What does one eat if they are wheat free, low carb, and low saturated fat? Can anyone give a sample day for this plan?

Have you tried T4/T3 adjustments with apo E4?

How can one find out if one has Apo E4?

Is it possible to have the same reactions to fats such as large increase in LDL, mostly large with little small LDL?  At one point i was 100% small LDL; restrcting carbs and increasing fats of all kind(good ones only) my NMR was 2098 LDL of which 200 were small were small.  HDL was 69 and TRGs 62.  Only way to get these numbers down is to be on statin and zetia.  Thought i was an ApoE 4, but test showed i am ApoE 3/3.
Perhaps i am a hyper-absorber of fats- maybe as bad as ApoE4?   With statin and zetia i can reduce the numbers to LDL total of 640 and <90 small.    So maybe the high fat diet is not so great even for those who are not ApoE4.
Thanks for your thoughts.

I'm getting my ApoE status tested soon.  I've been quite liberal with the healthy fats (olive, avocado, pastured eggs) and include saturated coconut oil and dark chocolate.  I also have high LDL particles - about 1500, but only 139 are small without statins.  I would love to find out I am 3/3 because I've already restricted grains and a variety of foods that I tested as allergic too including nuts.  I asked Dr. D on the forum if having <10% small particles was good news, but he was still worried about the total LDL.  I guess we will see how worried I should really be shortly.  BTW, I've got high Lp(a) at 26mg/dl, so I really don't need another strike against me in my plaque battle.

Lost a nice technical ApoE explanation  I spent a lot of my time on to "server error" .
I'll just lurk from now on.

Mighto:
Please stay here and enlighten us with your comments. Glitches can happen. I made it a habit a long time ago to just copy my text (Ctrl.A, Ctrl. C, on WINDOWS) before sending it. It is easy and takes no time. Text is preserved and you can try again.
I for one am enjoying your musings tremendously.
Cheers, Renfrew

What Renfrew said. I've run into this problem on blogger regularly where it decides to log me off while posting a comment. Now I always save any longish comment before posting. Better safe?

Digging into my 23andMe data, it reports back on APOE e4 status

You can find this as part of the https://www.23andme.com/you/journal/alzheimers/overview , or just check the rs7412 & rs429358 SNP's directly.

I am an APOE 3,4, and here’s what I eat on week days.
Breakfast.
Steamed raw vegetables (eggplant, zucchini, bell peppers, mushrooms, Mexican or yellow squash). Add yellow mustard and dry spices.
Natto twice a week (1 box Mito natto, throw away their soy sauce and mustard packages).
Frozen blueberries (1/8 cup), 3 tbsp flaxseed meal, 1 cup unsweetened almond milk - all microwaved for 2 min. Add ground cinnamon.
Half-ounce piece of part skim milk mozzarella cheese.
Coffee.
Lunch.
Frozen vegetables (California blend – cauliflower, broccoli, carrots) microwaved (reheat). Add a boiled egg, 1/4 avocado, yellow mustard.
Dinner.
Cooked or baked vegetables (cauliflower, bok choy, green cabbage, rapini).  
Sautéed or baked fish (tilapia, salmon, perch, trout), chicken breast, or ground turkey meat balls. Add yellow mustard, horseradish, and dry spices.
Generous amount of raw vegetables (green lettuce, pickles, tomatoes, bell peppers) with hummus.
Decaf tea with a 1/10 serving piece of 90% dark chocolate, half-ounce mozzarella cheese, and some almonds or sunflower seeds.

My daily fruit serving includes a cup of frozen dark berries (blueberries, raspberries, blackberries) from the Costco Three Berry bag.

back incollege i did a report on cancer and ottowarburg and i remember this gene being incredibly linked to cancer risk....any truth to that?

Hi, Steve--
There are indeed genetic predispositions outside of apo E4 that can provide for this response, e.g., apo B receptor variants. What is not known is when you've crossed a threshold of mostly or purely large LDL that is undesirable. Despite $2 billion spent on statin drug-related research, we still have no answer on this question.

Hi, Buck--
Similar issue as the question posed above by Steve: We just don't know what an "allowable" quantity of mostly or purely large LDL particles are. For a working value, I've been trying to keep NMR-derived LDL particle number 1500 nmol/L or less when LDL is purely large, but I have no endpoint data to justify this.

Great program, Gene, given your pattern. And I am impressed at your courage to eat natto!

Hi, Mallary--

Hardly my area, but I believe that the relationship between apo E4 and cancer in various sites is complex and modulated somewhat differently than in other apo E genotypes. Some discussion:
http://aje.oxfordjournals.org/content/170/11/1415.long

Hi, Simon--

The full diet is articulated in detail, including scientific rationale, in several reports on the Track Your Plaque website; link above. Chapter 9 of the New Track Your Plaque Guide is also devoted to this.

As you see, I will be putting out recipes here and on the Track Your Plaque website in coming months.

even 1 reconstructed paragraph just  lost to "server error"

ApoE joins with ApoB and is carried in VLDL and chylomicrons; it is ApoE that binds to tissue cell LDL receptors to start normal uptake. Inside the ApoB with lipids breaks off and heads into tissue cell lysosome.
Meanwhile ApoE and the LDL receptor head back to that cell's membrane, with ApoE carrying some cholesterol out of that cell to build into an HDL molecule for recycling.

I have the worst of both worlds, I think, as I am E2/E4.  Dr. Davis, do you have a specific program for patients with this genotype?

So, Gene, I'm curious.  It looks like you have an extremely low intake of protein.  How are your labs and what kind of activity do you do during the day?

