Tuesday, February 23, 2010

Saturated fat and sdLDL?

The post itself and the exchange of comments on Dr Davis' blog about genetic causes of sdLDL piqued the interest of many of us. You need to have read the post and comments to make sense of this particular post here. I'm not keen on decrying the concept of genetic sdLDL out of hand but, obviously, there is a great deal that can be thought about around the non genetic concept. My thoughts are down here as I don't want to go cluttering Dr D's post up with comments that are clearly mine, from my biased viewpoint, and very probably not congruent with those of Dr D. The situation is too interesting not to expand a little though...

I roughed out Stan and Ollie on Fitday, very crudely and making big guestimates.

Here they are:

Very crudely for Stan



I gave them both half a kilo of cabbage each, nuts as almonds, (slightly more for Stan as he is weight stable) and chicken, again slightly more for Stan to keep him weight stable. I also allowed Stan some cannola oil to make his total calories up to 2000kcal/d.


And here is a guess for Ollie


I assumed Ollie was burning 0.34lb/d of his own fat and entered this as lard. I allowed him a total (including the lard from his butt/belly) of 2,300kcal/d as he was carting a fair bit more weight around than Stan. Probably an underestimate.

Saturated fat "consumption" for Ollie (who near eliminated sdLDL) worked out as 67g/d, total fat was 83% of 2300kcal, MUFA 105g and PUFA 31g. Most of this fat was from belly-fat plus almonds.

Fat for Stan (who retained sdLDL) was from his diet only as he, quite correctly, lost very little weight over 6m. Results were saturated fat 17g/d, total fat 70% of 2000 calories eaten, MUFA 84g/d and PUFA 53g/d.

I find it hard to see that Stan's saturated fat is the reason for his sdLDL, unless one posits that 17g/d of saturated fat as chylomicrons (apoB48 labelled, gut produced) causes sdLDL in some way (sdLDL is apoB100 labelled and produced by the liver). While at the same time Ollie's 67g/d of saturated fat, available as FFAs after release by hormone sensitive lipase from his adipocytes, behaves differently to Stan's 17g/d saturated fat released from chylomicrons by lipoprotein lipase....

It's possible, but it seems implausible to me.

Dr Davis mentioned the tendency of this sub group of his patients to be borderline diabetic. This to me is far more interesting and makes my ears prick up. Both apoB100 and apoB48 have glycation-predisposed sites which, once glycated, inhibit their uptake by the LDL receptor (certainly for the apoB100 particles, probably something similar works for the apoB48 particle, I've not chased this).

If apoB100s are not taken up because they are glycated due to a borderline diabetes tendency we have a very plausible mechanism for "atherogenic" remnant particles both being formed and "remaining". It just needs a little sugar to get them there. And of course, some of us think sugar and arteriosclerosis might be linked anyway...

Peter

30 comments:

John said...

Ollie sure didn't eat much for a long time...

I would say those guestimates are accurate. Would someone who has a history of good eating have a different "belly" composition than lard, like tallow or butter? To what degree is stored fat reflective of diet?

Kurt G. Harris MD said...

But Peter, don't you see? They have opposite physiologic responses to saturated fat because one of them has a genetic disease.

And we must get tested to be sure we are free of this disease before it is safe to eat saturated fat.

Otherwise we'll need to stick to corn oil and nuts, if not twinkies.

But seriously, in the Stan and Ollie scenario, they BOTH showed improvement in sdLDL on low carb -so hasn't Stan's 17 g of sat fat already proved to be beneficial in lowering his sdLDL (even if less so than for Ollie on account of a lower dose as you astutely observe)?

And is this not actually the opposite of the stated claim?

Peter said...

Hi John,

The link between fatty acid composition of our stored fat and diet is complex. The PUFA and MCTs are diet derived. The ratio of saturated fat to MUFA is determined by insulin through delta9 desaturase, ie carbohydrate in the diet. But then you have to look at insulin resistance as well as insulin activity... We routinely desaturate some palmitic acid when we store fat. Otherwise we would set solid! There are interesting papers on delat9 desaturase knock out mice. Delta 9 desaturase activity is increased in obesity. Knock out the gene, stop obesity! Develop and inhibitor of D9desat and you have a world beating obesity treatement! Woo hoo.

It works too. Well the gene knock out step does. If you use a leptin deficient mouse that is (getting a bit tenuous in the link to the average fat Joe here!).

