

MCT Oil Kicks the Cr*pola Out of Olive Oil
St-Onge MP et al conducted a double-blind RCT comparing a low calorie, 'free living', 12% saturated fat/MCT Oil diet (medium-chain triglycerides, 50% of coconut oil) versus 12% olive oil diet for weight loss (Am J Clin Nutr. 2008 Mar;87(3):621-6). Free PDF click HERE. This is the only head-to-head trial I have found comparing MCT Oil and Olive Oil (another one used 24% saturated fat, 40% fat Canadian diet + 3% unesterified plant sterols + flaxseed oil which showed Pattern A 25.85 nm shifting versus 24% Olive Oil Pattern B mean peak LDL 25.45 nm in only 28 days; PDF click HERE, St-Onge MP et al 2003)
The MCT Oil and Olive oil diets were low-fat (naturally HIGH CARB) muffin diets.
The results were surprising.
Body fat recomposition.
Reductions in both subcutaneous fat and visceral fat which is highly associated with PLAQUE and heart disease.

One tablespoon of MCT Oil or coconut oil is ~ 15 grams of pure saturated fat. MCT Oil is liquid and can be heated (like olive oil) to a degree (though I wouldn't heat either). The participants in this study consumed about 1-2 tablespoons daily in a 4-month weight loss program, in the form of a muffin (10 grams) and cooking oil (8 or 14 grams).
DESIGN: Forty-nine overweight men and women, aged 19-50 y, consumed either 18 or 24 g/d (women or men, respectively) of MCT oil or olive oil as part of a weight-loss program for 16 wk. Subjects received weekly group weight-loss counseling. Body weight and waist circumference were measured weekly. Adipose tissue distribution was assessed at baseline and at the endpoint by use of dual-energy X-ray absorptiometry and computed tomography.

As part of the weight-loss program, the subjects were counseled to reduce their caloric intakes to 1500 kcal/d forwomen and 1800 kcal/d for men. Within this diet, all subjects received study muffins (either cranberry or blueberry; Krusteaz, Seattle, WA) that contained 10 g of their assigned oil and 8 or 14 g of liquid oil, for women and men, respectively, to incorporate into their foods during cooking. Therefore, all subjects received 12% of theirprescribed weight-loss energy requirements in the form of thestudy oil (18 g for women and 24 g for men). This level of oil was chosen because it was found to produce significant increases in energy expenditure (8). The subjects, along with the dietitian and clinical coordinator, were unaware of the oil each person was consuming. Muffins were given to the clinical coordinator in bags labeled with the subject’s study ID code and A or B to designate group. Oil was provided in opaque plastic containers, which were also labeled with the subject’s study ID code and A or B

High Saturated 12% Fat for Weight Loss

High Sat Fat 12% Diet: 1.7 kg (~4 lbs) More Weight Loss After 4 MonthsThe authors showed a significant trend in body fat recomposition with employing MCT Oil as the primary fat in a free-living weight loss program. It is unknown what precisely the carb, protein or total fat intakes were other than ' low calorie'. This is a major limitation of this little trial. On the other hand one of the strengths was the use of technology (DEXA and CT scans) to accurately assess body fat. Few studies examine body fat recomposition with diet.

(1) both olive and MCT oil produced average 2.4-2.5 cm waist circumference loss (p=0.0001)
(2) MCT oil produced more body fat reduction 1.46% BF decreases v. 0.58% BF (p=0.0037)
(3) MCT oil produced more pronounced weight loss 3.2 kg (7 lbs) v. 1.4 kg (3lbs) (p=0.001)
(4) Visceral fat loss (intraabdom) 6.7-fold more (MCT oil: 8.85 cm2, NS, n=14 heavy drop outs)
(5) Subcutaneous fat loss (abdominal) 2.2-fold more (MCT oil: 24.76 cm2, NS, n=14 only due heavy drop out rate)

Higher Saturated Fat and Higher Fat Intake Associated With Higher Testosterone

See below diagram discussed earlier HERE. Volek JS et al has already showed that higher baseline testosterone has been highly associated with appropriate total fat (30+%) , protein intake (15%), saturated fat and fat composition (low LOW omega-6, saturated to monounsaturated ~50:50) (J Appl Phys 1997).

Higher the testosterone when:
--higher the saturated fat intake
--higher the overall fat intake
--protein not exceeding 15% (when carbs high)
--lower the PUFA/sat fat ratio, e.g. lower the PUFA, higher saturated fat intake
--lower the PUFA (e.g. canola oil, soy, saff, sunflower, peanut)

Grassfed Australian meat is 'balanced' -- whether it is mutton, lamb, beef or veal -- the fatty acid profile is ~50/50 for saturated to monounsaturated fatty acid ratios. Please see Table 4 (at the very end). Click HERE for PDF. Muscle meat is only 5-8% fat whereas 'fat meat' is about 40-60% fat (rest is collagen, water, proteins).

Eat meat. ALL of it. Fat meat and muscle meat.


Testosterone: Male Fountain of Youth

We use testostosterone (topical cream and gels) for correcting lipoproteins and regression of plaque. Testosterone is great STUFF. Pound some saturated fats and do resistance training... the best way to naturally produce testosterone. I love Xfit. We do saturated fats + lifting/power exercises = Big 'T'. Testosterone is everywhere... I could lick it off the walls... *haaa*

Next Post:
Body Fat Loss: MCT Oil Kicks the Cr*pola Out Of Canola

Saturday, October 10, 2009

Low Carb Paleo: Nothing's Impossible

Low Carb Paleo

Why is low carb Paleo the way to go for not just heart disease reversal, but also for maximum vitality, lifespan and longevity?

What is Paleo?
--no grains
--no legumes
--no sugar, candy
--(if strict: no dairy, no A1 casein (goat milk is A2 and generally acceptable)

The above are the greatest sources of carbohydrates which drive insulin and thus inflammation and elevated, toxic blood glucoses and dense small LDL. Fruit -- fruit is high carb and most of us on the 'bandwagon' are low carb and minimize ALL FRUIT because Paleolithically it rarely existed.

Saturated Fat -- even Dr. Loren Cordain is getting into saturated fatty acids...! Yes really.