Eggs, natto, fish, poultry, and nuts are all rich in proteins, correct? I increase my portions of fish and poultry when I go to gym. I also add canned fish on these days like tuna in water or sardines in mustard sauce. I used to consume large amounts of tofu, but stopped recently based on some negative information I learned from a TYP member forum.
Every weekday I typically walk to and from the train station, 25 min each way. I work out two or three days a week following the slow burn routine; I do cardiovascular, too. I also ride my bike for 2 hrs every weekend.
I am a software engineer, so I spend most of my business hours in front of a computer.
Before I learned about my APOE 4, I used lots of olive and canola oil and was a vegetarian, but had already reduced carbs. My labs were pretty bad and actually much worse than when I ate lots of bread and oatmeal every day. In mid-December 2010, I started eating as described above plus taking niacin (500 mg) and Crestor (10mg). I was already taking the standard TYP supplements – vitamin D3, fish oil, iodine. At the end of March 2011, my NMR was the best I had ever had: LDL-P 568, LDL-C 70, HDL-C 55, Trig 24, HDL-P 29.5, Small LDL-P 293, LDL size 20.4, HDL size 9.7, Large VLDL-P 0.7, insulin resistance 16. I don’t have genetic lp(a). I know the results can be better, so I am looking forward to my next NMR due in the fall.

I'm confused. When you say 1 in 4 have this gene are you saying it's a *problem* in 25% of everyone? As in one-quarter of us should be eating like Gene K (above)? Or is a case where the gene isn't always active or something?

I recently wrote about Alzheimer's on my blog and this question came up in the comment section.  I think about APoE4 completely differently than you do and here is why.  APoE4 confered humans the ability to migrate out of the sahara and north and south to live in climates with less solar radiation.  It allowed us to live with lower vitamin D levels.  Moreover, its presence alone means nothing unless it is accompanied with the epigenetic triggers that make it dangerous.  Dr Davis you and I both know the disease you treat (heart disease) and the one I treat (Cerebrovascular disease) are the same disease just found in different organs.  SO i think we have a lot in common in what we do but how we think about thi sissue is different.  Here is my take.  I posted this answer on another forum and I think it needs to be discussed here.

I think the ApoE4 story is an interesting one and one I briefly touched upon in my AD blog.......I will revisit it.......but ultimately I dont think it is that important if you live an optimal life from 20-60. ApoE4 means much if you make poor epigenetic choices. I think people who come here do do what the rest of America does.

The other reason I think it means little is the epidemiology of ApoE4 in those over 80 yrs old. It does not have any major impact on healthy aging once you get to old age. That tells me that the epigenetic signals need also be present for it to matter.

ApoE4 is like dynamite.......and high insulin and high PUFA consumption and lowered total brain cholesterol (due to altered lipid uptake) are the major lit matches. If they exist by themselves they are harmless......but if they are brought together you are going to get heart disease and AD early and get taken out.

Dr Kruse

So everyone who is eating or planning to eat a high fat diet should get tested for E4, or are there some things that indicate it's probably unnecessary?

Dr Kruse -

It's pretty scary for me to think that maybe I am not supposed to be eating very much saturated fat. If it's true that is unbelievably lame. This is why I'm thinking I need to check to see if I am ApoE4. (How do I test for that?) If I am, then it may explain why, even on a Paleo diet, my LDL is mostly small dense. Are you suggesting that if I keep PUFA very low, like cut out my only remaining source (almonds/pecans), that this could be a key to producing more pattern A LDL? (By the way... I have chosen to eliminate all nuts and nut butters, regardless).

-Jack Kronk

Thanks so much for the thoughts - I am an E4/E4 eating a Paleo 2.0 diet.  As I understand it, high-protein is not a healthy diet, so low-fat & low-carb is not a good idea.  Fat is the healthiest macronutrient, so I'd love your opinion on which types of fat are best for E4s.

It sounds like you have concerns about saturated fat, and of course I avoid n-6 PUFAs and get lots of n-3s from grass-fed animals & fish oil.  What about coconut oil?  Olive oil?

What sort of HDL/LDL/etc  numbers would you look for in an E4/E4 as warning signs?  As health signs?

BTW, I blog occasionally on APOE4 at primale4.wordpress.com, am going to quote your post there.

Thanks for that, Gene.  I may need to go your route with my profile.  I'm following TYP pretty religiously and am having my 6-mo labs this month, so hopefully they will be improved from last time.

Jack as I mentioned to you on my blog I think you clearly need context.  I think your epigentics are telling you something.  But here is what I cant tell you and neither can anyone else.......without testing!  You need to be tested to get that context.  I think your diet you posted gave many clues......but even I did not jump to the easy conclusion.  I think your real underlying issue is multifactorial but your VAP strongly points to a leaky gut as a source of the sdLDL.  I think the bananas and cream are problems too.  Your O6/O3 ratio maybe bad and yes......you may have a bad set of allele's for ApoE4......but guess what!  Your HS CRP was very very low.  This tells me that your match is not lit.  So you may only be carrying a stick of dynamite.  Again......carrying dynamite is not going to blow you up.  This is why you need testing to get more context.

We send our ApoE4 patients to an nearby academic lab for testing.  One is likely available in your community because cardiologist and neurologist are ordering this test quite often now.  I think your PUFA content of your diet and of your tissues is critical.  In fact for AD the PUFA content is a major factor.  I believe it is a huge factor for CAD disease as well.  Wheat, Carbs, and PUFA's all drive sdLDL production.  Its not just one part of the diet that does it.  Moreover, the more leaky the gut the more sdLDL one will have as I laid out in my VAP blog that I dedicated to yourself.  I think your case is quite representative to many thousands of people and I am glad we are talking about it here because Dr Davis is a cardiologist and is coming at this issue from a different angle than I am.  I think however when the story plays out.......we will be in the same neighborhood because human biochemistry pathways are constant.  The fuels and hormone status and the situations in our guts are the covariables that make this issue more confusing.  I think people need to know why Apoe4 is important.  It conferred an adaptive advantage to move away from the equator to lower solar radiation and lower vitamin D levels.  This adaptation is seen in many american african americans.  The other interesting finding is that the liver of these patients makes more cholesterol to try to raise the D level and pregnenolone level to offset the deficit.  It never does.  But when this set of circumstance is mixed with a high carb low fat SAD (PUFA rich) it destroys the heart, vessels and brain.  This is what we see today in many parts of the world.  Their diet is now completely mismatched for the original adaptation.  I think if you tweek the diet when you know the epigenetic variables you can easily over come an Apoe4 positive test if youre willing to change.   But you need to test!

