FARMACY: Leras Family Farm in Santa Rosa

Local, Organic, Sustainable Farms like Leras Family Farm

My kids and I had the pleasure to spend a day at the Leras Family Farm in Santa Rosa last Tuesday. We had a total blast! We played with the two baby calves with Zak (intern), fed slop to the Red Waddle pigs, amusingly watched 24 piglets forage and root on their acreage, studied Danielle the intern making cheese, picked basil, berries and grapes, drank their kombucha and chased and played with their beautiful soy-free, free range chickens in two coups.

Thanks for Dave, WAPF chapter leader in Berkeley for helping to set up!

Mike Leras with my d Hannah and I

FARMACY

What's so awesome about the ecology and environment of an organic farm like Michael Leras and his family's (gorgeous wife Jill (former model), 2 sons, doggy Brownie) is not only the inclusive recycling of all the nutrients from produce and leftovers but the completeness of the system: animals + plants. It's a true farmacopeia of happiness nutrients that every brain, gut and body needs.

Michael and his family go to Three Stone Hearth in Berkeley for families to pick up their fresh products like soy-free eggs, pork, grassfed beef, etc every week on Wed night and Saturdays.



Antidepressant Microbes In Soil: How Dirt Makes You Happy

"Soil Microbes and Human Health: Did you know that there’s a natural antidepressant in soil? It’s true. Mycobacterium vaccae is the substance under study and has, indeed, been found to mirror the effect on neurons that drugs like Prozac provide. The bacterium is found in soil and may stimulate serotonin production, which makes you relaxed and happier. Studies were conducted on cancer patients and they reported a better quality of life and less stress.
Serotonin has been linked to such problems as depression, anxiety, obsessive compulsive disorder and bipolar problems. The bacterium appears to be a natural antidepressant in soil and has no adverse health effects. These antidepressant microbes in soil may be as easy to use as just playing in the dirt.
Most avid gardeners will tell you that their landscape is their “happy place” and the actual physical act of gardening is a stress reducer and mood lifter. The fact that there is some science behind it adds additional credibility to these garden addicts’ claims. The presence of a soil bacteria antidepressant is not a surprise to many of us who have experienced the phenomenon ourselves. Backing it up with science is fascinating, but not shocking, to the happy gardener.
Mycrobacterium antidepressant microbes in soil are also being investigated for improving cognitive function, Crohn’s disease and even rheumatoid arthritis." Read more HERE. Hat tip: Keith Bell.

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

Loren Cordain Is Getting Into Coconut Oil

Yes. It is true.

O F

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).




Ketones

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)
--starvation
--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 (greenpasture.org), 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.

DIET INFO:
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.

Results:
(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.

Don't fear B E I N G A MEATHEAD. Or FATHEAD.




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

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:
PPAR






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

Involvement of different nuclear hormone receptors in butyrate-mediated inhibition of inducible NF kappa B signalling.
Schwab M, Reynders V, Loitsch S, Steinhilber D, Stein J, Schröder O.
Mol Immunol. 2007 Jul;44(15):3625-32. Epub 2007 May 22.

Role of nuclear hormone receptors in butyrate-mediated up-regulation of the antimicrobial peptide cathelicidin in epithelial colorectal cells.
Schwab M, Reynders V, Shastri Y, Loitsch S, Stein J, Schröder O.
Mol Immunol. 2007 Mar;44(8):2107-14. Epub 2006 Oct 19.

PPARgamma is a key target of butyrate-induced caspase-3 activation in the colorectal cancer cell line Caco-2.
Schwab M, Reynders V, Ulrich S, Zahn N, Stein J, Schröder O.
Apoptosis. 2006 Oct;11(10):1801-11.

Shifting to Pattern ' A ' for Longevity

Increasing Saturated Fat Intake Shifts to Pattern 'A'

Krauss has shown that increasing saturated fat intake and reducing carbohydrates lowers sd-LDL and shifts to Pattern 'A' (Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Siri PW, Krauss RM. Curr Atheroscler Rep. 2005 Nov;7(6):455-9.).

Undeniably Pattern A with a dominance of Large-LDL is desired for regression, longevity and cancer protection. Again, Krauss has spelled out in seminal articles that Large-LDL-Particles are not associated independently with atherosclerosis (JAMA rebuttal: Is the size of low-density lipoprotein particles related to the risk of coronary heart disease? Krauss RM. JAMA. 2002 Feb 13;287(6):712-3.; Ion Mobility Analysis of Lipoprotein Subfractions Identifies Three Independent Axes of Cardiovascular Risk. Krauss RM et al. ATVB. 2009 Sep 3.)




What is independently associated with CAD???