Robb Wolf, his Paleo protege at our Crossfit network, mentioned it indirectly a few months ago and I alluded to it on our TYP forum. It is true. Read HERE with choice quotes from Don Metasz at his wonderful blog Primal Wisdom. Neither dietary cholesterol nor saturated fat are implicated in heart disease when the authors re-examined the literature. AAAAhhh... that is right on. Recall, Dr. Mozaffarian only found heart disease regression in the highest quintile of saturated fat intake > 12.0 %? And reduced progression in the quintile of the lowest carbohydrate intake?

Consensus. I like that.

Concordance among the critical thinkers... *haa* THINCers...

Here is a quote from Cordain et al...PDF click HERE Curr Treat Options Cardiovasc Med; 2009;11:289-301.

Low Carb, Mod-High Saturated Fat Paleo establishes all the metabolic parameters that Drs. Hecht and Davis support for optimum heart health:
--Lipoproteins dominated by buoyant large LDL particles, known as Pattern 'A' (versus 'B', for BBBBBAD)
--Regression of coronary calcification EBCT score with decrease in LDL-III (dense small LDL)
--Lowest Lp(a) values

Recall that Dr. Hecht (post: Cardio Controversies) compared a variety of lipoprotein factors with percentile rank of calcium scores. Again, total LDL made no difference at all. However if we look for patterns, one can observe a concentrated portion of high coronary calcifications around 140-160s and from his analyses, we know that the great majority of these are Pattern 'B' which are dominated with dense LDL. In the CAD patients, > 40-100% are typically dense small LDL particles. Our goal at TrackYourPlaque is to achieve < 10% or lower. We do see regression though even at < 30% so this is acceptable for some individuals who can improve the buoyant HDL2b substantially (like REALLY substantially).

Heart Disease LDL example (sdLDL = ~84 mg/dl):
Let's say that someone's LDL is 140 mg/dl.
Let's say it's solidly Pattern 'B' with 60% dense and small LDL. This is not unlike some of our subclinical atherosclerosis members (no event, no revascularization, no stent, no bypass graft). These are individuals with no symptoms who made the right decision to evaluate the coronary calcification status by having an EBCT or MDCT done. Easy -- 30 seconds -- hold the breath -- don't move. Low low radiation. DONE.

OK so how much is dense LDL? 60% of 140 is about 84 mg/dl. So on the graph above -- the L-sided red line is the actually dense small LDL. The R-sided red line is the 'total LDL'. The total LDL again does not mean a thing. The proportion of small v. large LDL is what matters and the context of HOW MUCH CORONARY CALCIFICATIONS exist to determine aggressiveness of treatment strategies (or not... since it is all controllable and reversible).

What about dense LDL created by eating low carb mod-high sat fat Paleo?

From several examples among my buddies on the blogosphere and at TYP and the seminal research on high sat fat diets of Krauss RM and Volek RS, we know that dense LDL can be controlled to... ZERO on NMR

Zero...'zero' LDL-3 on NMR, as reported by several Paleo folks at TrackYourPlaque on low carb mod-high fat Paleo, some in only 4 - 6 wks of diet implementation.

Or at most 5% (but who cares? it's less then Dr. Davis' ultimate goal 10%). Jimmy Moore's is 3%. (And, zero calcium in the coronaries -- Congrats again Jimmy! *wink* of course!)

So the 'paleo' dense LDL is orange on the graph.

Do you see it? On the FAR FAR FAR left side?

Paleo LDL example (sdLDL=~0 - 5 mg/dl):
Compared with 'non-low carb Paleo' 84 mg/dl dense small LDL. That's improvement of... infinity-times.

84 to zero.

What can be achieved by low carb, high sat Paleo?

Regression perchance...?

Complete ANNIHILATION and ERADICATION of coronary plaque...?!?

Seriously... other than avoidance of all AUTOIMMUNE diseases, congestive heart failure, DIABETES, DEMENTIA, cancer...
What can be achieved by low carb, high sat Paleo?

NOTHING IS IMPOSSIBLE (the bad*ss, brown-haired, beautOfaul broad-wide dental arches, Australian Merriweather, Last Skeptik remix, and losing his v-cherries at the V-Festival again)

Low Carb Paleo Controls Trigs and Raises HDLs

Other parameters also make a difference though these metabolic measures had less statistically related coefficients compared to Pattern B (particle size), Lp(a) and regression of coronary calcifications with reduction of LDL-III (dense LDL).

(a) Low Triglyerides (TG -- a reflection of our carb intake and insulin)

(b) High Total HDLs

Again... Paleo thrashes these metabolic parameters of heart disease. Without synthetic drugs. No statins. No fibrates. No zetia. No pletal.

Yes... again it controls Lp(a) as well. All Lp(a) is DANGEROUS when the 'death band' and low HDLs are present. Do you recall... butter and coconut oil beat the cr*pola out of canola oil and olive oil for reducing and controlling Lp(a)?

See prior animal pharm post for our wonderful TYP hall of famers and Paleo examples of PERFECT lipoproteins for PERFECT regression.

Low Carb Mod-High Sat Fat Paleo Raises HDLs OUT OF THE ROOF
In addition to all of the above metabolic parameters for control of atherosclerosis, HDLs are most stunningly and astoundingly improved. No drug can reach the height of these simple diet changes. Statins: -5 to 5% (this explains the utter lack of outcomes compared with regression trials with omega-3, niacin or vitamin D recall Cardio Controversies: Dr. Superko and his sumarai quote?). Fibrates: 5% (but they raise dense HDL-3 mostly). Zetia: 0-2% (again mostly HDL-3 and explains why all outcomes are negative and even worse than statin outcomes). Pletal: 0-3% (again HDL-3).

Our goal at TYP for HDLs is 60 mg/dl but obviously higher is not harmful if it is all the buoyant HDL-2 type which is associated with reductions in Trigs (see above) and dense LDL (see first diagram).

Never in my 10+ years pharmacological career have I ever heard of diet manipulations that substantially raise the heart- and cancer-protective HDLs until I found Paleo. *overwhelmed sigh* Yes -- sure niacin 30-50% (shift to 'A'). Yeahhh -- sure liquid GOLD that I oil 5-10% (generous shifting to 'A' and massive immeasurable immunomodulating anti-inflammatory benefits).

Low carb high sat fat Paleo: INCREASE BY 100-200%.