Hi, Tim--
Very rare, as you likely know.
I believe that you simply deal with this on a practical level, i.e., deal with the small LDL and insulin resistance issues and postprandial abnormalities from apo E2 as you ordinarily would. Then deal with the LDL-accumulating aftermath from the apo E4 component.

Thanks for the insightful thoughts, Dr. Kruse.
I'm not sure how your approach folds into mine, though fascinating. I do agree that apo E4 is made much worse by the means you cite, i.e., polyunsaturates, carbohydrates that trigger small LDL. This is why, despite the LDL-accumulating effect of apo E4, I focus first on reducing the small LDL component, in effect an anti-inflammatory, glycation-reducing, oxidating-reducing approach, followed only then by dealing with any large LDL-increasing aftermath.
What is not clear to  me is how atherogenic the large LDL is at higher levels in the setting of apo E4. As you know, one of the greatest concerns in apo E4 is that its effects may not be confined to lipid effects, but may extend into non-lipid effects. But that is such poorly charted territory.

Hi, Patri--
The formal data on the various fat fractions and apo E4 are, unfortunately, very skimpy.
Saturated fat clearly increases whatever LDL dominant form there is. However, other forms of fat, even omega-3 fatty acids, also increase apo E4. This become a problem, for instance, when we try to use high-dose omega-3 fatty acids to reduce Lp(a) in the presence of apo E4.
As I commented above in response to Dr. Kruse's comments, as a practical matter I believe it is best to address the worst fraction of LDL particles first, i.e., take dietary steps to reduce small LDL particles, meaning reduce carbohydrate triggers of small LDL. Then deal with the large LDL that emerge by varying fat intake and gauging effect.
Odd thing: Even among apo E4 people, fat intake yields variable LDL-increasing effects, quite variable sometimes.
Also, recall that health extends beyond LDL. So there may be benefits to monounsaturates or omega-3 polyunsaturates, say, that extend to issues like brain and liver health.

Hi Melinda,
Please copy and post this in previous thread for ApoE4 … .
Continuation about ApoE4:
% of ApoE4 messes dynamic inside tissue cell so that ApoB turns to use Scavenger Receptors to try to start cascade which gets signal transducer (Specificity Protein 1) to up-regulate the cell membrane transporter protein ( ABCA1, ATP binding cassette transporter A1) that puts excess cholesterol out from that cell. I believe this is where Doc Davis’ stated ApoB irregularities add to the problem with ApoE4 (since normal human ApoE3 works all by itself to get that signal transducer to bind to ABCA1 to work shucking cholesterol) . When cholesterol gets to build up inside the cell the large LDL can acetylate and form excessive “droplets” in that cell’s cytoplasm; while the small LDL can oxidize from CuSO4- and load up inside that cell’s lysosome.

Meanwhile % of ApoE4 doesn’t just dock with tissue cell LDL receptors and so the macrophage scavenger receptors pick up too much cholesterol laden ApoB/ApoE lipo-protein carrier molecules. Once in the macrophage the same problem of oxidized LDL piling up in lysosome and acetylated LDL burdening cytoplasm occurs; and for that matter, in macrophages, it is down to ApoB to get the signal transducer going if any cholesterol is to be put out by cell membrane transporter protein ABCA1. This is the recipe for risky pro-atherogenic “foam cell” formation; while the individual genetics of ApoE, ApoB, assorted receptor types, signal transducer and transport protein all make it hard to predict how ApoE4 plays out.

Dr. Kruse broaches ApoE4 in alzheimers and this is in large part because ApoE4 causes the brain neurons to get less than optimal cholesterol from the brain’s astrocytes. It is ApoA1 working in HDL complex that controls the astrocyte cholesterol balance and when there is inflammation there is a risk of ApoA1 mis-folding to foster amyloid aggregations. Low intact ApoA1 and ApoE4 together increase the risk factor for cognitive problems and dementia several fold.

Diabetics with ApoE4 have that % of ApoE4 as an additional limitation; however, irregardless of the ApoE iso-form diabetic dementia risk arises from their glucose loads impairing kidney tubules, and thus fostering the uremic environment that stymies ApoA1 bio-synthesis. The normal role of ApoA1 is to bind to the transport protein which secures cholesterol into a safe bond with HDL; so low ApoA1 from any factor will challenge the brain neuron over time. I suggest there are individuals whose age impaired kidneys contribute to senile dementia from impairing ApoA1 levels being made and also possibly speeding up the normal 4-6 days kidney elimination of ApoA1 ; and so Patri’s comment on limitation of high protein intake is relevant due to it’s demand on aging kidneys.

Reply

The above comment was written by Might-o'chondri-Al.  He asked me to post it in this thread as he is having trouble posting here.

Ok I will test! But I have been asking around how to test and still don't know how? Is this something that I would just ask my doctor about? Maybe I go to the same lab that did my VAP? Since I got my results 3 weeks ago, I have made the following changes: zero bananas, reduced my cream intake by about 70% or so, lowered my overall fruit intake signigicantly, added 2 teaspoons of red palm oil daily, decreased caffeine intake (and now I am doing no coffee in August). I have also decided to eliminate all nuts and nut butters as of 2 days ago. Now my only real source of PUFA left in my diet is bacon, occassional chicken, and avocado. It's weird too, because on SAD, I was probably getting 10 times the PUFA, at least. I cooked in canola, ate loads of grain bread and corn products like tortillas. Maybe adding the saturated fats makes everything more amplified. The only thing now that I am VERY reluctant to give up is starches like potatoes and white rice. If I do, I will surely be VLC again, as I don't eat breads and very little fruit now, and rarely ever indulge in sweets. This means, by default, that most of my calories would then be sat and mono fats. Isn't that not good if I am ApoE4? What a mess! Dr Davis is right about being between a rock and a hard place. Jeez!