(1) Small Dense LDL, particularly the 'death band' LDL-IVb produced by dietary deficiencies of saturated fatty acid and/or ketones and/or excessive dietary carb loads

(2) Low HDL-2 (ditto)


No individual at TYP with subclinical or post-CAD event fails to demonstrate the above two characteristics. Without a doubt, these 2 metabolic parameters describes all atherosclerotic processes that lead to obstructive disease, clinical events, morbidity and mortality. Some individuals with 2-4 stents or bypasses, exhibit zero HDL-2 at the start of our program and 100% sd-LDL.

No joke.

Of course it immediately changes on the TrackYourPlaque program (faster when it is STATIN-LESS).



Krauss and Pattern 'A'
Of all the literature I have reviewed on Pattern A, Krauss has performed nearly all the seminal, landmark research. He has explored a variety of manners to shift to Pattern 'A' (sans statins, sans niacin).

Lots of Fat. 46% minimum.

Saturated Fat. 18% saturated minimum.

Carb restriction. See first diagram, at top.



Can we obtain zero% Pattern B:100% Pattern A in individuals? Minimal and near-zero 'death bands' of LDL-IVb? It sure would be nice.

When the line breaks 'zero' fat intake is ~ 65% and carb intake 20%. Is 20% still too high for some inviduals? I believe so.

I consume about 20-50 grams daily when I am insulin resistant (around my mense when my body thinks I'm getting ready for a baby; during the year of synthetic hormone h*ll). How do I know when carbs are excessive for me (eg, eating a whole dark chocolate candy carb = 30-40grams)?? I ck my blood glucose on a meter 10-20min afterwards (because I peak fast on high GI foods) and it may be > 110-120 g/dl. After rice/sushi, the BG may peak to 180 g/dl for like... 5 min. I can tell the damaging high glucoses are followed by damaging high insulin (and a reduction in adiponectin, the hormone related to body fat loss) because I may have heart palpitations, rapid/racing heart rate, a little anxious (?? or is it the I.V. Caffeine), not relaxed, (HUNGER for 24-72hrs afterwards) and basically feel like... CR*P.

I weigh about 125 lbs now and consume about 1-2 g per kilo of protein daily (somedays more with more exercise, somedays less with IF) which is approx 45-56 grams daily (= approx 2 chicken breasts) which makes up about ~15% of energy (or more).

If I estimate I obtain about 1000-1600 cal/day and calculate 20% would be allocated to carbs as an example, then that would be equivalent to ~50-80 grams of carbs daily. WOW. That is a lot more than my current consumption and my experience is that I would gain weight on that dietary intake (esp during insulin resistant periods), even if I consumed 65% fat and 15% protein (or even 50% fat and 30% protein).

Perhaps if carbs were restricted further, more individuals would have achieved Pattern 'A'?

10% Carbs?

5% Carbs?

See below, same graph, I've extrapolated into Pattern A territory by extending the Fat%/Carb% x-axis.



Saturated Fat Intake Lowers LDL-IVa+b

In a trial in n=103 men, low-fat versus high-fat diet were compared. Krauss yet demonstrates again that increased dietary fat and specifically the saturated fat portion are statistically related with reducing small dense LDLs LDL-III and LDL-IV and shifting lipoproteins toward Pattern A. (Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Dreon DM, Krauss RM et al. Am J Clin Nutr. 1998 May;67(5):828-36.)

In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid, was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL. This study also showed that increases in dietary saturated fat were associated with decreases in HL activity. This finding, together with our previous cross-sectional analyses that revealed significant inverse relations of HL activity with LDL peak flotation rate (15), suggests an inverse association of HL activity with concentrations of buoyant LDL particles.

Diet Compositions

Low fat diet:
--24% of energy as fat (6% saturated, 12% monounsaturated, and 4% polyunsaturated)
--59% as carbohydrate, with equal amounts of simple and complex
carbohydrates.

High fat diet:
--46% of energy as fat (18% saturated, 13% monounsaturated, and 12% polyunsaturated)
--39% as carbohydrate. TOO HIGH!!

The main fat as described by the authors was "Palmitic acid (16:0) ... the primary dietary saturated fatty acid in both diets, followed bystearic (18:0) and myristic (14:0) acids, which are representative of the major saturated fatty acids in most human diets (3)." The carbohydrates would be considered high and associated with a higher incidence of Pattern B according to the first Krauss trial described earlier in the post. Nonetheless the results were quite fascinating. Only saturated fatty acids corresponded statistically with improvements in shifting to Pattern A, increased LDL diameter size and to reductions in small dense LDL (both LDL-III and LDL-IV). Please see below stats.




Reduction of LDL-IV by 39% With Increased Saturated Fat
The amount of dietary saturated fat tripled up from 6% to 18% of total energy. This change statistically correlated to reductions in LDL-IV by a total of 39%. The 'death band' which would have corresponded to LDL-IVb was not determined in this trial but definitely some proportion was significantly decreased. Between LDL-IVa and LDL-IVb, we do not know the precise proportional changes.