My HDLs nearly doubled (60s to 105 mg/dl with TYP + high fat Paleo, and probably higher now)

Most others report doubled or tripled total HDL values from baseline. See below examples and from the post: Part II Benefits of High-Saturated Fat Diets.

Is it really that easy?
--raise HDLs
--lower dense small LDL
--shift to Pattern A from BBBBAD
--feel more energetic, vibrant, younger with maximum vitality

N-O-T-H-I-N-G is impossible.

Summary of my favorite low carb high fat Paleo stories:

Dr. Richard Bernstein MD, Type 1 DM, 70-ish years old, no diabetic complications, low carb, high saturated fat lacto-Paleo: Triglycerides–50; LDL–53; HDL–118; and LDL subparticles - Type A.

Mr. Jimmy Moore (ultimate low carb high sat fat lacto-Paleo): Pattern A, small dense LDL 3%, HDL 60s, EBCT calcium score ZERO (percentile rank, big PHAT Z-E-R-O). Family heart disease risk: HIGH.

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

Mr. Stephan Guyenet (high sat fat semi-Paleo) TC 252 TG 49 HDL 111 Calc LDL-131 (wrong, but who cares)

Mr. Scott Miller (BF 9% -- low carb high sat fat Paleo TC 223 TG 51 HDL 98 (baseline: HDL 38-ish and BF 26%) Calc-LDL 125 Lp(a) 2

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

Mrs. Anna (Against the Grain blog GRRRLL! ) TC 230 (2007, still transitioning to sat fat/grain-free) TG 59 HDL 72 (from 60's) Calc LDL 146
EBCT calcium score ZERO (percentile rank, big PHAT Z-E-R-O)

My Labs (on coconut oil, low carb mod-high sat fat Paleo, [25OHD]=50 ng/ml) TC 249 TG 68 (TGs 30s when no drug adverse effects) HDL 105 Real LDL 125 Calc-LDL 130 Lp(a) 2

Dr. Bernstein: Why the Low Carb Diet is Best

Dr. Bernstein is a wonderful educator, researcher, and physician. My respect for him and his brilliant work could never be overstated. His lipoproteins also R-O-C-K.

Why the Low Carb Diet is Best (click HERE link)

Part 4 of a 5 part feature

Richard Bernstein, MD, FACE, FACN, FCCWS Apr 24, 2007

Dr. Bernstein's latest book, Diabetes Solution, 3rd Edition, was published in March 2007 by Hachette Book Group, USA. His prior book, Diabetes Diet, was published in 2005 by Little Brown and Co.

When I developed diabetes in 1946, physicians thought that the high illness and death rate of diabetics was due to dietary fat and the supposedly resultant elevation of serum
cholesterol. Since the DCCT trial, the scientific literature overwhelmingly supports the role of elevated blood sugar in all long-term diabetic complications.

Yet even today, many physicians ignore the need for normal blood sugars and focus on dietary fat. The 2006 Clinical Practice Recommendations (1) of the ADA advocate large amounts of dietary
carbohydrate (45 - 65% of total calories) and small amounts of protein and fat. This recommendation is preceded by the statement that "dietary carbohydrate is the major contributor to postprandial (after meal) glucose concentration."

The high carbohydrate load is justified by the claim that "the brain and central nervous system have an absolute requirement for glucose as an energy source." This statement, while only partially correct (ketones from stored fat keep the brain alive during starvation), ignores the fact that in the absence of dietary carbohydrate, the liver, intestines, and kidneys convert dietary protein into as much glucose as the brain requires.

Virtually the entire evolution of mankind occurred when our ancestors were hunter-gatherers, well before the inventions of agriculture and animal husbandry. (2) These people had scarcely any access to dietary carbohydrate and certainly no access to animal milk, cereal grains, whole-grain and refined breads, refined sugars, and sweet fruits. They ate almost exclusively lean meat and fish, plus small amounts of leafy and other
low carbohydrate vegetables. Some humans, such as Eskimos, consumed only fat and protein. Our pre-agriculture ancestors frequently had violent deaths, but no coronary, kidney, or arterial disease, no tooth decay, and no diabetes.

By 1969, when I first began to measure my own blood sugars, I was already suffering from about 15 major and minor long-term complications of diabetes, thanks to the
low fat, high carbohydrate diet I had been following for 23 years. By about this time, scientific studies of animals had demonstrated the prevention and even reversal of many diabetic complications by blood sugar normalization.

I soon discovered that even multiple daily
insulin injections (basal/bolus dosing) would not achieve anything close to steady normal blood sugars. It was not until I lowered my carbohydrate consumption to a daily total of 30 grams (mostly from leafy and cruciferous vegetables) that things fell into place. Today my A1c is 4.5% (normal is 4.2-4.6%), and my target blood sugar is 83 mg/dl (about mid-normal for young non-diabetic adults).
Most of my long-term complications, including advanced kidney disease and severe
gastroparesis, have normalized. Those that involved irreversible muscle loss (droopy eyelids, intrinsic minus feet (diabetic foot)) have not gotten worse. My lipid profile, which had been grossly abnormal, now shows: Triglycerides–50; LDL–53; HDL–118; and LDL subparticles - Type A. I see similar results in others who follow a prehistoric diet like my own (except for some type 1's with severe gastroparesis).

Until very recently, researchers were not comparing the effects of low carbohydrate diets to the ADA low fat/low protein diet. Recent results consistently support low carbohydrate, high protein¬ diets–not only for blood sugar control, but also with regard to
weight loss and cardiac risk. Many of these studies are posted on the Web site of the Nutrition and Metabolism Society, at

I am not alone. Thousands of type 1 and
type 2 diabetics are following very low carbohydrate diets. Many observe that both fat and protein bring about satiety, while carbohydrate leaves them hungry and craving more carbohydrate. Other studies have focused on the importance of dietary protein for prevention of bone loss (4) and for preventing blood pressure elevation (5).

