Sunday, September 27, 2009

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.

15 comments:

Adam Wilk said...

Dr. B G,
Again, informative, hope-giving, and just plain awesome posting!
Question(s) for you: 1) I busted out my jar of delicious, organic virgin coconut oil after reading your post this morning and took a tablespoon along with my usual tablespoon of Carlson's Fish Oil (thank G@d for the lemon-flavor!!)
You don't see any problems with someone taking both oils at the same time, do you? Just want to be sure...and 2) I'd like your permission to go slightly off subject--I'd love to pose a "what would you do" question not only to you, but to the obviously knowledgeable and kind folks who read this blog--would that be okay?
Thanks, Dr. B G!
-Adam

Steve said...

Weight loss led to the conversion of pattern B to pattern A in 58% of baseline pattern B men. Among men who achieved BMIs of <25 kg/m(2) (62% of pattern B men vs. 83% of pattern A men), 81% of pattern B men converted to pattern A.

The above is from the second Krauss study you reference. The research remains equivocal: There is data that shows that restricting carbs, increasing fat can lead to particle shift, but not in all cases.
For some of the TYP members you cite(Harry for example) substantial amounts of Niacin are also taken-2.5-3.0 grams. I question what the increased sat fat is doing to those who do not shift particles.
You clearly are on to something, and as always I appreciate your views; i hope they will not contain the zealous dogmatism of the low fat crowd! Thanks, Steve

Dr. B G said...

Adam,

Go for it! Post away...

I don't recall any interactions betw coconut oil and n-3 fish oil right off hand. As long as one does not suffer from steatorrhea (fatty stools), then any increase in fats (or carbs for that matter) should be tolerated within most limits. The caveat: those without a functioning gallbladder (either surgical excised or autoimmune-disabled). These are situations where exogenous digestive enzymes are a must to aid digestion and absorption of protein, fats and complex carbs (non-starchy veggies). Several of my diabetes individuals noted actually improved glucoses after starting digestive enzymes. Those who are not quite 'low carb' notice that GERD/reflux is either completely eliminated with dig enzymes or at least dramatically improved to the point their Prilosec (or other-acid-blocker) is no longer necessary.

Great!
G

kasing12 said...

9/29/09

Dr.B,
Another excellent article. I always look forward to to your new posts, as I know they are full of Gems, and backup with unbiased well researched science behind it.
By the way I posted my new NMR results in the TYP forum recently. If you remember, after Las Vegas, and intermitent fasting, my sMLDL had gone up from 11% to 76%. Well, my latest NMR on 8/5/09, this time dropped from 76% to 20%. My Niacin remain at 1500mg for two years. So, my conclusion is the reduction in my SmLDL is most likely due to my Saturated Fats. My Sm LDL, therefore is malleable or could be modified, by the amount of Saturated Fats and Niacin and other TYP Protocol. I must have unintentionally created a ruckus, when I stated that my goal is to reduce my SmLDL to 0%. Question is is there a harm in reducing SmLDL to zero(0) percent?

http://forums.trackyourplaque.com/topics.aspx?ID=2576

I added a link to my NMR.
By the way, how about writing a book?

Thanks,
kasing12

steve said...

Well, i was going to suggest you author a book, but i was beaten to the punch!
Anyway, i am thin, and have no weight isues whatsover. Based on your thoughts i have added more eggs to the diet, eliminated fruit which was only berries, eat cheese,but not to often(don't really care for it that much, but when do is blu or parmean(real kind)). Eat grass fed beef, but actually prefer fish and Avocado daily. No sugar, no starch and will try some coconut oil and see what happens. How best to use it-add it to Whey shake? I have actually decreased those and from time to time will skip breakfast(IF). Will see how it goes.
For me at least, Niacin worked real fast: dropped my LDL particle count in half in weeks to 598, and 10% become large LDL. Take vit D3 6000, CoQ 10, magnesium as supplements, and Centrum multi w/0 iron. Also, take Carlson fish oil and ground flax and Metamuceil. Any other suggestions, and thank!
Oh, Blood Glucose is around 79 w/o Niacin; jumped to 83 with it as did liver enzymes. Since i seem to be sensitive to it(good and bad) may reintroduce it at verylow leve and see what happens. In meantime with your suggestions, am tightening up the carbs.
Would be interesting to have a dialogue with Krauss!