"high protein is not a healthy diet". you mean specifically for ApoE4 folks? I haven't been tested for it yet, but I suspect I may be ApoE4. I take whey protein daily and eat lots of eggs and beef. I do this on purpose because I do weight training 5x per week and am building muscle. Could it be true that people who are ApoE4 are not supposed to build much muscle? (logically speaking, due to the restriction on protein)

Is server cooperating now ?

ApoE4 degrades more readily than ApoE 3 or ApoE2; ApoE4 protein fragments that get into a tissue cell's cytosol can have bad effect on that cell's mitochondrial membrane lipid binding . This decreases the mitochondrial efficiency  when they try to perform glycolysis for generating energy.

ApoE4 degradation in a cell cytosol can  decrease the level at which that cell advances it's bio-genesis of  robust mitochondria; this is due to how ApoE4 fragments depresses PPAR gamma expression & PPAR gamma is what promotes making good mitochondria. (Specificly in the case of human fat tissue PPAR gamma is what regulates transcription of pre-adipocytes differentiation into true adipocytes. Hence Avandia & glitazone drugs that target the receptor of PPAR gamma do short out adipocyte differentiation;  and yet risk the side effect of increasing heart disease due to mitochondrial impairment.)

In Alzheimers the form of ApoE makes a difference; and the brain amyloids react to insulin differently with different ApoE iso-forms. The ratio of insulin in cerebro-spinal fluid as compared to insulin in plasma changes with different genotypes of ApoE.   Alzheimer patients tend to have lowered glucose utilization in their brains with  less insulin and insulin-like growth factor receptors, despite the Alzheimer brain harboring fewer insulin degrading enzymes. Which engenders a paradox whereby diabetic brain neuro-pathy experimentally improves with administration of nasal insulin; and similarly,  individuals  with ApoE4  receiving nasal insulin improved their cognitive function, with the boost being higher in ApoE4 carriers than folks with any other alleles of ApoE.

Higher amounts of Alzheimer amyloid  formed tangles are seen in Type 2 diabetics and in those with ApoE4; leading to the conclusion that "normal" ApoE3 fortuitously forms a complex with brain amyloids.
Apparently ApoE iso-forms other that ApoE4 can more readily bring an amyloid to where the molecule LRP-1 (lipo-protein related protein 1) can move that amyloid out across the brain blood barrier .

Hi Melinda,
Thanks for repost, looks like Doctor D hammered his server into shape again.

With regards to the large LDL content.  Again I am not a cardiologist, but a neurosurgeon.  The heart and brain work on the same principles of biochemistry.  And since these two organ take up much of the CO in the body they share much in common.  It is also why when we see neolithic disease affect the heart their is also a similar effect in the brain.  The Apoe4 story is one such case.  But so is the large LDL story.  Cardiology CW today believes that LDL matters.  In neurosurgery today its clear in neurodegenerative disorders we are lacking LDL and cholesterol more often than not.  This is incongruent to biochemistry.  Dr davis has said here in this thread the jury is out on large LDL in his field.  I am submitting that LDL matter little in any field.  Why?  If it did the body would have a specific detailed regulatory control method in place to deal with it and it does not.  In nature, with the consumption of organic, unprocessed parent essential fats rather than adulterated oils (PUFA's) and transfats, LDL cholesterol is supposed to be made up of significant amounts of properly functioning “parent” omega-6, linoleic acid (LA), and is not supposed to be harmful. It is the natural transporter of parent omega-6 and parent omega-3 into the cells. It is thus not critical to lower LDL cholesterol, nor is the absolute LDL number as important, if the diet contains sufficient unadulterated parent essential fats. These are unadultered PUFA's of both the omega 6 and 3 variety for clarity sake.  Also take note that the body has no natural “cholesterol sensor” in the bloodstream—it would if its levels had to be maintained within exact limits; such as, sodium, calcium, and glucose levels are monitored in many systems. For example, glucose levels are maintained to an amazingly tight 0.1% in each of us!  So Nature implemented biological mechanisms if required. There is no need for a cholesterol sensor because the absolute number is irrelevant.  That was my advice to Jack Kronk three weeks ago when he posted his VAP numbers and when I blogged about his numbers.  I understand that Dr Davis may not want to go out on a limb as I have here.  But I dont view it as a limb when the biology and biochemistry support my beliefs fully that LDL cholesterol levels are completely irrelevant to heart disease propagation.  This is why I advocate copious amounts of coconut oil to patients with heart disease and all neurodegenerative disorders including brain tumors and seizure patients.  In fact, my literature is loaded with thousands of papers supporting my belief made here.  I think its long over do that cardiologists start reading "other pathways" of data to reach conclusions that their own field muddies.  As a neurosurgeon, I read Dr Davis literature quite a lot and in comparing the two it is clear that our two fields are on a collision course from two different paths.  I got extreme clarity reading circulation over the last thirty years that cholesterol has nothing to do with heart disease.  Dr Davis has reach conclusions that are quite different from most of his fellow cardiologist as well.  I applaud him.  I just think he is still caught in the lipid hypothesis nightmare and that is the only reason he is not traveling down the road with me in unison.  Since he is a fine doc and one who clearly is ahead of his peers......i'll gladly wait for him on that road because we need him to alter what ails his branch of medicine to get to where we both need to be going for all patients.

Dr. Kruse,

What is your response to the fact that people with familial hypercholesterolemia (FH) have an exaggerated risk of CVD versus those who are not lacking ldl receptors? Why do so many of them have cardiac events in their 20's and 30's? Surely, you would not relegate this phenomenon to increased consumption of PUFA's and/or higher insulin?