3X Increase in Saturated Fat Increased HDL-2 by 50%

Recall in the HATS regression trial (NEJM, 2001) where 90% reduction in death and events were observed, the niacin arm was associated with a 70% shift to large buoyant LDL and HDL-2 increase of 60%. With an increase in saturated fats of from 6% to 18% daily, the HDL-2 subfraction increased 50%.


'Death Band': Percent-LDL-IV Changed from 6.0% to Only 3.4%
Examing the relative amount of the 'death band' LDL-IV, Percent of LDL-IV changed from 6.0% in the low-fat group to only 3.4% in the high-fat group. Recall in the previous post Krauss observed that regression (where stenosis is > 30%) was highly associated with quartiles of LDL-IVb less than 2.5%.




Summary of Heart-Healthy Improvements with a High-Saturated Fat (18%) Diet in only Six Weeks:

(1) Increased total HDL-Cholesterol 18% and the improvements were in vast increases of the regression subspecies HDL-2 of 50%

(2) Reduced Triglyercides by 30%

(3) Increased total LDL-Cholesterol by 13% which is a good indicator that large buoyant LDL are starting to prevail because this change is accompanied by increases in HDL-Cholesterol. An increase in LDL-C is a good thing and associated with regression when the HDL-C is increasing concomitantly. This is not the case in Metabolic Syndrome. Increasing LDL-C in MetSyn are ONLY associated with higher small dense LDL-C which translates to Pattern B (for extremely BBBBAAADD).

(4) Decreased small dense LDL (LDL-III) from 27% on the low fat diet to 18% on high saturated fat. Not bad. The TYP is goal is < 10-30%. For our TYP members who restrict dietary carbohydrates (eg, grains, fruit/berries, etc) and add significant amounts of saturated fat, in 4-6wks they observe basically eradication of small dense LDL to ZERO. These members may have struggled with dense LDL of even 70-80% for years.

(5) Decrease in the deadliest, smallest LDL (LDL-IV) from 6.0% to 3.4% with high saturated fat intakes.




Longevity: Small Dense LDL and HDL-2
We learn so many lessons from the regression trials with niacin, vitamin D (Dr. Davis publication, CKD hemodialysis patients HERE) and the omega-3 trials. The longevity observations in centenarians fascinate me to no end. I enjoy reading them since they conceptualize the same principal components that Krauss, Superko, Callister, Davis and other forward-thinking, visionary cardiologists and physicians advocate for heart health:
(a) achieve low small dense LDL
(b) bank on high HDL-2

The centenarian study that we reviewed earlier HERE is worth another mention at this time (Unique lipoprotein phenotype and genotype associated with exceptional longevity. Barzilai N et al. JAMA. 2003 Oct 15;290(15):2030-40.).




Centenarians Exhibit Pattern 'A+' With sd-LDL << 10%

The Ashkenazi Jewish study compared centenarians, their offspring and population controls (both short-living Ashkenzi Jewish as well as Framingham). Corollaries exist between the long-living (probrand) centenarians and the CAD regression pattern in the trials that we have reviewed here. The long-living typically have resistance against hypertension, diabetes, cancer and coronary artery disease. Uncannily, these centenarians have Pattern A and an extremely low percentage of small dense LDL subparticles, not unlike our Paleo (low carb, high fat) friends and Paleo/ TYP members who achieve all of Dr. Davis TYP goals.



Figure 1. Frequency Distribution of Lipoprotein Properties in Female Probands, Offspring, and Controls. The frequency distribution of plasma high-density lipoprotein (HDL) oncentration levels and particle sizes, and low-density lipoprotein (LDL) particle sizes in female probands, their offspring, and an Ashkenazi control population. [To convert HDL oncentration to mmol/L, multiply by 0.0259. The solid lines represent the mean and the dotted lines represent 1 SD of control.]


What strikes me is that the centenarians (probrands) exhibit generous quantities of large buoyant LDL (60-70+%), only < 10% sd-LDL, Pattern 'A' lipoproteins and an inordinate amount of large-sized HDL-2. Even with modern eating (refined processed foods), their children also similarly exhibit a prevalence of high HDL-2 and high buoyant LDLs. Like good wine, the centenarians' HDL-2 and buoyant LDL appear to have gotten better with age!



Maximize Genetic Expression
Burst your genetic ceilings and boundaries! With the appropriate diet low in carbohydrates, wheat/gluten-free, containing sufficient saturated fatty acids, we can achieve similar longevity-associated lipoproteins. Many are doing it and it's not that hard. Clinical studies support the validity of the benefits of high-saturated fat diets for achieving regression, shifting to Pattern ' A ', controlling small dense LDL, and raising HDL-2.