Dr. B G said...

Steve,

I was wondering what post your referring to... gosh I had 4 Krauss citations and none linked up to what you posted but now I know what you are referring to.

What you brought up is Krauss' latest findings:
Obesity (2009) 17 9, 1768–1775, titled 'Reversal of Small, Dense LDL Subclass Phenotype by Normalization of Adiposity.'

Are you identifying with these study participants? They are obese and therefore highly insulin resistant and/hyperinsulinemic.

This study was 'moderate-carb' which means A LOTTA CARBS and explains (to me anyway) the lack of complete 100% conversion to Pattern B.

Your fruit and berry intake... do you think this is holding up your conversion to Pattern A??

Lack of saturated fats in your diet? What percent would you estimate you get 5%? 10%? 15%?

This obese study population consumed a high-fat diet (which I can't access and get detailed info -- it's probably not completely unlike the one in this post 47% fat, 18% saturated).

Have you tried plugging in your nutri data into one of the online free sites for analysis? Many at TYP 'think' they are consuming enough fats but honestly hardly anyone is unless they are POUNDING butter, cream, cheese, coconut oil and lard leaf. We are all (incl me) just hard-wired from all the years of brain-washing and medical establishment indoctrination.

Hyman likes coconut oil -- for as well it is a 'convenient' vehicle. A wonderful thing my sis and I discovered is (I believe but not 100% certain, casein-free) grassfed butter by Purity Farms at Whole Foods and most health food stores. YYUUM YUM!

As you know Harry35 just posted here. He is POUNDING saturated fats. He cut out the AWESOME YUMMMY baked goods from his lovely wife. Yes of course the niacin doesn't hurt but you must be aware that niacin takes 24-36 months to work its 'magic'.

Diet takes only 4-8wks. As Harry appears to have shown!

The reasons for 'resistant' Pattern B is three-fold imho:
(1) fear (fear of sat fats)
(2) overstatination
(3) excessive carbs

Too much fruit which Peter refers to as 'nature's junk food.' Evolutionarily fruit only existed briefly and seasonal. Berries took a lot of time/energy to forage for.

Statins hold on to CETP activity and this has numerous adverse effects namely increasing insulin, diabetes and glucoses. Crestor is the most potent on CETP and thus is about the only statin that shows a significant increase in the diabetes incidence in the treatment arms compared with placebo. The excessive suppressive effects on CETP all increase sdLDL upon prompting (whether its niacin, olive oil, sat fat or fish oil). All the new LDL is 'forced' to be small and dense, just like the owner, unfortunately. ?? May raises blood pressures too? (maybe kinda like Torcetrapib that AWFUL, deathful drug) Anything that raises insulin and diabetes incidence, raises blood pressures. Statins PREVENT ALL large LDL from forming, unless this mechanism is 'overcome' and it appears apparently that high high sat fat/low low carb can do so (sev members were cutting back there statins and this worked very successfully; their small LDLs went to ZERO).



Hang in there -- you are getting there... I see the cogs rolling in the rust *haa* (I was there too once and I know it is HARD). As progressive as you'd like I am, my sis actually had to bring over the first bottle of coconut oil! And... a great book, which I have given fondly to friends :)

-G

Dr. B G said...

Hey Dr. K!

Thank you for the link. I looked it up and saw your RANT. *haa* I really enjoyed reading it because it was unbiased, from the medical standpoint, intelligent and accurate.

Yes -- that Vegas trip was a doozy... for the lipoproteins... I'm glad you quickly recovered and the #s are fantastic!!!! Congrats!