Richard K. Bernstein, M.D.,F.A.C.E., F.A.C.N., F.C.C.W.S. Mamaroneck, NY 10543

1. Amer Diabetes Assoc Clinical Practice Recommendations, Diabetes Care, Vol 29 Suppl 1, Jan 2006, p. 513.
2. Cordain et al, Origins and Evolution of the Western Diet: Health Implications for the 21st Century, Amer J Clin Nutr; 81:341-54, 2005.
3. Science, 307:840, Feb 2005.
4. Bonjour J-P, Dietary Protein: An Essential Nutrient Factor for Bone Health, Jnl. Amer. Coll. Nutrition 24:6, 5265-5365, 2005.
5. Obarzanek et al, Dietary Protein and Blood Pressure, JAMA 275:20, 1598-1603, May 1996.

Wednesday, October 7, 2009

Case: 45 yo Female, Perfect Framingham, Perfect Cholesterol, Perfect PLAQUE PROGRESSION

When I see a female with Peripheral Vascular Disease (plaque in the legs) or angina/CAD (heart disease: plaque in the coronary arteries) or Chronic Kidney Disease (plaque in the kidney arteries)... invariably Lp(a) and low HDL2b are the PRIME factors for plaque buildup.

Another factor is a positive family history of a coronary event in the father prior to age 60 yo.

Review: Goals for Regression

Dr. Hecht has ten case studies which I will review one by one here. Earlier (Cardio Controversies: Dr. Hecht) we reviewed the success case study of the the young male with strong family CAD history, high Lp(a) and 15% EBCT regression after only 15 months on niacin 4000mg daily (and low low dose weak statin). This gentleman had regression after doubling the HDL2b from 12% to 24% and the small LDL shifted to buoyant Pattern 'A' LDL subspecies. Most notably, his Trigs started in the 200s then reduced to only 30s. O-u-t-s-t-a-n-d-i-n-g. Drugs alone? No. He must have lost weight, changed the diet, gained some body recomposition and started a good exercise program. Drugs alone cannot lower to Final Trigs 30s from the 200s. TYP goal for Trigs is 60 mg/dl however this is typically exceeded by most members especially those who are able to shift to Pattern 'A' and reach the other TYP goals. Trigs are an expression of our carbohydrates in our diet (starchy and sweet foods/beverages), saturated fats, and omega-3 fatty acids (ALA flaxseed; EPA DHA fish oil). As Trigs drop, buoyancy goes to the particles, both LDL and the HDLs. HDL-2b, the regression particle is the most buoyant, largest HDL subspecies. HDL-2b is associated with extreme longevity in centenarians, cancer-protection in remission cases and vascular regression of plaque in heart trials and at TYP.

HDL-2b are like good, loyal friends who watch out for you and your family.

Can you ever have too much?

Case Study: Perfect Scores, Perfect P L A Q U E

Dr. Hecht presents a case of a young female, no symptoms, with perfect plaque progression. She has a double-digit coronary calcification score of 95 which takes her to the top 98th percent for her age for plaque. Normal heart disease stratification at this time in conventional medicine uses the Framingham score. With her perfect baseline lipids, her score is quite good.
The Framingham 10-year risk is calculated to be < 1%.

Translation: 0-10% = 'low risk'. (10-20%=mod; >20%=high)

Her risk, in fact, is estimated to be insignificant, negligible risk.

No worries???

Yes, worry.

Alarmingly, she has the highest heart calcifications and the 'real age' of a 98 year old female.

Real Age, Real Baloney: Coronary Calcification Tells Age

Some experts Dr. Hecht discusses want to use EBCT or MDCT percentile scores as the 'real age'. This makes sense to me. It is the internal metabolic milieu, chaos and entropy which reflect our longevity and status.

Just as well, the internal metabolic calm reflect our regression and control of lifespan.

Advanced Metabolic Testing
Her results for the metabolic testing show perfect CRP (C-reactive protein). CRP is bunk. It could be elevated if you sneeze. If it is chronically elevated, then you have issues but it is no more telling of plaque than the traditional, conventional lipid panel.

On further examination, the metabolic testing which is identical to what we look at TYP program shows:
--elevated apoB (goal < 60-70)
--mildly elevated homocysteine (goal < 8.0)

Both of these indicators are related to inflammation and high carbohydrate intake. Inflammation may stem from excessive omega-6 and/or fructose, deficiencies (n-3 omegas, vitamins ADEK, B-vitamins B3 B6 B1 folate B12, minerals Magnesium Selenium Zinc Chromium Iodine Iodine, vitamin C, vitamin "O" optimism *haa*, carotenoids, mitochondrial components Carnosine CoQ10 ALCAR Carnitine; hormones adiponectin T E2 E2 P preg DHEA, etc), food allergies (wheat, gluten, A1 casein, nuts, etc), heavy metal and environmental toxicity (mercury from seafood, estrogenic pesticides, etc).

Ultimate Testing Lipoprotein Subfractionation:

The 'death band' is evident.

Recall according to Krauss, goal LDL IVb is less than zero. Just kidding, the goal is to get this subfraction which is the most dense, most lethal to as low as possible. In patients with large amounts of plaque where stenosis was > 30%, Krauss found < 2.5% of LDL-IVb was highly statistically significant for regression on angiogram. For those with 'less' plaque (read: less stable), LDL-IVb of 2.5% was still too high for regression to occur. What is good? I believe as low as possible. We see at TYP even when LDL-IVb is 1.5%, EBCT progression still occurs at 10-25%.

I don't find this acceptable.

The death band should be as low as possible. Or none.

Ultimate goal: Shift the LDL from dense to buoyant (known as LDL1 + LDL2a+b on BHL) and annihilate the 'death band'. Stop stuffing the face with fructose (fruit). Cut back olive oil and replace with some saturated fats.

Major Risk Factors for CAD: Low HDL2b, Lp(a)

Diagnosis: This young lady has extensive 98th-percentile plaque. Dense LDL, the death band LDLIVb, low HDL2b, and Lp(a).

Conventional Prognosis: No action on her doctor's part until she comes in with throbbing, painful legs or shortness of breath, back ache, jaw pain, heartburn (extensive plaque leads to vague, non-specific anginal symptoms in females). Worse case scenarios: tries to run a half-marathon or marathon and has a coronary event and is resuscitated with brain damage. Or SCD (sudden coronary death) where the first sign of heart disease is silent and fatal.
Unconventional TYP Prognosis: Longevity and shifting 98th-percentile calcifications to 15-50th-percentile less each year. Shortly... her real age will be 17 years old.

Yes, shaving YEARS off of her real age, coronary calcification percentile rank.