Palmitic Acid+ CARBS = Mouse Skeletal Muscle IR

Peter at Hyperlipid and Stephan at Whole Health have dispelled yet again myths regarding the indictment of the 16:0 long-chained saturated fatty acid Palmitic Acid as the prime instigator of insulin resistance (IR). Researchers are always wrong -- it's... HIGH CARBS PLUS Palmitic acid.

Their brilliant posts discuss below:
--Sportzaid (FRUCTOSE) + Palmitate = IR RETARDNESS
--High Carb Lab Chow + Palmitate = IR in the brain

Yes. Such inferences applied to low carbers (LCers) is pure ridiculousness. Non-applicable.

Low/no carb + Palmitic Acid = GOOD THING. All the low-carb/high saturated fat (palmitic acid) and ketosis trials by Hays JH, Volek JS, and Krauss RM have shown reductions in blood insulin, blood glucoses (BG) and peripheral tissue insulin resistance (IR). Directly contrary to the high carb animal or human studies.



Palmitic Acid (16:0 SFA)

Palmitic acid has a special evolutionary, adaptive role in mammalian metabolism. Stephan showed that it likely 'fills in' when blood glucose starts to decline.

G E N I U S ! !

Our mammalian *sses are full of palmitic acid. We release palmitic acid into our blood streams during b*tt-burning long low-intensity cardio, physical exercise, ketosis, starvation, and intermittent fasting.

What is the most important organ in the body? (Some males may argue otherwise. Hey, get your mind outta the gutter for a second -- and I apologize gentlereader if the last post had anything to do with it.) The organ of the most vital importance is understandably controversial but in reading Stephan's post and given that he is a neurobiologist, let's say for a moment... it's the B R A I N. The brain like other vital organs (nerves, retina, kidneys) have unregulated glucose access because glucose is the valued currency of energy. Few GLUT transporters (or none) exist in these tissues. Whatever is in the bloodstream, is in the tissue. These also are the first organs to be damaged by high, unremitting, toxic blood glucose concentrations. We tell individuals with diabetes on hypoglycemic medications, if the BG goes below 60 g/dl, they are in a lot of trouble. Consciousness, rational thoughts, driving (yes, DUIs can be cited), physical movements SHUT DOWN. Comas occur at below BG 40 g/dl, including fatal ones. Of course this rarely happens to those not taking pharmaceuticals because the liver and other tissues have the ability to make ANYTHING into glucose. Protein, fatty acids, glycogen via gluconeogenesis turns into blood glucose for the brain and other vital tissues (eyes, kidneys/adrenals, peripheral/central nervous system). So after a good 8-hour sleep, your blood glucose continues churning on at 70s-83 g/dl (non-diabetic, normal range) when the sun glows on your happy shining face every morning.

When protein, carbs and fat (eg, FOOD) become scarce, by default, ketones become the currency of brain-energy. Our brains are hard-wired to run well on two different types of fuel depending on the energy 'environment'. Ketones can be generated from ANYTHING with prefential production from fatty acids. Proteins from muscles are protected as long as possible. Muscle-wasting was NOT an evolutionary advantage for survival. This is why with intermittent fasting, I rarely notice any degradation of my hard-earned HIIT, Crossfit and jogging muscles! Atrophy occurs when I sit on my b*tt all day.




IR at the Skeletal Muscle Level

From the skeletal muscle point of view, a bunch of the same inaccurate inferences have been made by researchers de Wilde et al (Physiol Genomics. 2008 Feb 19;32(3):360-9. Free PDF HERE). They looked at the induction of genes and glucose/insulin levels in mice on high-HIGH-carb, 10%-Palmitate v. HIGH-carb, 45%-Palmitate diets in skeletal muscle. Mice were sacrificed at Day 3 v. Day 28 and their quadricep genetic and fatty acid profiles were compared (quads are a mixture of Type 1 Slow and predominant Type II Fast twitch muscles). At the skeletal muscle level, with both diets, both glucose and insulin increased over time. The researchers have concluded that insulin resistance has occurred to a higher extent however in the high-fat group. This makes sense if evolution-wise, little carbs existed and Paleo man intermittently hunted and ate gamey-meat. In this experiment, high carbs enter into the picture and sets off another metabolic pathway. Insulin (?and IR) appears to have spiked exponentially in the high-fat +carb group; blood glucose actually declined by Day 28 in this group.









Bizarre Love Triangle

In nature, paleotologically speaking, 3 things never rarely occurred together at one time as they do in research trials such as the ones that Stephan, Peter or the one highlighted here.

These are indeed BIZARRO COMBINATIONS:
--high carb + high SFA ('large kill') + no omega-3 DHA
--high carb + low SFA ('small kill')+ no omega-3 DHA
--high carb + no SFA (no kill) + no omega-3 DHA

Palmitic acid is always consumed with DHA if one is eating grassfed meat/fowl or wild seafood. Or if I ate these study mice. :) J/k. And . . . in a 'paleo' environment... with scarce dietary carbohydrates.

