Tuesday, June 9, 2009

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


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

The NEW Track Your Plaque Diet:
Part 3 Special Issues

-- Lp(a)
-- Apo E
-- Diabetes
-- Pre-diabetes
-- Metabolic Syndrome (MetSyn)


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

[Edit: I don't agree with Davis' remaining 'edicts' because they do not appear to work and raise inflammation per clinical trials... =< 200mg cholesterol per day, =< 20 grams saturated fat per day and 15+% omega-6 vegetable PUFAs daily and LDL =< 60 mg/dl]


The Track Your Plaque Basic Diet Principles

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



Regression or Stabilization

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

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

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

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

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

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

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



So...Easy. To gain control.

Choose any 3.



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

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

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

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

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


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

7) control of inflammation (unfortunately few 'markers' to TRACK):
  • dietary (avoidance of gluten, food allergens, casein, etc; adequate ADE K1 K2 MK4-9 vit C B-vits the right ones and minerals Iodine Mg Zn Se, fiber (if tolerated), saturated fatty acids, CLA, GLA, cholesterol, CoQ10/quinones, plant sterols (esp stigmasterol), etc)
  • environmental (stay away from plastics/bisphenols/ heavy metal exposure/ pollution/ pesticides, etc)
  • mental /psychosocial (stress, excessive physical training, etc)
  • hormonal (optimization of thyroid, vit ADEK1K2, omega-3, SFAs, E T P DHEA preg, insulin, cortisol, melatonin, etc)
  • pharmaceutical/xenobiotic (adequate intake of antioxidants/ omega-3/ phytochemicals/ FOOD to thwart toxins; avoidance of synthetic hormones, certain drugs (excessive statins), synthetic vitamins (eg, Lurotin, D2/Ergocalciferol, etc), omega-6-PUFA seed/legume oils, etc))




Original TYP Goals for Regression: 60-60-60

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

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

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




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

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

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

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

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

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

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








Healthy Centenarians Attain ~4 of 7 TYP Goals

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

See picture (top)

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

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

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

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

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


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


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



Polymorphism in CETP Gene and Phenotype of Exceptional Longevity

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

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

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


Previous animal pharm posts:

13 comments:

Calvin said...

Hi Dr "incognito" BG,

Without question, your blog has not only with the most current, right on the mark, health and fitness info on the web, but also your witty-sassy-spunky-style is always pure delight to read. That said, this health and fitness guy thinks your awesome!

Best wishes,

Calvin

Peter said...

Nice posts G, getting these refs tied together is excellent...

Peter

Dr. B G said...

Peter,

I learn from the best... generous, brilliant, critical THINCers... *smile*

Thanks!
G

Dr. B G said...

Hi Calvin,

SWEET! *ahaa* Yoga-MovNat brawn, beaut, evolved brain... ur positive comments are always welcome here! Flattery... HHhMm...

-G

Kiwi said...

"control of inflammation (unfortunately few 'markers' to TRACK)"
What about CRP?

Is Niacin in the pot (not mentioned in part II?)

Is K2 supplemented or just dietary?

Many thanks :)

Kiwi said...

"Original TYP Goals for Regression: 60-60-60

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

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

Ah-Ha!
Are you a heretic or is that an "official" TYP policy change?

Dr. B G said...

Hey Kiwi,

CRP -- HEYYYUGELY irrelevant unless chronically elevated (secondary to high carbs, gluten/autoimmunity, lack of omega-3/vit D, excess omega-6 PUFAs, exercise deficiency, etc) BTW oral contraceptives and any synthetic hormones RAISE CRP

Niacin -- I still love niacin! It is exercise in a pill. It's also ketosis and intermittent fasting in a 'pill' form! I metnioned 'B-vits'; niacin is vitamin B3

Vitamin K2 -- MK4 to MK9s (the longer-chained, the better... like omega-3 PUFAs and carotenoids) -- are fantastic. They are found in organ meats, offal and muscle meats and dairy and fermented stuff. FOOD is good and if one isn't assured and confident, then supplementation is not a bad thing. Two wks ago I started sourcing my K2 from (not bad tasting) cinnamon-tingle-flavored fermented CLO from greenpastures.org! My gums have never felt BETTER (as I have a rotting crown that I'm waiting for insurance *urrrg* to replace).

THANKS for your comments,
G

Dr. B G said...

Kiwi!

R u being an incidiary?

I am surely SOMETHING.

-G

David said...

This is not a healthy diet. Eating a diet high in saturated fat will cause many diseases. Animal flesh takes much longer to be digested than natural plant foods. Sugars and carbohydrates in fruits are completely natural and it is absurd to think you should put a limit on them. They are without question the healthiest foods available. If you want vibrant health then look up a raw vegan diet.