Hecht-Treatment: Hecht discusses niacin 4 grams per day and some statin (why? I dunno why because he contradicts himself when it comes to bashing LDL and LDL-goals; I sense some 'cognitive dissonance' on his part). Most cardiologists and physicians don't know a lick about diet, nutrition, what organs/hearts require, and basic micro- macronutrients. Didn't the father of medicine, once say 'let food be thy medicine'? We in the Paleo/Primal and TYP communities already know food can be poison (e.g. gluten, wheat, grains, legumes).

Is Hecht's therapeutic strategies enough? No. Some cases are 'treatment failures' which we'll later breakdown why.

Optimal Longevity Treatment To Reverse Vascular Dysfunction:

(1) Statin-less (statins increase Lp(a), OxLDL, OxLDL/apoB, %-dense LDL and prevent shifting from pattern B to A+++; causes autoimmunity and auto-antibodies, cellular level mitochondrial and myocyte damage, depletes antioxidants ubiquinols and coenzyme Q10; Crestor is associated with higher incidences of diabetes and kidney problems (proteinuria) in clinical trials)

(2) Niacin

(3) Omega-3 fish oil 6000++ mg EPA DHA daily for Lp(a), low HDL2b, high dense LDL, shift to pattern A, optimize n-6:3 ratio (goal ~1.5-2.0 per Dr. Barry Sears PhD and medical literature involving CKD patients)

(4) Correct Vitamin D deficiency (goal [25OHD] 60-80 ng/ml)

(5) Correct Saturated Fatty Acid Deficiency: Stop the AHA-low-fat-low-cholesterol-diet. Obtain Saturated Fats 15-20+% daily to increase HDL-2b, lower the death band LDLIVb, shift to Pattern 'A', and lower the atherogenicity of Lp(a)

(6) Correct Vitamin K2 deficiency (Sources: fermented cod liver oil, casein-free butter, hard cheeses if not allergic, natto, vitamin K2 100mcg daily MK7)

(7) Correct thyroid and adrenals by initially supporting (egg yolks, vitamins ADEK K2 Bs C; tocopherols, tocotrienols, minerals: Magnesium Selenium Zinc Chromium Iodine Iodide; saturated fatty acids, omega-3 fats ALA EPA DHA, carotenoids, avoidance of n-6 PUFAs) and if not sufficient then thyroid replacement (Armour +/- T4) and adrenal support (read HERE and HERE) to achieve optimal metabolism and stable core body temperatures 98.2 - 98.6 degrees F.

(8) Correct insulin disparities (exercise, C-A-R-B RESTRICTION, stress reduction, SLEEP, yoga, resistance train, weight loss, ketosis (diet, intermittent fasting), insulin-sensitizers: R-alpha lipoic acid, L-carnitine, Chromium, Leucine, Taurine, Glutamine, whey protein, flaxseed and fish oil, bittermelon, celery, pycnogenol, krill oil, astaxanthin, other antioxidants and proanthocyanidins, etc)

(9) Correct other calcified organ dysfunction: pineal (melatonin), hypothalamus (yoga, relaxation, breathing ex, etc), thyroid (see above), pancreas (see insulin above + digestive enzymes), gallbladder (digestive enzymes), colon (probiotics)

(10) No w-o-r-r-i-e-s ! *winky*

What about 4 grams per day of vitamin B3, niacin?

Does overdosing on niacin aid the above? Unfortunately 'no'. The mechanism of action is that niacin mimics all of the above (increases hGH, testosterone, steroids, ketosis, fasting and exercise). Adverse effects of niacin include: gout, diabetes and liver test elevations. Again I like niacin b/c it works but I don't love it. It doesn't appear to work on everyone in the year 2008-2009 and likely the future. Numerous nutritional and environmental toxicities apparently have shifted the cardiology and endocrinology playing field since the niacin trials were published, including the HATS 2001 NEJM publication by BG Brown et al.

Dr. Davis' Nutritional Wisdom and Recent TYP Topics (Members) to Reverse Vascular Dysfunction:

o Fructose: Dangerous at Any Level?
o Anthocyanidins: Eat Purple
o S-L-E-E-P -- Quality and Quantity
o Iodine Deficiency -- Importance for Heart Health
o Thermoregulation -- Thyroid and Adrenal Dysfunction
o TYP Part 3 Diet: 40% Fat Diet for Lp(a) and read more HERE

Friday, October 2, 2009

Cardio Controversies: Lp(a) Dangerous at ANY Value

What the heck...?

Can Lp(a) create more damage than we previously thought?

Dr. Hecht has apparently showed it with his examination of lipoprotein, cardiac and metabolic parameter comparisons with the real measure of heart disease risk: EBCT-determined plaque burden. Lp(a) was 3rd after HDL and LDL particle diameter in being highly associated with coronary calcifications. See below. Free PDF HERE. Normally at TrackYourPlaque we consider Lp(a) greater than 20 mg/dl as a high contributor toward accelerated plaque burden. When I look at Dr. Hecht's graphs, what I notice is that indeed this may not be true.

It appears to my observations that at ANY Lp(a) value, plaque burden is quite high reaching even 97th, 98th or 99th calcium percentile for CAD risk (of population norms) at severely low Lp(a) levels of 5 mg/dl or 10 mg/dl.

OK...what the heck?

I can make the same observations for my CAD (heart), PVD (peripheral), or CVD (stroke) patients and individuals with extensive diabetic complications. At any Lp(a), the extent of disease can still be quite pronounced.

What other factors are correlated to vascular damage?

1. Low HDL2b

2. High small dense LDL.

These THREE factors determine almost entirely the extent of disease. Both visionaries Dr. Davis and Dr. Hecht focus on these predominantly to control and halt the progression of calcifications.

How are these 3 metabolic parameters created in the first place?
--low fat SAD AHA low cholesterol low saturated fat diet
--saturated fat deficiency
--excessive carbs (>10 g/d, >20 g/d, >50 g/d, >100 g/d -- depending on a person's insulin and insulin sensitivity and pancreas/adipose/hormone status)
--inflammation (excessive omega-6 oils)

Not... necessarily... a Slo-niacin or Niaspan deficiency...