So paleolithically speaking, high carb was not an environmental norm and therefore no genetic norm was ever established. Studies show human metabolic machinery is mainly set up for intermittent/daily consumption of fats and proteins (Huss, Kelly. Circ Res. 2004). However... the machinery for carbs does exist and for survival, these ancestral pathways seem to override and take precedence above all else. The ability to store fat for the purpose of reproduction, growth, and surviving harsh winters may have been key in determining that genetic material would be passed along in certain geographic niches. Anabolism of adipose is the metabolic pathway chosen when environmental 'carbohydrates' became readily available, eg fruit harvest at the end of summer (+/- big game 'kills'). Ingested carbs become post-prandial triglycerides, then small LDL and oxLDL, then into adipose eventually. Dr. T discusses a role for small LDL in evolutionary terms. It makes sense. Some research suggests a role for small LDL in delivering triglyerides to non-LDL-receptor sites perhaps for the same reason ultimately, fat storage for winter, a winter that never comes.

You can see inherently in mice (despite eating lab chow), in the muscle fat breakdown of the experimental mice -- DHA is about 10% of the total fatty acids in the quad muscles. Palmitic about 25-30%. DHA is an omega-3 PUFA associated with longevity and reduced cancer and coronary artery disease. Consuming more saturated fat and less carbohydrates, these mice had a noticable increase in DHA content and lower content of toxic omega-6 in their muscle-meat in the high-palmitate group (see below).



High-carb scenarios did not exist as humans evolved over 200,000 years.
-- Fruit didn't grow on acres of groves. Honey and ripe fruit were available for only a very short weeks at the end of summer.
-- Tubers, potatoes and yams didn't grow in 50 lb bushels at Costco
-- Grains and legumes were pre-ag


High carb actually has little bearing for those who are LC and semi-Paleo. After a 'kill', Paleo man was glycogen-depleted and running on ketones (if not already earlier). His BGs had already flat-lined at 70-80s g/dl for who knows how many days the tribe had been tracking and following herds of game. Gluconeogenesis and ketotic processes were in full force to keep Slow twitch Type I fibers on the go (walking muscles Gastronemius/ Gluts, Heart, lower back Trapezius, Psoas ('filet mignon' like other dark meats). Below table courtesy of Drobson. Type I Slow Twitch muscles require less glycogen (stored carbohydrates) than Fast Twitch. Conversion to Type I Slow Twitch musculature makes some evolutionary sense to prepare for certain physical tasks and energy demands when one considers the nature of how food was scarce and how it was intermittently obtained (hunting v. foraging v. fishing).







Insulin Resistance Increases with HIGH CARBS

Naturally IR increases with HIGHER Palmitic Acid/HIGH-carb digestion MORE than with the high-HIGH-carb, lower Palmitic Acid mouse diet. The mouse metabolic system was utterly CONFUSED -- two energetic systems were switched on concurrently:
(1) HIGH CARB/ Metabolic Syndrome (MetSyn), related to fat storage
(2) HIGH Palmitic Acid/Ketotic Efficiency, related to fat burning


Dr. T talks about MetSyn as 'evolutionary suicide' in some recent wonderful, concise and explicit posts (Part I and Part II). PPAR-gamma, the nuclear steroid involved with carbohydrate metabolism and energy balance, are normally whacked out and completely degraded in those with obesity and diabetes. In these mice, on the other hand, both groups exhibit expression of PPAR-gamma. This is not expected. Both 10% and 45% saturated Palmitate did it. (that's because Palmitate like omega-3 EPA DHA are agonists and activate the PPARs gamma and delta).

In fact, PPAR-gamma is turned ON in similar fashions with diabetic drugs (Avandia Actos which are PPAR-agonists), life-extending Resveratrol, ketosis, niacin and omega-3 PUFAs (fish oil EPA DHA). How PPAR-gamma is related are in prior animal pharm posts HERE.













Authors Conclusions Are Correct Except...

The authors are in fact correct -- insulin resistance occurs as Stephan and Peter agree as well and it is a good thing under certain circumstances. Low carb. Under high carb circumstances, it appears that MetSyn consequences are unavoidable and perhaps even hastened by Palmitic acid (perhaps via two ancient metabolic pathways both being induced simultaneously). When food sources are low and we need to continue walking/moving/hunting/foraging/carrying carcasses etc, we want to turn on the ox phos in the Type I slow twitch muscles as these authors discovered so that we can obtain more ATP which requires phosphorylation. We want morphogenesis -- change more muscles to Type 1 slow twitch as we are going to keep physically exerting ourselves after consuming a nice tasty high fat/protein-containing meal or in preparation for the next physical demand. If carbs are very scarce, we want some insulin resistance to continue to shunt any available glucose to the brain and eyes and nerve endings to the ears to see/listen for predators. We want decreased protein and carb catabolism (save all the stores in the muscles). We want increased fat catabolism.