I'm in Dr. Davis boat that anything < 30% sd-LDL (Pattern 'A' in other words) with concomitant high HDLs will induce regression. In Vegas, I bet you were still eating saturated fats (but probably lots of nasty omega-6 too) therefore the HDL-2 did not suffer at all (actually it improved a teeny bit there). It appears in the literature that HDL-2 provides the antioxidant protection (probably via PON1) against oxidation on small dense LDL. Omega-3 fish oil and flaxseed oil and other antioxidants play a HUGE role here.

On your latest NMR the HDL-2 is 25.1 umol/L which is 350% higher than the initial. Total HDL improved from 45 to 72 mg/dl. WOWO!!! Strong work, doc! Who cares what the small LDL is!

No, niacin didn't do that. I would concur with you. It didn't hurt but not likely to have affected the #s to this degree.

OK, first let's question 'zero' small LDL. Does that really physiologically occur? If we look at the metabolism cascade for lipoproteins, no. There is a brief interchange betw large and small/medium particles. Perhaps below a threshold, NMR fails to detect small LDL? Chuckerino reported 'zero' on NMR yet on other methods small LDL were detected. Very few members do simultaneous testing and of course we have very few members IMHO with low %-sdLDL so it is difficult for me to determine. Even in the ketosis trials, it cannot be determined either since study subjects ALL invariably lose tremendous weight which makes the lipoproteins very funky transiently and uninterpretable. Longer term studies would probably show the same effects as you others have experienced (and me) on the annihilation of sdLDL. The Paleo peeps in the blogosphere don't waste their money on NMR... (we have to pay for grassfed beef *haaa*).

OK you know I have a weird mind. I think of LDL as an account. Some people have no debt, right? That is good or neutral depending on your financial background. Some people have no debt and lots of investments, or even a mix of debt and investments (I've been watching too much Poor Dad, Rich Dad infomercials my lifetime *haa*).I make analogies also to monks/nuns -- no property, no debt, yet rich in deeds.

Large LDL to me is like INVESTMENTS (or DEEDS). I think our goal should be > than a certain # because this is what longevity and centenarian studies show. Large LDL are necessary for immune upkeep, infectious disease protection, and even I believe BP and diabetes control. Same with Apo E and Lp(a). These all have functional roles in mammalian systems for precisely ID control.

Centenarian (and C. elegans/ worms) studies also teach us that low insulin is desirable and associated with extended lifespans (including low insulin post-prandially -- no CAD patient has low insulin post-prandially unless they are low carb or ketotic imho).

'A preponderance of small dense LDL is associated with specific insulin, proinsulin and the components of the insulin resistance syndrome in non-diabetic subjects.' Haffner SM,et al. Diabetologia. 1995 Nov;38(11):1328-36.

How low can we go? Well, how low can debt go? How high can good deeds/ investments go?

Personally, I don't believe there is a threshold with the caveat other metabolic parameters are not suboptimal. And... if it is done non-pharmaceutically.

Book?!? That is what my patients beg for too... Dr. Davis and Nephropal have asked... You are always right-on with your insights and I will perhaps... (someday!) I already told Mr. 'Living Dangerously' for my vigorous 70-something yo HAAAWWWT Type I that I'm naming it after him, who has inspired me teaching that we are all walking miracles... just like ALL the members at TYP!

-G

Adam Wilk said...

Dr. B G,
Thanks so much for allowing me this opportunity.

Being a pessimist (I know it's bad for me--I'm working on it) I'm always preparing for the worst, an event that may never actually happen.

The issue is control. In this scenario, I've walked into the ER on my own power, but with chest pains.

So, from my experiences with my poor father, I know an angiogram will be performed. I don't know what the blockage percentage is, but I know if an angioplasty/stent is required, the surgeon will perform it on the spot--there won't be any asking me "hey, Mr. Wilk, do you mind if I unblock this artery?" That I understand and accept.