But what happens when you can't store fat? Think Berardinelli-Seip congenital lipodystrophy and diabetes. Yes, your mouse becomes a slim but diabetic double knock out mouse (they used ob/ob mice).

That's what happens when you give lots of money to a group of idiots to sort out a problem generated by cardiological crooks in the 1950s. Hysterical.


Well Kurt, that's how I see it too. I think Dr D is really hung up on lipids without the wider picture. It's a pity. I don't like to keep on about it, but I agree that this example shows the potential therapeutic effects of high saturated fat diets. Which Dr D does not seem to use. If he did it would put him over with JK, ie beyond Atkins, which may not be a comfortable place.......

On a lighter note we did have that throw away comment from Dr D that he sees an association between high Lp(a), which must be reduced, and intelligence. Bit of a compliment, if a little backhanded, when said to someone with an Lp(a) of 84mg/dl who's not looking to reduce it!

Peter

donny said...

"4) The "floor" of 600 nmol/L can be broken. We've had success

achieving really low body weight

and inconsistently with several supplements, e.g., phosphatidylcholine."

This further elaboration by Dr Davis might be telling. When Stan does manage to wring some calories from his smaller fat stores, his small dense ldl decreases. So calorie restriction still works for these people. Insulin and blood sugar both go down in semi-starvation. Or in ketogenic diets where both protein and carbohydrate are more strictly controlled.

Ned Kock said...

Excellent analysis Peter.

When I saw the original post by Dr. Davis, I thought that a key difference between the two individuals was that one was burning significantly more fat than the other; body fat, as you noted.

One thing that I am not sure of is whether the mechanisms for transport and metabolism of fat change much depending on whether the fat is exogenous or endogenous. More specifically, are chylomicrons involved to the same extent whether the fat being burned is dietary fat or body fat?

As for pockets of the population having retained a group of related genotypes that would make them look like Stan, I think that is a distinct possibility. Genotypes may evolve into fixation for all kinds of reasons, and once they become fixed and are dominant in respect to a phenotype, it may be hard to “get rid” of them:

http://healthcorrelator.blogspot.com/2010/01/how-long-does-it-take-for-food-related.html

http://healthcorrelator.blogspot.com/2010/01/evolution-of-costly-traits-challenge-to.html

donny said...

Somebody posted this over at Nephropal;

http://www.ajcn.org/cgi/reprint/20/2/139.pdf

They gave it as evidence that a high fat diet was not for everybody. It has a very blunt measurement of serum cholesterol, undifferentiated. The study involved pretty much a zero carb diet, with varying ratios of protein and fat, in both obese and normal weight subjects. So when I say higher protein in the following, I also mean lower fat.

CF was a normal weight subject; his blood cholesterol spiked when compared to the other subjects in his group; but if you look at figure 1, it spiked at the higher intakes of protein rather than at the higher intakes of fat. At 70 percent fat, 30 percent protein, his cholesterol is only slightly higher than the other subjects. Between 40 and 70 percent protein, serum cholesterol is highly elevated compared to other subjects, there seems to be a high plateau for serum cholesterol in that range of protein intake.
Of course, can't say what's going on with the small ldl or anything like that. But I'm suspicious. CF's triglycerides seem to increase at increasing levels of protein. Er, lower levels of fat.

Talk about "through a glass, darkly..." but maybe CF is a Stan?

donny said...

"Spiked" should maybe be replaced with "was most elevated."

Dr. B G said...

Donny,

That study used unnaturally GINORMOUS amounts of n-6 PUFAs 13-35 GRAMS. The max people should consider that mirrors ancient/primal man is 3-6 g/day (with appropriate n-3 PUFA 3-12 g/day).


Peter,

I've read there are genetic and gender-specific predispositions to n-6 where sdLDL increases more than others-- perhaps this is Stan?

If Stan is pre-diabetic/MetSyn (and likely highly n-6 sensitive), I concur: the dietary carb intake is more of a factor for the formation of sdLDL and the glycalated disformed apo B-100 and apo B-48 particles.

With a saturated dietary fat 'deficiency' and elevated postprandial glucoses/insulin, indeed Stan is looking at hardcore CAC progression 10-20+ % and who knows what the soft-Lp(a)-core plaque progression is annually... from my observations. (Because again, only lower carb, n-3, sat fats and good immunity control Lp(a)... as the fishing Bantu exemplify)

Y E S -- *haa* Rx: MORE statins and PUFAs and pound that LDL further to oblivion...