Repeat... increased fatty acid (FA) catabolism. Easy release of the palmitate OFF of our cheeky b*tts.

They are CORRECT in the genetic analysis... Except... The authors surmise (see above Figure 3) that the entry of saturated fats like palmitate into the cellular membranes is associated with poor benefits including reduction in detox and immune function. How did they get that?!? They also extrapolated to the membranes of mitochondria. I think that these researchers have failed to take into account that again humans never consumed palmitate alone, always with omega-3 PUFAs DHA and EPA, and paleolithically always low carb. Palmitate and n-3 PUFAs balance the fatty acids and cholesterol of the cell membranes, providing structure and rigidity and important hormone signalling (see Hulbert below). The authors appear to also have forgotten or failed to reconcile the evidence for Palmitic acid in IMPROVING immune function (see last 2 citations below). Additionally the authors fail to recognize the role of high dietary carbohydrates, its downstream increase of LA omega-6 content in muscles, high dietary omega-6 intake or the role of dietary omega-3 PUFA deficiencies in instigating Metabolic Syndrome.

• The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension.
  Tran LT, Yuen VG, McNeill JH.
  Mol Cell Biochem. 2009 Jun 18.
• High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation.
  Rayssiguier Y, Gueux E, Nowacki W, Rock E, Mazur A.
  Magnes Res. 2006 Dec;19(4):237-43.
• Temporal changes in dietary fats: role of n-6 polyunsaturated fatty acids in excessive adipose tissue development and relationship to obesity.
  Ailhaud G, Massiera F, Weill P, Legrand P, Alessandri JM, Guesnet P.
  Prog Lipid Res. 2006 May;45(3):203-36.
• Omega-3 and omega-6 fatty acids in the insulin resistance syndrome. Lipid and lipoprotein metabolism and atherosclerosis. Rustan AC, Nenseter MS, Drevon CA. Ann N Y Acad Sci. 1997 Sep 20;827:310-26.
• An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?
  Ailhaud G, Guesnet P, Cunnane SC.
  Br J Nutr. 2008 Sep;100(3):461-70.
• Dietary fats and membrane function: implications for metabolism and disease.
  Hulbert AJ, Turner N, Storlien LH, Else PL.
  Biol Rev Camb Philos Soc. 2005 Feb;80(1):155-69.
• Membrane fatty acids as pacemakers of animal metabolism.
  Hulbert AJ.
  Lipids. 2007 Sep;42(9):811-9.
• Effects [beneficial] of palm oil on cardiovascular risk.
  Chong YH, Ng TK.
  Med J Malaysia. 1991 Mar;46(1):41-50.
• Dietary palmitic acid influences LDL-mediated lymphocyte proliferation differently to other mono- and polyunsaturated fatty acids in rats.
  Tinahones FJ, Gómez-Zumaquero JM, Monzón A, Rojo-Martínez G, Pareja A, Morcillo S, Cardona F, Olveira G, Soriguer F.
  Diabetes Nutr Metab. 2004 Oct;17(5):250-8.
• Dietary palmitic acid modulates intestinal re-growth after massive small bowel resection in a rat.
  Sukhotnik I, Hayari L, Bashenko Y, Chemodanov E, Mogilner J, Shamir R, Bar Yosef F, Shaoul R, Coran AG.
  Pediatr Surg Int. 2008 Dec;24(12):1313-21.

Benefits of High-Saturated Fat Diets (Part V): The Traditional Okinawans

Goya Chanpuru dish courtesy of TastyIsland

According to Dr. Willcox, Principal Investor for the Okinawa Centenarian Study that started in 1975, "Among the entire population, which takes a sparing approach to food, there is 90 percent less coronary artery disease than in the wider world, a third less incidence of cancer, and breast cancer is virtually unheard of." HERE. In long-living Okinawan and Japanese, their dietary intake as surveyed in the 1970s was higher in both protein and dietary saturated fatty acids (see below abstract) compared to their shorter-lived peers at that time. When Okinawans move away (like to Brazil) heart disease risk factors appear (see last abstract). Diet is 80-90% of our health I believe because our bodies are designed to express what is dictated by our environment and food macro- micronutrients (foraging/hunting v. lounging; fecundity v. fasting). (These are the PPAR alpha gamma and delta receptors; their role is to 'sense nutrients' and to 'sense energy demand' in order to ultimately balance our energy needs). To me, the observations from blue zones and centenarian data always seem to reinforce that the physically active, low carb mod-high fat Paleo/TYP approach is the most optimal at this time, as it was for centenarians studied in the 1970s.