Here's the doomsday scenario, the one where the doctor doesn't even bother doing anything but ends the procedure and I end up groggily coming out of the semi-anesthesia with a family member (let's say it's my wife) telling me "they're saying you need bypass surgery, honey."

Okay.

Now, this is where it gets tricky. Sure, they're going to try scaring the hell out of me to have this, and I'm sure my family would be pressuring me (you have to do this, or else you'll die!!)
But realize, I did walk into the ER on my own, I can probably walk out, too.

Here's my thinking--do I begin a water-only fast immediately to clear my body, whilst I begin slamming chelation suppositories? Do I run for EECP while ingesting massive doses of vitamin E, CoEnzyme Q10, vitamin D, vitamin C and L-Lysine?

Do you see what I'm thinking? The list is full of possibilities, and I wouldn't want to make a decision out of fear.

I absolutely enjoy reading your entries, because I learn quite alot about preventing this whole nightmare scenario to begin with.

But I'd love to hear (and yes, I know, this isn't medical advice that's being given, but merely opinions on the subject-I hold no one accountable!) what you and the other brilliant minds here have to say about this scenario.

You, Dr. Davis, and other pioneers are wonderful with the prevention--I'm just curious if any of this advice extends to when they have some poor soul on the table. Hmmph.

Thanks!
Adam

reinman said...

Dr. B.G.,

Great post as always. Thanks.

I began eating paleo about 7 weeks ago in an effort to improve my health and lose weight. Me:6'1", 56 yrs., 205 lb. to start and 188 now. Goal somewhere around 170. I've been using the Protein Power diet as a basic blueprint, and slightly modifying based on information I pick up along the way. I've become an avid reader of your blog, as well as Whole Health Source, Hyperlipid, PaNu, Nephropal and others. Great stuff with invaluable information, although I had to brush the cobwebs off Lehninger and Stryer and do a little reviewing before tackling some of the posts. (majored in biochem in college).

My wife and I have been eating plenty of good saturated fats. We're lucky in that we live in Montana, and great quality grass fed beef, and pastured eggs and dairy are readily available at very reasonable prices from our friends and neighbors.

My carb intake is 20-30 gm/day all from vegetables, no grains at all, and I've been supplemeting with fish oil, krill oil, vit. D,K,and A among others. Also Niacin 2 gm/day. Several months ago my Dr. put me on statins (simvastatin 20mg.). I lasted about 6 weeks- muscles aches, mental confusion, the whole works. Nasty stuff. I refused to take it any longer and my Dr., while not happy, suggested the niacin and red yeast rice, both of which I've been taking. Labs on 6/30/09: TC 270, LDL(calc.) 167, HDL 54, TG 247. Will be retested in about 6 weeks.

I think I'm on the right path here, diet wise and with what I've learned from reading all these great blogs, but I'd like to know what you think about the red yeast rice. I've seen very little discussion about it.

Additionally, any suggestions about getting my Dr. on board with all this? His attitude is that of tolerance for a misguided patient who sooner or later will see the light. For example, when I asked him about an advanced lipid profile, he turned up his nose, and said that while it my be of some academic interest, whatever the results were wouldn't alter what he'd do clinically, and that the only people really benefiting would be Berkeley Heart Lab and others who make money from the test. He's a nice guy, very sharp, but his inflexibility on this bothers me some. It would be nice to have a Dr. whose on board with this, but I guess that's pretty hard to find. Seems like the do it yourself route is the one I gotta follow.

Hope I didn't go on too long. Thanks again.

Dr. T (Nephrologist) said...

I love coconut oil. But what about raw cacao nibs? I good source of fat with a high antioxidant amount. I put them in my salads to give a nice crunchy texture.

Dr. B G said...

Hey Dr. T!

Mmmmhh... cocao nibs in salad!! You are so creative as usual :) That sounds truly wonderful!!

I've read about the fiber and flavonoids but don't know beyond that. Some of the highest flavonoid dark chocolate lowers blood pressure so they appear to good anti-inflammatories. They make me HIGH. *haaa*

-G

Dr. B G said...

reinman,

Congrats!! WOW -- 17lbs loss in only 7 wks! I hope you posted at Mark's site to let him know. I think he LOVES stories like yours!! Keep up the strong work.