There are five major classes of FH due to LDLR mutations.  FH is a collection of genetic defects.  Many believe that the end result of these defects (IE high LDL or cholesterol) cause the diseases associated with it.  I do not.  Why?  When these people live past their 6th decade they have extremely low levels of neurodegeneration.  I believe the cause of the early on set  CAD is tied to secondary effects of what the primary genetic disease does to the liver to alter its function.  If one looks at FH patients and their VAP results one sees a pattern of chronic gut inflammation that is the real source of the atherosclerosis that causes higher incidences we see in FH.   These patients all have altered gut biofilms and some of the lowest levels of Vit K2 and vit D.  They also have extremely low DHEA S and pregnenolone levels are pointing to a chronic inflammation......due not to the high cholesterol level but to an altered gut axis.  Read my blog on this here.    http://jackkruse.com/your-vap-brain-love-not-war/   My views on this topic are radically different because even with severe LDL lowering treatments the disease patterns these people face remain unchanged.  Why?  because their gut remains the source of the inflammation that damages their arteries for their entire life.  We need to focus our efforts on the gut side of the equation and not the LDL side.  Ironically Dr Davis has done this with his assault on wheat.  Wheat drives sdLDL via what mechanism?  It screws up the liver and increases gut permeability to cause issues.  His current ideas and mine are very close.......but no one is tying this together.  I think my VAP post on the gut provides you the link.

Genetic high total cholesterol is related to the over 50 amino acid variations of PCSK9 (pro-protein conertase subtilisn/kexin 9,  which comprises 692 amino acids). Individuals producing an excess of PCSK9 more extensively degrade their cholesterol receptors with surface defects; and so don't readily take up LDL out of circulation, which lets blood levels of LDL rise higher. Conversely, those making sparse PCSK9 can't degrade their LDL receptors, which pull lots of cholesterol into a tissue cell where it can pile up over time in that cell's lysosome; and blood levels of LDL seem to drop.


PCSK9's worst version is D3744; where total cholesterol trends to 4 times normal and risk of death is estimated to be even +/- 10 years sooner than even other problematic PCSK9 genetic variations that affect maybe 1 in 500 westerners and account for +/- 5% of all pre-mature coronary heart disease. As regards the "older" age survival ability of those with familial high cholesterol  this may be due to the way over time plaque holds less lipid content and acquires more collagen with calcium infiltration. In other words younger plaque is less stable and more likely to burst free and be perilous.

If fretting about plaque be aware that the average duration of carotid plaque is +/- 9.6 years; according to Carbon 14 dating from autopsies. Plaque may even form multiple times during one's life and the statistically dangerous symptoms take 5 - 15 years to manifest. Increased levels of circulating plasma insulin accelerate the rate that plaque forms; and also adds to a plaques instability (ie: potential to rupture) due to insulin's interaction with genes involved in the immune response;  like how those with insulin resistance make more pro-inflammatory cytokines. This bolsters Doc Davis' insistance to control glucose, since the down stream result is a more stable plaque.

Noteably, there is the so called "protective cytokine" TGF beta which can allay plaque rupture. This is hard to predict for individuals because we have no way to assess who has what types of TGF beta receptors around , since normal and then plaque ridden blood vessels can harbor different TGF beta receptors. TGF  is considered a vital player inside vascular smooth muscle cells because it forms part of the interactive sequence that stops the smooth muscle cells from altering; and it bears mentioning that excess cholesterol can inhibit some TGF beta pathways.

For those who asked (Jack Kronk, Peggy, et.al.) about where and how one can get tested for ApoE it's simple:   Virtually any large commercial lab in the U.S. can do the test, e.g., Labcorp, Quest, etc.   Also, Atherotech (VAP) and Berkeley Heart Labs will do the test as well.   Since it's a genetic test, it's only run once during a person's lifetime.  The test can run anywhere from around $100 on up, depending on which lab runs it for you.

In my last lipotropen test, I do not absorb chol not do I make it.  Am I a closed system?  My lp[a] is 41.  I am very puzzled.

Dee

That was from the Boston Heart lab.  I am a AP03/3.

Super interesting!

Do you know what SNP is PCSK9 ?  I'd like to look up it in my 23andme info.
Thanks,
George

Plasma PCSK9 levels correlate with cholesterol in men but not in women
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


Janice Maynea, , , Angela Raymonda, Anna Chaplinb, Marion Cousinsb, Nadine Kaefera, Charles Gyamera-Acheamponga, Nabil G. Seidahc, Majambu Mbikaya, Michel Chrétiena and Teik Chye Ooia, b

aHormones, Growth and Development Program, Ottawa Health Research Institute, The Ottawa Hospital, University of Ottawa, Ottawa, Ont., Canada

bClinical Research Laboratory, Division of Endocrinology and Metabolism, Department of Medicine, The Ottawa Hospital, University of Ottawa, Ont., Canada

cLaboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Que., Canada

Received 29 June 2007.  Available online 18 July 2007.

Abstract
Proprotein convertase subtilisin kexin-like 9 (PCSK9) is a secreted glycoprotein that negatively regulates low density lipoprotein receptor (LDLR) levels. Several single nucleotide polymorphisms (SNPs) in PCSK9 have been linked to autosomal dominant hypercholesterolemia (ADH). Conversely, hypocholesterolemia associates with both ‘loss of function’ nonsense and missense SNPs in PCSK9. We examined the association of plasma PCSK9 with lipoprotein parameters in 182 normolipidemics. For men (n = 98) plasma PCSK9 averaged 6.08 ± 1.96 μg/ml and Spearman analysis revealed significant correlation between it and total cholesterol (TC), LDLC, and TC/high density lipoprotein (HDLC) (r = 0.276, 0.282, and 0.228, respectively). For women (n = 84) plasma PCSK9 averaged 6.46 ± 1.99 μg/ml having no correlation with TC, LDLC or TC/HDLC. The ratio of plasma PCSK9/LDLC increased in men carrying ‘loss of function’ PCSK9 variations. Our results suggest a gender difference in PCSK9 regulation and function with PCSK9 correlated to TC and LDLC in men but not women.