Kurt G. Harris MD said...

@Peter

Speaking of genetic diseases, I was re-reading your posts on FH last night and came across a definition for FH including LDL of 195 mg/dl

On the SAD, my calculated LDL was around 120. Now on 70/20/10 it is 191, so if it goes up just a smidgeon, I will have actually changed my genotype to heterozygous FH!

Diet is apparently even more important than we thought. It can now cause genetic diseases like FH and congenital sdLDL.

PS My LDL-P is 1100 - true LDL is therefore 110.

Also, my Lp(a) of 85 is in mg/dl. Is there a size effect for Lp(a) similar to that with LDL when eating high fat?

donny said...

Dr BG; yes, way too much omega 6. But I still wonder about the protein. Have you seen the wikipedia entry for rabbit starvation (pretty sparse), or tried to find studies of it? All I can find that comes close enough to matter are studies on anorexia, articles about the extremely high (as a percentage) intake of protein of some gymnasts (just more anorexia, there, as far as I'm concerned), protein-sparing modified fasts in the obese (doesn't count), anecdotal evidence from people who were thrilled with their results from Kimkins early on, but later on started having symptoms, low energy, hair falling out etc. A young guy showed up at freetheanimal, he went paleo and his cholesterol went up, he started feeling like crap. He didn't start out overweight. I have to wonder if there isn't a danger to grass-fed beef. Grass-fed is leaner, and it might be healthier in a lot of ways, but maybe we have to feed the leaner parts to the dogs, like some of our ancestors did, or add lots of coconut fat. What's worse, rabbit starvation or too much corn oil? Heck if I know.:)

I don't know that feeding a high protein low fat low carb diet will derange cholesterol metabolism in lean subjects, I haven't really seen anything to say that it won't, I just haven't seen the studies.

donny said...

"During each dietary period, two of
the four men received a small supplement of 50
g of carbohydrate, primarily using bread plus
a small amount of orange juice as sources of
carbohydrate."

"The two subjects, ND and TR, who received
the supplement of 50 g of carbohydrate
daily (mainly in the form of starch) exhibited
a smaller increase in serum cholesterol."

At some point in the study, I guess these two guys were actually on the Optimal diet, if you ignore the corn oil.

Peter said...

Donny,

It's a very interesting study on several fronts. I notice they mentioned to loss of hunger in the women on high fat diets, offset by the awful monotony of eating steak followed by double cream on some LC dessert all the time.

Personally I really miss hunger. Drinking the odd half pint of cream whenever I feel like it, or not bothering to eat if I'm busy... Gawd, the awful, terrible tedium.

Perhaps I ought to go back to Weetabix for breakfast and hunger by 10.30am. At least I wouldn't be bored!

Seriously, 70% of calories from protein is going to be rabbit sickness. I looked through the literature for studies in rodents using gross protein overload/unit calories but never found anything interesting enough to blog about.

Obviously we're not in a position to comment on sdLDL or any other LDL (that ad hoc patch had not been thought up back in the sixties it seems!). But the diets seem to have been designed to maximise problems and mostly failed, as far as I can see...

Peter shakes head, 70% of calories from protein....

James said...

Hello,

Could you provide analysis on this recent study when you have time?:

Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet .
American Journal of Clinical Nutrition, 2010 91: 578-585.

Peter said...

Hi James,

The abstract says it all really. A low fat starvation diet gives you sdLDL so the LDL guestimated figure drops.

The high fat group group increase large bouyant LDL so increased their guestimated LDL.

You notice this is described as "increased" but no statistical significance is given in the abstract (it is for everything else).

They may or may not be exceptions to the sdLDL vs lbLDL picture but Krauss' work shows that, on average, this is the case.

Only the high fat group dropped fasting insulin, while "Both dropped 24h insulin". Guess which dropped it most! They don't say....

What is not included is that the low fat group were HUNGRY. The high fat group weren't.

I'm loathe to pay per view for another endorsement of high fat LC eating whith an abstarct which is a devious as a corkscrew!

You can bet your bottom dollar they didn't measure lipoprotein subgroups. These people are not stupid!

High fat eating is ALWAYS associated with more FFAs in the plasma than high carb eating. What are you going to run your metabolism on during high fat eating if it's not FFAs? It's certainly not going to be glucose and, as fat gets styored between meals, it has got to get from adipocytes to muscle cells. Short of beaming aboard they travel as FFAs!