Protein and Fats?

Dietary Protein and Fatty Acids activate PPAR alpha gamma delta. (Like drugs but no adverse effects and gosh so yummy...)
(a) PPAR Delta: Omega-3 PUFAs, Fish Oil, Grassfed Beef
(b) PPAR Delta: Dagger in the Heart of CAD
(c) PPAR Delta: Prevent Sarcopenia, Poverty of the Flesh
(d) PPAR Delta: Saturated Fatty Acids Are Anti-Atherogenic


Okinawan culture not only embraces one of the most heart-healthy diets (high seafood, animal meat, milk, eggs, saturated fats, high minerals and low carb) but also a very physically active lifestyle. Additionally, like other long-living societies, they display a distinct community spirit and lifestyle that values every members' contributions including elders, daily prayer, frequent festivals honoring ancestral spirits, playing/dancing (Bali, Polynesian style) regularly, exercising/tai chi together, working diligently until the day they pass away, hot baths (sweat out toxins) daily, avid music listening, folkmusic singing, instrument playing (sanshin) and is tied around all generations of extended families yet promotes self-sufficiency and self-reliance. Traditional Okinawan livelihoods and common activities are still farming, fishing and gardening.


Internet? I am not sure if it would be embraced by these happy, busy, peaceful inhabitants of this subtropical semi-Paleo-fantasy island... They are too busy LIVING. *ahaa*



Carbohydrate intake (less than mainland Japan, ALL GLUTEN-LESS):
--sweet potato
--rice
--mochi (sticky rice dessert)
--buckwheat noodles
--raw goat milk (alkaline, more similar casein profile to human milk)




Here are some 'secret' foods from this ancient society:
--goya (twice the vitamin C as citrus) Okinawan version of Chinese bitter melon known to lower blood glucoses and inflammation; the above pictured dish goya chanpuru is a staple (goya, eggs, pork, lard, bonita shaved taurine/fish)
--nigari (more Magnesium and Calcium than trad'l tofu)
--sweet potatoes (anti-inflammatory, rich in carotenoids and hormone precursors)
--fish fish fish seafood seafood seafood (taurine, iodine, omega-3s, carotenoids, krill oil, astaxanthin)
--goat meat: stewed, stir fried
--raw goat sashimi which is considered a delicacy (taurine, omega-3s, CLA, and other muscle building/fat-burning fatty acids)
--raw goat milk (plant sterols, short and medium-chain saturated fatty acids, CLA)
--LARD LARD LARD (anti-inflammatory, lowers sdLDL-particles and %-sdLDL, increases particle buoyancy like other saturated fatty acids like lauric acid)
--BOAR PORK BOAR PORK BOAR PORK (pork belly, stews, stock, etc)
--miso (centenarian Okinawans have ME-SO-PRETTY skin and coronary arteries! ..."source of vitamin E, saponin, isoflavones, lecithin, choline, and dietary fiber from soybeans; vitamin B2 from koji mold; and vitamin B12 from lactic or propionic acid bacteria" ...fermented foods and probiotics that promote longevity are staples Japanese food)
--fermented fish sauce (source of vitamins B12, K2, MKs) Ishiru/squid, Ishiru/sardine, Shozzuru (pickled juices of mackerel-sardines-anchovies)--red tofu (fermented source of vitamin K2 MKs)
--seaweed (iodine, marine minerals and antioxidants like FUCOIDAN/ fucoxanthin)

Nutrition for the Japanese elderly.
Shibata H et al Nutr Health. 1992;8(2-3):165-75.

The present paper examines the relationship of nutritional status to further life expectancy and health status in the Japanese elderly based on 3 epidemiological studies.

1. Nutrient intakes in 94 Japanese centenarians investigated between 1972 and 1973 showed a higher proportion of ANIMAL PROTEIN to total proteins than in contemporary average Japanese.

2. High intakes of MILK and FATS and OILS had favorable effects on 10-year (1976-1986) survivorship in 422 urban residents aged 69-71. The survivors revealed a longitudinal INCREASE in intakes of ANIMAL foods such as EGGS, MILK, FISH and MEAT over the 10 years.

3. Nutrient intakes were compared, based on 24-hour dietary records, between a sample from OKINAWA Prefecture where life expectancies at birth and 65 were the LONGEST in Japan, and a sample from Akita Prefecture where the life expectancies were much shorter. Intakes of Ca, Fe, vitamins A, B1, B2, C, and the proportion of energy from PROTEINS and FATS were SIGNIFICANTLY HIGHER in the former than in the latter. Intakes of CARBOHYDRATES and NaCl were LOWER.