Saturated Fats Like Butter Beat the Cr*pola Out of Canola in Lowering Lp(a)

We've discussed Dr. Mozaffarian earlier in Part IV Benefits of High-Saturated Fat Diets where he showed higher sat fat (> 12.0%), lower n-6 PUFA and lower carb were associated with less coronary artery stenosis; in fact in the quartile of the highest sat fat dietary intake, regression of coronary artery stenosis was signficantly observed. No other parameter was correlated to regression. Right...! ONLY higher dietary saturated fat consumption... (this quartile also was found to smoke more and took less pharmaceuticals).

Is Krauss in the house?? OK, Dr. Mozaffarian at Harvard has come through again (sort of). He did the right study again (though... 'wrong' conclusions). In his most recent publication Mozaffarian showed that after switching human subjects off of various concentrations of dietary trans fats to different fats (saturated and n-6), dramatic changes in cardiac parameters were noticed (Mozaffarian D, Clarke R. Eur J Clin Nutr. 2009 May;63 Suppl 2:S22-33. Free PDF HERE. ) Butter and other saturated fats were shown to lower the baseline Lp(a) to greater degrees than n-6 PUFAs like soybean, cottonseed, or canola oil.

Butter, palm oil and lard beat canola and other n-6 PUFA oils by 3-4-fold.

Mechanism of Action of: B U T T E R

Butter is comprised of part monounsaturated fats and part saturated fatty acids with one of the predominant acids being BUTYRIC ACID, a 4-carbon chain entity. It turns out that ALL the saturated fatty acids behave much like the omega-3 PUFAs that we enjoy for their plaque-regression, lipoprotein improving, immunomodulating and anti-inflammatory properties. Omega-3 PUFAS bind the whole-pan-PPAR receptor family to shift to LDL larger particles and increase HDL2b. Saturated fats bind most strongly to PPAR-gamma which raises HDLs and and lowers both Lp(a) and Small Dense LDL (particularly LDL-IVb, the 'death band'). They bind weakly to PPAR-delta but sufficiently to paradoxically and P-O-T-E-N-T-L-Y lower inflammation (NFkB, TNF-alpha).

Recall: PPAR-Delta is the Dagger in the Heart of CAD

Saturated fatty acids in fact behave like hormones and bind like steroid nuclear hormones to the PPAR family of receptors (like vitamin-D-to-VDR, carotenoids-to-RXR, vitamin-A-to-RAR, thyroid-to-TR, estrogen-to-ER, etc). This research was done many years ago by Glaxo researchers Eric Xu and others (Molecular Cell, Vol. 3, 397–403, March, 1999). See below. Other researchers defined further the benefits of butyric acid (butyrate) by elucidating its binding activity of PPAR convincingly.

Our b*tt is made out of saturated fats and we eat saturated fats (almonds, coconuts, olives, fatty fish, grassfed beef, free-range eggs/fowl, wild duck, etc). Our body creates, metabolizes and burns saturated fats all day (recall: palmitic acid) esp when we are between meals, intermittent fasting, carb restricting, ketotic, exercising or starving.

Do we make butyrate??

Make Butter (Butyrate) In Your B*TT

Just kidding... North of the rectum (e.g. b*tt), in the colon , short-chain fatty acids like butyric acid (butyrate) one of the fatty acids found in butter, cream and cheeses is produced via anaerobic fermentation of dietary fiber. Our friendly happy gut flora actually produces butyrate (not us). We either consume it or we absorb it from our intestines from bacterial production.

Yes... *haaa* make BUTTER in your colon from vegetable fibers...

Butyrate Protects Against Colon Cancer by Lowering NFkB by Binding PPAR

Furthermore, butyrate has been shown in trials to be anti-inflammatory and immune-modulating. Deficiencies in luminal butyrate synthesis are associated with chronic bowel inflammation. Schwab M et al state:

"Previously, we have demonstrated that the nuclear hormone erceptors Peroxisome-Proliferator-Activated-Receptor (PPAR) and the vitamin D receptor (VDR), transcription factors with anti-inflammatory capacities, are up-regulated and activated by butyrate (Gaschott and Stein, 2003; Gaschott et al., 2001; Schwab et al., 2006;Wachtershauser et al., 2000). PPAR and VDR are highly expressed in the colonic epithelium indicating that both receptors are important agents in the physiology of the human colon (Desvergne and Wahli, 1999; Nagpal et al., 2005). Ligands for both receptors have been shown to interfere with the activity of NFkB and to influence the ability of olonocytes to express immune-modulatory cytokines (Segain et al., 2000; Sun et al., 2006)."

Independently in two labs in 2007, butyrate was found to control NFkB, one of the most potent pro-inflammatory cytokines of our immune system implicated in ALL chronic and acute diseases known to man, including colon cancer and coronary artery disease (Schwab M et al. Molecular Immunology 2007;44: 3625–3632.; Usame M et al. Nutr Res 2008;28:321–328. See end.) The anti-inflammatory power of lauric acid from coconut and palm oil and butyric acid from butter originates from their ability to bind and activiate PPAR-gamma as shown by these studies. PPAR, like the vitamin D receptor (VDR), is one of the master controllers of inflammation. Schwab shows in several publications that butyrate does in fact configure, bind, and activate PPAR receptors. Butyrate is like a DRUG. It binds the most potent receptor for energy balance, immunomodulation, control of lipids (Lp(a), HDL2b, sdLDL), and inflammation! End result... it knocks out NFkB. For the heart, this translates to kicking the cr*pola out of canola in terms of shifting to Pattern 'A', increasing HDL-2b, annihilating small dense LDL and Lp(a) and eradication of vascular atherosclersis.

See Prior Posts:

Trying to Target Butter-Receptors: How About Grassfed GHEE??

"There is increasing evidence that the expression and activity of PPARg and VDR are under the control of butyrate implying that the receptors may participate in butyrate-mediated suppression of NFB activation (Gaschott and Stein, 2003; Gaschott et al., 2001; Schwab et al., 2006; Wachtershauser et al., 2000). PPARg and VDR are both ligand-activated transcription factors that belong to the nuclear hormone receptor family and participate in a variety of immune processes (Tirona and Kim, 2005). VDR is widely expressed in epithelial tissues, cells of the immune system and several cancer cell lines including colorectal cancer cells (Giuliano et al., 1991; Segaert and Bouillon, 1998). PPARg is activated by natural ligands such as fatty acids and eicosanoids and is highly expressed in colonic epithelium, indicating an important role of the receptor in the physiology of the human colon (Desvergne and Wahli, 1999). All these characteristics make both receptors potential targets in butyrate-mediated inhibition of NFkB signalling."