Peter

Peter said...

Actually, what would be really interesting would be the chylomicron remnants compared between groups when they were on adequate calories to be weight stable.

But, as I mentioned, these people are not stupid.

P

Dr. B G said...

Donny,

Peter knows rabbit studies... If the whole bunny were consumed (brain, liver, organs, etc), would there still be a metabolic problem? I guess so. Rabbits are too lean -- gimme a musk ox or bison or pig with 20-25% body fat!

In the 70/30 group where 70% protein and 30% fat, I think the protein is providing an insulinogenic response -- hence the trends of higher TG. The weight stabilized in the men.

You know though this study is kinda junky, the 70% fat group still had the lowest Trigs and best weight delta's.

-G

Kurt G. Harris MD said...

Look in your inbox - I've sent you that article.

I agree, the abstract says all you need to know.

Peter said...

Thanks Kurt,

It gets a bit boring blogging about these studies, but this one has to be one of the worst I've read. Actually, the study is quite good, it's the research group and their twisted writing which are appalling.

Yes, the rise in LDL in the high fat group was completely non significant.

Yes, the low fat group did drop HDL significantly while, yes, the HDL drop in the high fat group was non significant (how the hell did they drop the HDL in the high fat group at all, ad libitum trans fats??? Oh, they advised participants to avoid saturated fat...Duh).

Yes the high fat group were on ad libitum food until satisfied and the low fat were on aggressive Weight Watchers restrictions. Each gave identical weight loss but the poor starving folks on Weight Watchers must have suffered for science...

It just goes on. Total misinformation. Once you translate the study in to an honest dissertation you can sum it up by saying that the atherogenicity of LDL goes DOWN in association with rising free fatty acids. If you think LDL is atherogenic at all, which these clowns obviously do.

Huh. Got me ranting didn't you!

Tee hee

Peter

Kurt G. Harris MD said...

I see the true Peter fired a salvo over on the amazon thread: )

When will they learn the only way those veggie diets work is by stuffing you full of so much non-nutritrive roughage that you are forced to "eat" your own fat - and only then if you have any!

Nigel Kinbrum said...

It was I who posted Some Metabolic Changes Induced by Low Carbohydrate Diets, merely to illustrate that we are all different. I can't see any mention of omega-6/omega-3 in that study, but linoleic acid is generally cholesterol-lowering according to Fig. 2 of Types of Dietary Fat and Risk of Coronary Heart Disease: A Critical Review.

LynneC said...

A couple of comments, re Dr Davis and sat fat. I'm a member of his TYP program, and although he's not in the sat fat camp (yet), he's certainly not advocating consuming corn oil and twinkies! (I know that was tongue in cheek,Dr Harris, but a bit insulting, nonetheless)

A large focus of the TYP program is related to blood sugar and carb control, with recommendations to eliminate wheat, conrstartch and sugar,and test for blood sugar response to other grains and eliminate or reduce them, based on individual blood sugar response.

Dr Davis’ recent report, available at TYP, discusses elevated postprandial triglyceride response as it relates to fat consumption, and the conclusion that he reaches is that fats should be limited to 25-50g per meal, to minimize elevated postprandial trig responses. The ‘official’ TYP recommendation on sat fats is to consume less than 25g per day, but many members are eating a much higher total of sat fats than that, based in part on what works for them.

LynneC said...

Peter, JAMA report on non-fasting trigs and relationship to CAD

http://jama.ama-assn.org/cgi/content/full/298/3/299

Kurt G. Harris MD said...

@lynn

I said corn oil and nuts, IF NOT twinkies. I did not say AND twinkies.

Peter said...

Hi Lynne,

I realise that Dr D is heavily in to normalising blood glucose levels and low carbing to get there. This is excellent. Where I disagree is the toxicity of post prandial triglycerides. If you eat a meal based on 150g of animal fat you will have a surge of chylomicrons. These are, of course apoB48 containing and will carry a mix of un-damageable saturates, modestly damageable monounsaturates and some small amount of unstable PUFA. Why these should become remnant particles, if they are not glycoxidised, is what is beyond me.

To compare them with elevated fasting triglycerides, which are essentially a surrogate for fructose intake, seems illogical. Even to condemn fasting triglycerides (VLDLs) per se, without looking at the toxicity of the fructose they are derived from, also seems illogical to me.