You know the labs get funky after tremendous wt loss. The best labs are after wt stabilizes for a while. Don't worry -- it's a weird, benign (as far as I know from Dr. Davis' experience and what I've observed), totally transient occurence.

"Labs on 6/30/09: TC 270, LDL(calc.) 167, HDL 54, TG 247. "

I find that any doctor who is willing to be openminded is worth their weight in gold in this day and age. The good ones work hard and they try to look out for the patient's best interest with their current knowledge. How about trying to increase their knowledge? Most of the articles I post I believe are free PDFs which you could certainly print off for them. They may not be used to self-education since most of the mandatory continuing eds for MDs is kinda spoon-fed at this point by Pharma.

OK I'll give you some of my 'lipid luminations' *haaa*

If everything was stable, I'd probably be concerned about the extremely high Trigs and small LDL (which go along with high Trigs). Since this lab was shortly done after significant wt loss, I'd consider just letting it go.

On niacin, don't forget to have the uric acid, CPK and fructosamine checked. Fructosamine is a 2-wk sugar average. If you are having glucose excursions, it will show up. I aim for non-diabetic norms like < 180-200. On rare occasions, niacin may raise blood glucoses but I find this only occurs in those still consuming too much carbs or fruit (even one fruit daily is WAY WAY too much).

Montana BEEF and bison is the BEST. Had some bloody rare delicious bison at Yellowstone this past summer!! OH WOWOWOW. You and your wife are so lucky!

-G

Dr. B G said...

Hey Adam!

Please feel free to vent it all out!!! What you are describing is absolutely normal fear of the known (your father's) and unknown (yours). It's not irrational at all. You must talk to other people, survivors, sons like yourself who have gone through what you have... Are you a TYP member? I don't believe I ever saw you at the forum?

I believe why the forum is so popular is that it is a great place to commiserate and find common ground with others. Fighting heart disease can be lonely... sort of. It definitely helps to bounce experiences and pearls... and even better coaching others. We learn deeply actually through teaching others. The generosity and kindness of many of the members with sharing knowledge and comfort is just staggering and mindblowing.

I think you will be quite fine :) On the hand if you ever have non-traditional or traditional anginal pains, then guess what? You need to call '911' for debrillation (time is life). Or, obviously go to the nearest ER for prompt medical evaluation. Do you have nitro on hand (not that you really need it)?

Interventional procedures and surgeries are necessary and life-saving if someone is symptomatic with heart tissue damage. It can prevent heart failure and cardiomyopathy later.

Hope that helps?

You're right, I'm limited here coz I don't give medical advice... it's my psychobabble.

It is wondeful that you have found nearly all the solutions to avoid similar premature tragedies in your family history. I have the utmost confidence you'll reach all your cardiac and longevity goals!

-G

reinman said...

Dr. B.G.,

Thanks for you reply!

I think I may have inadvertently created a little confusion by not being clear enough (not the first time I've done that!) in my previous post. The labs I presented were pre paleo diet and weight loss. Am going to be retested in about 5 weeks, which will be about 3 months on paleo. I'm hoping to see some significant changes for the better.

Glad you made it out our way last summer. We live up in the Beartooth Mountains,just about 60 miles from Yellowstone. Amazing country.

Dr. B G said...

reinman,

Oops -- ok then, the pre-paleo labs show some degree of hyperinsulinemia and carb sensitivity.

Niacin and carb restriction are FANTASTIC. You probably do some primal fasting which will help too do wipe out glycogen reserves and improve insulin sensitivity. What you do basically emulates NIACIN.

Robb McLeod at Entropy Production is great. He some some other tips that are brilliant.

Three Basic Strategies
Feasting and Fasting: Dichotomy of INSULIN


Can't wait to hear the post-paleo numbers later!

-G