PMID: 1407826

Impact of diet on the cardiovascular risk profile of Japanese immigrants living in Brazil: contributions of World Health Organization CARDIAC and MONALISA studies.
Moriguchi EH et al. Clin Exp Pharmacol Physiol. 2004 Dec;31 Suppl 2:S5-7.

1. Japanese immigrants from Okinawa living in Brazil have a higher mortality from cardiovascular diseases and have their mean life expectancy shortened compared with their counterparts living in Japan.

2. A cross-sectional study comparing Okinawans living in Okinawa (OO) and Okinawan immigrants living in Brazil (OB) was designed to characterize the dietary factors that could interfere with the profile of cardiovascular risk factors and with this reduction on the life expectancy when Okinawans emigrate to Brazil.

3. In total, 234 OO and 160 OB (aged 45-59 years) were recruited to the present study to undergo medical and dietary history, blood pressure measurement, electrocardiograph (ECG), blood tests and 24 h food/urine collection.

4. In the present study, OO subjects presented with 37% less obesity and 50% less systemic hypertension than OB. The OB subjects used threefold more antihypertensive medication than OO. Meat intake was 34% higher in OB than OO, whereas fish intake was sevenfold higher in OO than OB. Serum potassium levels were 10% higher in OO than OB. Urinary TAURINE (an index of seafood intake) was 43% HIGHER in OO than OB. Urinary isoflavones (an index of the intake of soy products) were significantly lower in OB than in OO. Of (OMEGA-3 PUFAs) acid (20:5) and docosahexaenoic acid (22:6) were TWO- TO THREE-FOLD HIGHER in OO than OB, respectively.

5. The rate of ischaemic ECG changes in OO subjects was only 50% of that of OB subjects.

6. There were no differences in the smoking rate between OO and OB subjects.

7. The results of the present study suggest that coronary risk factors and cardiovascular health are not only regulated by genetic factors, but that the impact of LIFESTYLE (MAINLY DIET) can be large enough to modulate the EXPRESSION OF GENES.

PMID: 18254187



The Food of Paradise: Exploring Hawaii's Culinary Heritage

By Rachel Laudan (Kolowalu Books, 1996) HERE






Read more about Okinawan food, culture and lifestyles:

Diary of Local Okinawan TASTY Dishes *YUMM* Goat sashimi, boiled testicles with miso and vinegar, slow cooked stews (fatty pork), goya chanpuru
Children of Heaven Interview: Live SLOW Live LONG
Okinawan 'Lard' Recipes *ahhhha*
The Way of ChoJu: Consuming Longevity in a Rural Japanese Village (Masters Thesis by J. Busch)
Mashed Okinawan Purple Sweet Potato Recipe (americanized)
Goat Meat and Milk Productivity in Subtropical Okinawa for last 80-130+ years
Goat Meat and Pig Rearing in Okinawa Prefecture
Traditional Yagi (Goat) Dishes and changes in modern Okinawan youth -- Yagi-jiru Goat soup, stir-fried goat, raw yagi-sashi goat sashimi, etc
Raw Grassfed Goat Milk in an Okinawa Study Tolerated due to different type of non-allergenic beta-A2 casein and better saturated fatty acid profile (butyric, propionic, lauric, caprylic, etc)
Okinawan Goat Milk
Traditional Japanese Condiments: shoyu, miso, ishiru, preparations
Truth About Saturated Fats by M. Enig and S. Fallon: "In Okinawa, where the average life span for women is 84 years—longer than in Japan—the inhabitants eat generous amounts of pork and seafood and do all their cooking in LARD (Franklyn D, Health, September 1996, 57-63 .)" This is not apparently the case currently... as canola and other refined omega-6 oils which oxidize super rapidly increased to predominant use after the 1980-90's; canola is not great but less omega-6 compared with corn, soybean, safflower, sunflower, cottonseed, grapeseed, or peanut oils.
Okinawa Centenarian Study and Genetics
Ex-Pats in Okinawa and Crossfit Asia/Okinawa
Bizarre Food's Andrew Zimmern checks out: traditional Okinawan sea snake soup, raw goat ball and testicles, yako-gai (giant sea snail), squid ink soup, and giant tuna eyeballs, stewed in mirin, garlic, ginger, and brown sugar
"Blue Zone Okinawans formed moais to support each other in good times and bad" HHhmmmmm.... sounds like... our TYP forum? our Paleo blogoshere? our Xfit gym networks?
Goat's Milk, Blue Zones and Longevity: "Goat's milk - 80 percent of all people over 90 have consumed goat’s milk many times per week throughout their life. It is rich in blood-pressure lowering tryptophan and antibacterial compounds."
Blue Zone concordance: Ikaria, Greece similar to Okinawa, Japan in lifestyles, hot baths (?Magnesium, Iodine), raw goat milk consumption, wild greens, tea-drinking, relaxing, embracing community and family closely, etc