Originally total fat was ranged against sucrose in the competition for the cause of CVD. Anyone with fat phobia has to explain how we got from 1953 to today without throwing out the lipid hypothesis in 1957 and never paying any attention to it ever again! Y and H destroyed Keys, but the lipid monster lives on ...

Now, omega 6s from nuts and healthy oils like olive oil and cannola, that's a whole different ball game... as we know, linoleic acid is THE lipid of apoB100 particles, if we must cling to the apoBs are out to kill us paradigm. Maybe if they carry lots of healthy glycoxidised (in situ) linoleic acid they are assassin's bullets.

I keep thinking Dr D getting there, but he continues to frustrate! Perhaps give him more time and results via CAC scores and maybe he'll cross the divide! But how can you check results without trying the fats?

BTW, re the Copenhagen study: non-fasting trigs and diabetes, look at table 1

http://jama.ama-assn.org/cgi/content/full/298/3/299/JOC70073T1

Nice to know they adjusted for diabetes in amongst a host of other factors, but I personally doubt they could adjust for people with post prandial hyperglycaemia which still makes it down to acceptable levels after a 12h fast. This uncontrolled-for IGT is mangling your arteries, nerves and lipids, without the label of diabetes. Type two diabetics have usually had sugar dysregulation for 10-15 years before diagnosis. I like table 1. I don't like hyperglycaemia. ApoBs? What's in the lipids underneath them and why are they still there are the questions in my mind.

Peter

Mindscaper said...

Can you elaborate on this statement?

"the atherogenicity of LDL goes DOWN in association with rising free fatty acids. If you think LDL is atherogenic at all,"

Do you not think that LDL is atherogenic? or if I've missed this point could you point me to a previous post?

Another question: Is it possible if one is on statins and plavax to still benefit from a diet that adds N-3's, reduces N-6's, raises saturated fat intake by adding fish oil, coconut oil, butter, includes adequate vit D, magnesium and Q-10, + raw dairy and kefir, gf beef, cold water fish, and fermented foods, as well as very little sugar or fruits, no beans or grains? I was told that I had to stay on the plavix for at least one year (or possibly have another clot and die).I became a captive of the cardiologists one year ago when they implanted 4 stents during my most vulnerable moments following an MI. That decision cannot be reversed (but I wish I could have first tried to reverse the atherosclerosis through diet and lifestyle changes). I didn't know that it was possible then. I did ask and the doctor told me that it wasn't!

I hope to be able to free myself from the pharmaceuticals so I have abandoned the initial recommendations from my doctors for a "heart healthy" low-fat diet (follwed by a recommended Mediterranean diet). Instead, I arrived upon and have been following a fusion of paleo and a Japanese diet that I researched, myself. I just had my one year lab tests today and will have a one year follow-up on Wednesday. I can't wait to see the results.
I have learned a lot from following Peter,Stephan's, and Kurt's blogs (as well as Art Ayers and Dr. Davis). It is a lot of information to decipher and relate to ones own needs but I read all the discussions and then make up my own mind about what I think is right for me. I appreciate all the time and care you take to reference your work and state your opinions (including your biases). Thank you.

LynneC said...

Peter said:
I keep thinking Dr D getting there, but he continues to frustrate! Perhaps give him more time and results via CAC scores and maybe he'll cross the divide! But how can you check results without trying the fats?
I agree; even in the short time (7 months) that I have been a member of the TYP program, I have seen a shift regarding sat fats. There are enough members now who are eating a highish sat diet that we should be able to see trends forthcoming.

Peter said...

Hi Mindscaper,

Is LDL atherogenic? Certainly not. The hypeglycaemia which converts apoB to remnant apoB, which cannot dock with the LDL receptor (assuming this is what is meant by remnant particles), is certainly damaging. Whether the glycoxidation involved in this makes the apoB particle toxic per se is slightly open to negotiation, it certainly damages many other structures by random glycation. I suspect glycation of apoB is a normal phenomenon driven to extremes by on going damage from hyperglycaemia and the cellular response is amplified by insulin. Without the hyperglycaemia I doubt any LDL would become a remnant particle to worry about.

But never forget that first cholesterol was the problem, then only LDL (the apoB subgroup) and now it is only sdLDL which is atherogenic and the large fluffy LDLs are not, though both have apoB100 on their surface. Has the shift in the goal posts stopped yet? Don't bet on it!