Keywords: Plasma PCSK9; Loss of function; Hypocholesterolemia; Hypercholesterolemia; Single nucleotide polymorphisms

Article Outline
Materials and methods
dI found this on the internet, I'm not sure if this is what you need?  

Dee

All patients with FH need to have their thyroid optimized.  This issue was hashed out at the Ancestral Health Symposium on August fifth at UCLA.  Jack Kronk's VAP is helping many patients learn how to raise their HDL to increase endotoxin clearance from the portal circulation to prevent oxidation of slow moving cholesterol because of A lack of their LDL receptor.  Thyroid optimization can overcome this to a degree but it requires a physician who knows precisely how to do this and not create an unsafe situation.  Their diets has to be a strict low carb moderate protein paleo diet high in coconut oil.

This too can be assessed by looking at thyroid beta receptors......it is associated with down regulation or resistance of this specific thyroid receptor.  A company in Denmark has a clinical trial on going about this specific receptor.  Thyroid hormones bing to both thyroid alpha and beta receptors.  But disease that affect the LDL receptors seem to preferentially knock out the thyroid beta receptor.

I apologize if I sent the wrong ifo.  Didn't read it through.
Dee

Dr K. -

I am inquiring with the my Doc about getting tested for ApoE. I will let you know how that goes.

Regarding hypothyroidism, yah the issue that I'm running into is that "it requires a physician who knows precisely how to do this and not create an unsafe situation".

This is the problem with our medical system in America. I live in San Diego, one of the biggest, most advanced cities on earth, and I am having trouble finding anyone over here that can truly help me with this. My doctor situaiton is pathetic. Sorry to say that, but I'll call a spade a spade. All they want to do is put me on Lipitor and go low fat whole grain. So then I am stuck with doing my own diligent research, and appyling knowledge that I can learn from people who actually know what they are talking about, and right now, for me, that means the internet. Incredible when you think about it.

When you say low carb, do you mean no starch as well, not even potatoes? By the way... the name of this post is "The Exception to Low Carb". So... that's why this is so confusing. Some very knowledgable people think it's best to raise my intake of starches and lower my fats. If my body is creating more LDL (even small dense) because of my saturated fat intake, then it makes sense to replace sat fats with something else. I already get enough protein, so then I am left with carbs. If it has to be carbs, isn't safe starch my only real option? It can't be 'sugar'. It can't be 'fructose', or grain starch, right? Should I eat loads of salads? Or I am on the wrong track completely? Should I look at upping my mono fats in place of saturated, like using mac nut oil for cooking? Or would mono fats be just as problematic?

You see? Honestly, I know this stuff stone cold. I know what *most* people do well with, but if we don't figure out how being pre-disposed to having issues with LDL receptors really changes things, we are going to (deservedly) get hammered by the low-fat whole grain camp when a fair amount of people who thought they had it all figured out are dropping dead from eating fats because they are ApoE and had no idea.

I'm genuinely glad that my example is helping people. No doubt I am. But I'd be alright with feeling like I'm getting somewhere with all this in my personal case as well. At the moment, I can't really say that I feel that way just yet.

Patients with apoe4 have a higher rate of AD and AD is associated with a cholesterol deficiency in the brain.  So for me apoe4 is a signal to load with the MCT of coconut oil which has massive benefits to the brain metabolically.  I find it hard to believe this is bad for the heart at any level because CAD tends to mirror CVD across all measures.  I think only cardiologist have this problem with Larger particle LDL because of the faulty lipid hypothesis.  cAD is an inflammatory condition.  It ha little to do with cholesterol itself.  If the cholesterol is oxidized then there are issues but this can be followed by acute phase reactants from the liver like HS CRP.  When it's up HDL tends to be low......and it's low because the liver is being bombard by gut endotoxins and this is a direct measure of the oxidation potential of an overwhelmed portal circulation.  To further the point......thyroid hormone, testosterone, estrogen, and high vitamin D levels all raise liver HDL and this is how they protect against heart disease.  I maintain large LDL confers no risk without inflammation.......and a low HDL is a great way to know if your liver is being overwhelmed in the portal circulation.  This is why vitamin K2 confers a great cardiac benefit.......it comes from a healthy gut biome.  vAP tells you a ton about your portal circulations inflammatory burden.

M-Al, just copy your text prior to the post, or write it in the editor. I don't know which browser you use, but in Chrome if you use "back" on "server error", it will return what you typed in a reply.

Following your diet I took an NMR last summer and this summer.  The small LDL particles went down (835 to 709) but the total particles went up (1800 to 2100).  Should I stick with your diet (low carb, no wheat, D, omega3's), one Walmart glucometer) or go back to rice and beans?

I got quote at $390 for just an ApoE genetic test. Is that normal?

Have you seen any reduction in your LDL following this diet?

I've been eating paleo/primal for about a year, dropped 10 pounds, and brought my triglycerides down from a high of 325 three years ago to 130. Unfortunately, my LDL-p is over 2600 (first time it was checked), and I found out I'm APO e4/e4.

The doctor says e4/e4 should go vegan, which seems about as anti-primal as you can get.

Any suggestions for where to start looking for eating guidelines?

My goodness, how very confusing!!  I'm hypothyroid.  My HDL is 95. My total C is 285. Ny LDL is 186. But my LDL fractions are mostly big and plumb and my small total 23. So, I think I'm ok...buy my doc thinks I should go vegan. I want coconut oil, little red meat.  I evercise 5x week. My heatt stress tests were all 'well within'   So, it sounds as though I need to get the E4 tested   More?

I would be deeply grateful for your advice. I am doing my best to understand how to cope with my aPOE 3/4 status. I have Alzheimer's on both sides of my family, which has killed or is in the process of killing several relatives, including my father and maternal grandmother. Unsurprisingly, I have received much conflicting data.