In Vivo (Live Humans) High Intake of Butter Associated with Reduced Colon Cancer

Of course Swedish researchers examined their nutrition data registry for the Swedish Mammagraphy Cohort and lo and behold found distinct correlations between high dairy intake and low colon cancer (Am J Clin Nutr. 2005 Oct;82(4):894-900.) Those in the upper 2 quartiles of CLA consumption and > 4 servings daily of high-fat dairy was highly associated with reduced colon cancer risk. The author's conclusions were: These prospective data suggest that high intakes of high-fat dairy foods and CLA may reduce the risk of colorectal cancer.

Diary Fat Potential Anti-Carcinogenic Agents

Parodi reviews the literature and reports that... "About one third of all milk triacylglycerols contain one molecule of butyric acid, a potent inhibitor of proliferation and inducer of differentiation and apoptosis in a wide range of neoplastic cell lines. Although butyrate produced by colonic fermentation is considered important for colon cancer protection, an animal study suggests dietary butyrate may inhibit mammary tumorigenesis. The dairy cow also has the ability to extract other potential anticarcinogenic agents such as beta-carotene, beta-ionone and gossypol from its feed and transfer them to milk (J Nutr. 1997 Jun;127(6):1055-60. Free PDF HERE). Grassfed cheese, cultured milk, yogurt, ghee, and butter also contain CLA. Parodi discusses that, "Recent research shows that milk fat contains a number of potential anticarcinogenic components including conjugated linoleic acid, sphingomyelin, butyric acid and ether lipids. Conjugated linoleic acid inhibited proliferation of human malignant melanoma, colorectal, breast and lung cancer cell lines. In animals, it reduced the incidence of chemically induced mouse epidermal tumors, mouse forestomach neoplasia and aberrant crypt foci in the rat colon. In a number of studies, conjugated linoleic acid, at near-physiological concentrations, inhibited mammary tumorigenesis independently of the amount and type of fat in the diet."

Beef Tallow SYNERGISTICALLY Beats the Cr*pola Out of Corn Oil (n-6 PUFA)

In another interesting animal study (mice), beef tallow (25% palmitic acid; 50% oleic acid) increased the potency of CLA in decreasing mouse mammary tumor metastasis. (J Nutr. 2006 Jan;136(1):88-93.) "Linoleic, oleic, stearic, and palmitic acids, either did not change or enhanced the cytolytic effects of CLA isomers on mouse mammary tumor cells in culture." The authors found that oleic + palmitic enhanced cytolytic CLA-derived tumor cell death, whereas n-6 PUFAs (linoleic acid) were associated with dose-dependent increases in tumorigenesis and blocking CLA-benefits.

See Prior Post:
Happy Cows and CLA (CLA is found in grassfed beef, dairy, lamb, pastured pork)

Rat Study: ONLY Olive Oil and n-6 PUFAs Associated with Cancer Model in High-Fat Diets

Rats are not humans but they have no gall bladders... so they are not unlike 80% of the individuals that I see who fail to have functioning gallbladders. Anyhow in this one study 4 high fat diets (corn, lard, beef tallow and coconut oil) and 1 low fat corn oil were used in 5 rat groups (Chan PC et al. Cancer Res. 1983 Mar;43(3):1079-83.). Mammary tumors were induced with N-nitrosomethylurea. Incidence of tumors in the high-fat groups was the lowest in the coconut oil group. Upon further analyses (these researchers were GOOD), they concluded, " the total oleic and linoleic acid intake in the five groups of rats correlated positively (r = 0.95) with mammary tumor incidence."

Role of Oliv-ola (Canola+Olive oil) Induced Colon Carcinogenesis:
Coconut Oil Beats the Cr*pola Out of OLIVOLA

Nair J et al in Germany have been conducting research in DNA damage associated with oils (Nair J et al. Mutat Res. 2007 Nov 1;624(1-2):71-9.) They tested LA (linoleic acid, n-6 PUFA), oleic acid and coconut oil in rats by lavaging them for 30day, sacrificing, then measuring etheno-DNA adducts in the organs. Etheno-DNA adducts are associated with j*cked up gene expression, mutations and carcinogenesis. They are produced by oxidative stress and lipid peroxidation. Their research showed that n-6 PUFAs have gender-specific toxicity and other surprising results. Not unlike the Israeli 'Paradox' (see below), female LA-treated rats showed increases in etheno-DNA adducts in the DNA of their circulating immune cells, the all important WBC (white blood cells). For both genders, colon was the target for stress-derived DNA-adducts in omega-6-PUFA treated rats, which supports the role for omega-6 induced colon cancer, the authors concluded.

'Unexpectedly, olive oil treatment enhanced entheno-adduct levels in prostate 3-9-fold' the researchers observed.

What... the... H E C K ?

So... olive oil (n-9 monounsaturated) is highly implicated in TWO studies with cancer: mammary and prostate. Is this only seen in certain situations?

Lame-o retard-o dietary fat composition?

Saturated fatty acid deficiencies?

Omega-3 deficiencies?

Most lab rats are vitamin D deficient as well...

Here is other provocative (ok, not really) research showing the same thing in more in vivo animal cancer model studies:
--coconut oil beats the cr*pola out of n-6 PUFAs
--MCT oil (50% of coconut oil) beats the cr*pola out of n-6 PUFAs
--the lower the rat cholesterol, the higher the incidence of mammary tumorogenesis... in other words (switch around), the larger the LDL particles induced by saturated fatty acids which results in a higher total cholesterol, the lower the risk of breast cancer in rats. Applies to humans too.

Dietary fat and mammary cancer. II. Modulation of serum and tumor lipid composition and tumor prostaglandins by different dietary fats: association with tumor incidence patterns.
Cohen LA, Thompson DO, Choi K, Karmali RA, Rose DP.
J Natl Cancer Inst. 1986 Jul;77(1):43-51.