David said...

Eating a diet high in meat will cause the body to become very acidic. Eating a diet high in fruits will promotes alkaline.

Dr. B G said...

I believe your vegan diet is making you B12 deficient, and thus explains why your comment sounds demented to me and unfounded by the heavy weight of omnivore evidence. Add'lly the vegan/vegetarian diet is responsible for RAMPANT heart disease and demented people where vegetarianism is 'popular'.

Ann Nutr Metab. 2006;50(6):485-91.

B-vitamin status and concentrations of homocysteine in Austrian omnivores, vegetarians and vegans.Majchrzak D, Singer I,et al.

BACKGROUND: A vegetarian diet is considered to promote health and longevity and reduce the risk of cardiovascular diseases and cancer. However, a vegetarian diet may be deficient in some nutrients. Exclusion of animal products in vegetarian diets may affect the status of certain B-vitamins, and further cause the rise of plasma homocysteine concentration. OBJECTIVE: The nutritional status of various B-vitamins (B(1), B(2), B(6), B(12), folic acid) and the concentration of homocysteine in blood plasma of omnivores (n = 40), vegetarians (n = 36) and vegans (n = 42) in Austria was evaluated. METHODS: The evaluation was done using the functional parameters erythrocyte transketolase (ETK), glutathione reductase (EGR) and glutamic oxaloacetic transaminase (EGOT) activation coefficients. Enzyme activity was measured photometrically. The quantity of vitamins B(1), B(2) and B(6) in urine and the concentrations of vitamin B(6) and homocysteine in plasma were determined by HPLC methods with fluorescence detection. Plasma concentration of vitamin B(12) and folic acid were measured with radioimmunoassay. RESULTS: Most of the subjects showed a satisfying vitamin B(1) status. Vegans presented a significantly lower mean plasma vitamin B(12) concentration than omnivores and vegetarians and deficiency in 2.4% of the volunteers but the highest mean value of plasma folate among the investigated groups. A deficient status of folate was found in 18% of omnivores and in approximately 10% of vegans and vegetarians. The status of riboflavin is considered to be deficient in about 10% of omnivores and vegetarians and in over 30% of vegans. According to the activation coefficient of GOT, approximately one third of all subjects showed vitamin B(6) deficiency. Elevated homocysteine concentration in plasma was observed in 66% of the vegans and about 45-50% of the omnivores and vegetarians. Vegan subjects had significantly higher mean plasma homocysteine levels than omnivores. CONCLUSION: Thiamin and folate need not be a problem in a well-planned vegan diet. Vitamins B(12) and B(2) may need attention in the strict vegan diet, especially regarding elevated homocysteine levels in plasma. Pyridoxine status appeared to be independent of the diet.

PMID: 16988496

Dr. B G said...

Ann Nutr Metab. 2005 Nov-Dec;49(6):366-72.

German vegan study: diet, life-style factors, and cardiovascular risk profile. Waldmann A, et al.

BACKGROUND/AIM: Evaluation of cardiovascular risk profile in 154 German vegans. METHODS: Cross-sectional study, Germany. Study instruments: 2 FFQ, 2 questionnaires, analyses of fasting venous blood samples. RESULTS: The total study population had a low BMI (mean: 22.3 kg/m(2)), a moderate blood pressure (mean: 120/75 mm Hg), an extremely low consumption of alcohol (mean: 0.77 g/day) and 96.8% were nonsmokers. Moderate physical activity (PAL) was reported by nearly 50%, whereas 22.7% declared to have a high PAL (>3 h/week). Median triacylglycerol (TG) was 0.81 mmol/l, total cholesterol (TC) was 4.33 mmol/l, HDL was 1.34 mmol/l. The mean TC/HDL-ratio was 3.3. Lipoprotein(a) (Lp(a)) was 8.13 mg/dl, concentrations of >30 mg/dl were prevalent in 25% of the participants. In general, status of folate and pyridoxine were sufficient, while 49.7% showed cobalamin concentrations <150 pmol/l. Plasma homocysteine levels were slightly elevated (median: 12.5 micromol/l). Cobalamin concentration and duration of vegan nutrition were the main determinants of homocysteine in the total study population. CONCLUSION: Although TC and LDL concentrations were favorable [low LDL; translation: all small and dense like your comment], low HDL and elevated homocysteine and Lp(a) concentrations were unfavorable. Overall, these results confirm the notion that a vegan diet is deficient in vitamin B(12), which may have an unfavorable effect on CHD risk.

PMID: 16219987

russ said...

very informative articles thanks it leaves food for thought http://diets.netai.net