I am 46. I eat a strict Paleo diet (grass-fed, wild-caught, etc.) except for some resistant starch in the form of parboiled rice and unmodified potato starch. I consume approximately 50-60% fats (majority saturated fats including daily MCT oil), 30-40% protein and 10-20% carbs. I exercise vigorously and non-vigorously -- but not every day. (Incidentally, over three years I naturally increased my testosterone by 38% using this approach, going from the low 3's to 5.3.)

My LDL is 128. My HDL is a distressingly low 33. Triglycerides are 59.

MY NEXT MOVE: Seek out an LDL particle-size test. If that reveals my LDL particles to be of an unhealthy size then I will need to consider a different approach in regard to sat fats. Also, looking  to improve my sleep, which has been my Achilles' heel (consistently get only around six hours). Finally, using super-consistent exercise and increasing oyster intake to boost the HDL.

I would appreciate any guidance.(!)

Best / Mario

A similar experience happened to me. In my case I had a stroke, a triple bypass on my left coronary artery, a stent the size of Rhode Island on my right coronary artery, all preceded by v-tach.

It was a near death experience and surprizingly enough, I never had a heart attack. I am in my mid-50's and very fit when this happened and it wasn't until my final meeting with my Heart Surgeon where he asked, "how did this happen?"

Not one Doctor previous to that asked me why I had heart disease. I had an answer yet nobody bothered to ask.

I refuse to take a statin. When medicine has an answer for LpA I will be all over it!

Awesome essay, Dr. Davis.

Question: How could this be improved upon via Medical Education? It appears to be a deeply-seated cultural problem, aside from the prevailing financial reasons for why we treat instead of prevent:

"In other words, the prevailing community standard is to stent, bypass, prescribe statin. It is not to understand why the disease occurred in the first place, correct the causes and minimize or eliminate any future danger or need for procedures."

In other words, is there a cultural / professional development approach to (partially) attacking this problem; or, is our maligned financial landscape the sole culprit that must be changed?

Thanks,

Brent

My fiance's dad is being treated in a similar matter. Unfortunately, he won't listen to her or info that I've found and modify his diet much. He also seems highly sensitive to Niacin so won't take it all anymore. Fish oil and Vit. D3 are no starters as well. It really saddens me how people could make simple inexpensive changes and improve their health and yet they don't due to lack of information or unwillingness to believe or make change.

This is exactly my story. I'm 49, heart attack and stent in rca in May, script for 80mg lipitor and plavix. Heart Association diet, etc. and see me again in 6 months. When I googled lipitor, I ended up here eventually. Thank God. A goldmine of information and advice and pointers to many other resources. Thanks Dr.Davis for providing this service to the public. It should be required reading for anyone in cadiology, and all their patients as well. One day when time permits I'll post my entire experience, maybe it will help someone else. Thanks again.

OMG! that's not good. why most people heart disease is the problem? I think this kind of disease will happen to those people who are working in offices and no limit in oily foods.

Absolutely!   There is a very simple and effective defense against this kind of new medieval "culture" you have described - science and reason.

I am surprised how little of that is being used or taught.

Stan (Heretic)

This totally rings true with many and/or most of my personal experiences with the medical profession. Many doctors seem to be only interested in treating the symptoms, not getting at the underlying root causes.  When I've pressed them on the issue of cause, I've gotten vague answers along the lines of "sometimes these things just happen, and you have to learn to live with it" (direct quote from an ophthalmologist recently).  It's hard to determine whether they don't care, or don't know, and won't admit it.  
I wish there were more sources available online such as Ratemds.com where you could get info on a doctor before you see them - it seems I can be better informed about the company coming to clean my carpets, than the doctor who may hold my life in their hands.

Hi, Brent--

I think that change needs to come from several directions, including changes in education and attitude.

However, I believe that the quickest way to change the system is for patients themselves to agitate with their doctors and express their dissatisfaction with their care. The system still supports 2nd and 3rd opinions and free-market access to doctors who try to do better.

I was on that merry-go-round. Age 54 and had my 1st stent. My cardiologist came into my room and told my husband "I fixed her." Funny, he did not say that when he did #2, #3 and #4 stent. He did once mention that my heart reblockage was probably due to inflammation, but no one was looking for the source. Not surprising I went on to have bypass.

I have noticed that doctors seem to be focused on diagnosis. They want to give a name to the disease and then there are evidenced based treatments to do and prescribe. What is missed is looking for underlying causes. CAD may be a diagnosis, but it does not reveal anything about what might have caused it. When my doctors looked at my heart, they saw a plumbing problem. When I started looking at my heart, I found low vitamin D, low B12, low folate, low B6, hypothyroidism, hypertension, insulin resistance, gluten sensitivity, belief that trans fats were safe, low fat/high carb AHA diet and probably low EFA's. Slowly I am figuring out how to truly improve my health.

Physician are rewarded for procedures. There is little money in counseling a patient about diet and lifestyle. Nutrient levels are rarely tested. Patients too often want the quick fix and are unwilling to make lifestyle changes.

Forgive me for this--but what is heartbreaking are the infants and children I transcribe consultation letters for.  And this is for a large Eastern children's hospital, pediatric cardiology department.  The doctors are true believers, are genuinely interested in helping their young patients, and deal with heart disease and anatomical problems, but still the families are referred to the dieticians and the low-fat diet.  Some conditions are prescribed Gatorade and salty snacks like pretzels...carbs, but perhaps some electrolytes in fluid and/or fluids and just plain salt might help (I am only a transcriptionist, obviously not a doctor) but I transcribe consultation after consultation where I wonder what lies ahead for these youngsters when the heart disease you address here piles onto their congenital problems because of the dieticians and cardiologists' take on how to treat.  They have saved many an infant or young child though but that is not the whole picture.