Dietary fat and mammary cancer. I. Promoting effects of different dietary fats on N-nitrosomethylurea-induced rat mammary tumorigenesis.
Cohen LA, Thompson DO, Maeura Y, Choi K, Blank ME, Rose DP.
J Natl Cancer Inst. 1986 Jul;77(1):33-42.

Influence of dietary medium-chain triglycerides on the development of N-methylnitrosourea-induced rat mammary tumors.
Cohen LA, Thompson DO, Maeura Y, Weisburger JH.
Cancer Res. 1984 Nov;44(11):5023-8.
Medium chain triglycerides (MCT) in aging and arteriosclerosis.
Kaunitz H.
J Environ Pathol Toxicol Oncol. 1986 Mar-Apr;6(3-4):115-21.

So I've digressed... let's get back to the heart of the matter...

n-6 PUFAs Shrink LDL-Particles... To Pattern B (BAD)

Shrinkage... Not. Good. The rest of the Mozaffarian and Clarke's conclusions are not so justified by the medical literature. They further try to discuss the cardiac benefits of the n-6 vegetable oils without acknowledging the metabolic parameters that Drs. Hecht, Krauss, Superko and Davis support as the factors that are most highly correlated to plaque burden: LDL particle size, HDL2b and Lp(a). Unfortunately I find their so-called cardiac assertions kinda b-u-n-k-y. They employ parameters (TC/HDL ratio, apoB/AI ratio, CRP) that are not borne out to be associated with coronary calcium plaque burden or serial plaque progression according to Hecht's 2003 publication.

n-6 PUFA and olive oil are necessarily heart healthy?? No. In a study with rapeseed, olive oil or sunflower oil, LDL particles significantly (p=0.012) shifted to smaller, dense particles with all the oils tested, after a switch from a two-week saturated fat diet. BUNKY!!! See below.

Dietary mono- and polyunsaturated fatty acids similarly affect LDL size in healthy men and women.

Kratz M, et al. J Nutr. 2002 Apr;132(4):715-8.

The goal of this study was to investigate the effect of the dietary fat composition on LDL peak particle diameter. Therefore, we measured LDL size by gradient gel electrophoresis in 56 (30 men, 26 women) healthy participants in a controlled dietary study. First, all participants received a baseline diet rich in saturated fat for 2 wk; they were then randomly assigned to one of three dietary treatments, which contained refined olive oil [rich in monounsaturated fatty acids (MUFA), n = 18], rapeseed oil [rich in MUFA and (n-3)-polyunsaturated fatty acids (PUFA), n = 18], or sunflower oil [rich in (n-6)-PUFA, n = 20] as the principal source of fat for 4 wk. Repeated-measures ANOVA revealed a small, but significant reduction in LDL size during the oil diet phase (-0.36 nm, P = 0.012), which did not differ significantly among the three groups (P = 0.384). Furthermore, affiliation with one of the three diet groups did not contribute significantly to the observed variation in LDL size (P = 0.690). In conclusion, our data indicate that dietary unsaturated fat similarly R E D U C E S LDL size relative to saturated fat. However, the small magnitude of this reduction also suggests that the composition of dietary fat is not a major factor affecting LDL size.
PMID: 11925466

n-6 PUFAs Cause Inflammation and Cancer: Israeli Experience

Shapiri discusses how changing from traditional oils (saturated fats like schmaltz (rendered goose or chicken fat w/onions) or beef tallow) to a high consumption of n-6 PUFA oil is postulated to have lead to the astronomic rise in cancer in Israeli Jewish women (Eur J Cancer Prev. 2007 Oct;16(5):486-94.)

It is discussed HERE as well.

Wanna CUPPA of CANCER? Increase your n-6 PUFAs, reduce your saturated fatty acids.

Small Dense LDL, OxLDL and Lp(a) SYNERGISTICALLY Grow Plaque

Why is Lp(a) so extremely toxic and an accelerant for all damage whether it is diabetic complications (microvascular: eyes - kidney - nerves - penile - brain (e.g. Type 3.0 Diabetes)) or atherosclerotic disease (macrovascular: heart, carotid, peripheral)? Apparently Lp(a) binds oxidized phospholipids of apoB 100 which is attached to all LDL, including Lp(a). What is Lp(a)? It is just LDL + apo(a) combined. Large LDL are rarely oxidized -- they are protected by size, buoyancy, high cholesterol content (yes, cholesterol is an 'antioxidant') and a high content of vitamins and fat-soluble antioxidants (ubiquinols, carotenoids, menaquinones (vitamin K2s), tocopherols, tocotrienols) and apo E (carriers of minerals and other vital micronutrients).

A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma.

Bergmark C, et al. J Lipid Res. 2008 Oct;49(10):2230-9. Free PDF HERE.

Oxidized phospholipids (OxPLs) on apolipoprotein B-100 (apoB-100) particles are strongly associated with lipoprotein [a] (Lp[a]). In this study, we evaluated whether Lp[a] is preferentially the carrier of OxPL in human plasma. The content of OxPL on apoB-100 particles was measured with monoclonal antibody E06, which recognizes the phosphocholine (PC) headgroup of oxidized but not native phospholipids. To assess whether OxPLs were preferentially bound by Lp[a] as opposed to other lipoproteins, immunoprecipitation and ultracentrifugation experiments, in vitro transfer studies, and chemiluminescent ELISAs were performed. Immunoprecipitation of Lp[a] from human plasma with an apolipoprotein [a] (apo[a])-specific antibody demonstrated that more than 85% of E06 reactivity (i.e., OxPL) coimmunoprecipitated with Lp[a]. Ultracentrifugation experiments showed that nearly all OxPLs were found in fractions containing apo[a], as opposed to other apolipoproteins. In vitro transfer studies showed that oxidized LDL preferentially donates OxPLs to Lp[a], as opposed to LDL, in a time- and temperature-dependent manner, even in aqueous buffer. Approximately 50% of E06 immunoreactivity could be extracted from isolated Lp[a] following exposure of plasma to various lipid solvents. These data demonstrate that Lp[a] is the preferential carrier of PC-containing OxPL in human plasma. This unique property of Lp[a] suggests novel insights into its physiological function and mechanisms of atherogenicity.

Butyrate NFkB References

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PPARgamma is a key target of butyrate-induced caspase-3 activation in the colorectal cancer cell line Caco-2.
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