Re the reversal of CVD with diet, Dr D says yes, even within the sdLDL centered camp. I see no reason why not. The problem you have is that you personally can only look at surrogate markers as the stents are going to mess up any imaging. I know Kurt is not keen on repeat testing but I have more time for getting marks out of ten for what you are doing personally on an n=1 basis. Surrogate markers are always just that, but they are all you have even if they do not necessarily reflect the actual disease process. The conundrum is that if they are bad, what are you going to do? Assuming you are confident that what you are doing is correct... But if you find yourself between the sat fat vs healthy oils debate and your numbers are not good it might be time to change camp, or, better still, look at glycation, hyperglycaemia and insulin response to food, rather than lipids per se...

Lynne,

Good. That will be worth watching...

Peter

Mindscaper said...

Thanks for your reply, Peter.
Actually, I have switched to sat fats and eliminated vegetable and seed oils (except for occasional ev olive oil--as dressing-- and very little sesame seed oil in Japanese cooking).

Because I didn't feel like I was getting enough saturated fat I made little wafers of coconut oil, walnut pieces, and extra dark choc to raise my fat intake. I take them with my fat soluble vitamins.

I'm a little confused about nuts, seeds, and Omega 6s. I have been using almond meal and coconut flour regularly as a flour substitute and about 4 walnuts a day because of recommendations stating they work to reduce atherosclerotic plaque. Also to replace my nemesis (potato chips) I eat some cashews and pistachios. Is there good reason to eliminate these entirely even if I use a lot of fish oil (~8 caps/d)?

My lab results are in: In one year I have reduced my T cholesterol from 206 to 140; triglycerides from 201 to 115; HDL from 34 to 51; VLDL from 39 to 23 (and I have the large fluffy type); LDL from 131 to 66; C/HDL Risk Factor 6.0 to 2.7. Fasting Glucose (Feb) a year ago was 129, (June) 119, (Now) 100. Weight from 170 to 157.

Overall I think these numbers indicate pretty good progress. I still would like the glucose to be lower and I would like to lose more weight but I've only been doing paleo/japanese since September and I'm still refining it as I'm learning.

Even with these good results, I bet my cardiologist claims that the drugs are the responsible agents and will want to keep me on them!I will probably have to wean myself and then test again. The funny thing is my lipid profile was not that out of range to begin with (compared to a lot of people walking around and lying on couches who didn't have heart attacks with numbers far worse than those). . .which makes me question the whole lipid hypothesis anyway. So if these surrogate markers don't really tell me much which ones should I really pay attention to? I will look more into glycation, hyperglycaemia and my insulin response to food as you suggest.

Are you saying that because I have stents that a heart scan won't tell me much either? I was planning to have one of those on March 13th but I'll have to pay for it myself since insurance doesn't cover it. I had tests done by Quest labs in June which showed my APOB100 to be 64mg/dL and remnant lipoproteins (IDL+VLDL3) to be 30--didn't say anything about APOB48. Still that was way before I swtiched to high fat diet and cut out grains sugar and other carbs. My cardiologist doesn't request those tests--D.O does but I have to pay out of pocket for them!
Sorry to ramble. Thanks again for your response. Cee Mathers

Kurt G. Harris MD said...

@Mindscaper

Stents are roughly the same density as calcium, so assuming your stents are in the place with the calcified plaque, it's very hard to get an accurate CAC reading anywhere there is a stent. If you only have one and the stent does not obscure most of the plaque, it might be worthwhile but stlll may be hard to interpret accurately.

As far as CAC in general, i believe it's best use is in those who've already proved to have a non-zero scan but is now eating right -someone like Peter can repeat their scan in one year (or better yet, two) and if the score does not progress much, reassure themselves it is unlikely their diet is accelerating the atherosclerosis. No progression of an established CAC score is almost as good as a very low score prognostically.

In your case, a CIMT by ultrasound might make more sense, as it is easy and radiation-free and with the right diet can actually show regression of intimal thickening. (See Peter's later post he just put up.)

Dr. B G said...

Lynne,

Correction! Davis mantra is max 20 grams sat fat daily (not 25).

Perhaps this explains the lack of improvements in HDL2b, Lp(a) and CAC, no? For those compliant (~97% of the membership).

Obviously this is not the case for those noncompliant with the high omega-6, 20g max sat fat, high carb, non-Paleo TYP part 3 diet where arteriosclerosis regression is more potentially possible.

-G