A friend who was moving Labor Day weekend in 2004 developed chest pain and tachycardia and so presented to the emergency room and there was narrowing in two vessels (do not remember which ones), was stented (the cardiologist even went so far as to call the Italian cardiologist who had stented before in an awkward junction of vessels to get advice before he proceeded).  So my friend ended up with two stents and lost the house she was moving into, so I offered to have her stay with me.  She then suffered a heart attack---right at the stent where the "awkward junction" was.  So what caused this heart attack?  In my lay opinion, the cardiologist's approach to treatment is partially to blame here, but legally his treatment was up to the community standard of care.  My friend and I parted when I moved to another state but as much as i talk to her about sugar--she is addicted to cake and sweets, takes more drugs then I know anyone takes, has ignored the Vitamin D Cure I sent her, the Carlson's fish oil I sent, and the Carlson's Vitamin D3 I sent.  She is on statins/2, pain killers galore (I wonder why she hurts), antihypertensives/2, but she is on Armour thyroid.  Still thinks that cardiologist knows what he is talking about.  I have tried.

I went for a cardiology workup as I have some blockage in one artery. I was prescribed Crestor, and told to eat some tuna once in awhile.  Not even close to what I know to do already, thanks to the Track Your Plaque web site information.

Dr. Davis,

PLEASE stop stereotyping dietitians as if we were all Stepford bots programmed to relay the same canned information.  Would you not take offense to me categorizing you as a typical doctor who knows nothing about preventative care, prescribes medications only offered to him by pharm reps, and adheres to everything the AMA decrees?

Perhaps instead of blasting us, you could encourage dietitians to build on their knowledge and training base by providing some resources?  Maybe offer seminars?  Research?  

Also, how do you expect us lowly dietitians to make radical changes when the cardiologists and other docs we work for have limited knowledge and certainly no support for dietary intervention and non-pharm therapy?

Hi, Tara-

You are absolutely correct.

A good friend of mine is a dietitian. She eats no wheat, cornstarch, or dairy. She's slender and has corrected a complex lipid abnormality with her diet.

So there are good dietitians and there are plenty of "Stepford bots." Sadly, most are the latter.

I absolutely agree that my colleagues are failing miserably in delivering intelligent preventive nutritional care. So don't yell at me; yell at my colleagues and your colleagues.

Hospitals employ dietitians. How many dietitians are willing to go out on a limb to buck current,dated, nutritional recommendations?
Wheat? C'Mon! They must go with the flow.

There is a similar "neglect" following treatment that may be quite widespread.  I was treated for depression and after the prescription medications were over, I was 25 lbs heavier.

I asked the prescribing psychiatrist what to do to get the weight off, and he said, "Go on some kind of diet, I suppose".

I then and now consider this response inappropriate and inadequate and unprofessional.

Same here in Sydney. MI in June, five stents then discharged with paltry dietary advice and the usual list of poisons. Only by searching the web was I able to find sites like this and advice that made sense. Needless to say its over the counter treatment all the way for me now.

Still unsettling having to steer a course on my own. None of the medicos I've spoken to have been willing to consider a programme for being healthy, they just want to treat me

Super informative wriitng; keep it up.

At last! Someone who unedrsatnds! Thanks for posting!

HnAd8V , [url=http://ycrmvcyplpfr.com/]ycrmvcyplpfr[/url], [link=http://gykunjxbxkja.com/]gykunjxbxkja[/link], http://bingzdlwberl.com/

Dr. Davis,

You mentioned gelcap VitD. Isn't the liquid form administered via dropper easier to take, and better assimilated?

Would Pres. Clinton have the courage to go against the grain of conventional wisdom? I don't know the answer to that question, my hunch is that it is just "easier" to get treated then to take charge and responsibility.

My sister 46 (highly highly educated) will not listen to me at all. Won't even take the time to read some of the resources I point her to. Result? She just has been put on beta blockers for high blood pressure and a heart that beats to "fast and erratically" (her words)

Thank you Doc., for the wealth of knowledge and information you so freely share.
Have a great weekend.

Marc

Thank you for this post!

I am getting so tired of the pontificating statinators who practically blame the patient, or say there is no cure for heart disease, this can't be arrested, interventional cardiology is the only way, etc., while they either withhold the vital therapies you mentioned, or worse yet, don't even KNOW about them.

I just keep wondering how such a smart guy can have so little intellectual curiosity about the origins and ALL the modes of treatment of the disease that has come to rule his life.

Each of his events is a teaching moment, but unfortunately, what is being taught is intervention oriented, not oriented to stopping or reversing the progression of his disease, and that's just a pity.

Dr. Davis, you are a voice in the wilderness. Keep on Tracking, because many of us ARE listening, even if Mr. Clinton and his doctors aren't!

madcook

Dr. Davis:

Re: Vitamin D, why do you recommend only the gel capsules and not the liquid drops (Carlson's drops are in coconut oil I believe)? Much thanks, great great blog.

-Kyle Schneider

Great post, Dr. Davis.  Just about everything one needs to know to avoid heart disease all in one short list. Should be read by everyone. Thanks for taking the time to put it up.

Dr. Davis, it would appear that people with heart disease risk fall into two categories.
1. Metabolic Syndrome: High TG, low HDL, high fasting glucose etc. In these people small LDL is very high contributing to heart disease risk.
2. High Lp(a): These people may not have high blood glucose levels yet because of their high Lp(a) levels they are at risk for heart disease.

Mr. Clinton's triglycerides were at around 53 many years back. While he clearly has coronary artery disease he does NOT appear to exhibit signs of metabolic syndrome, i.e. high TG, low HDL, high fasting glucose etc. There are many people in this category that do not have metabolic syndrome yet show advanced coronary artery disease (possibly due to a high Lp(a) level).

Now Dr. Davis, you have stated that one of the ways to track small LDL and other risk coronary risk factors is to track blood sugars. However, in Mr. Clinton's case it appears (from his TG numbers) that both his fasting and possibly postprandial glucose levels are reasonable. His small LDL should thus be reasonably normal. He may very well have significantly high Lp(a) levels which appear to be independent of whether a person has metabolic syndrome. Therefore in Mr. Clinton's case heart disease appears to be a result of a high inherited Lp(a) than his value of small LDL.

Please correct me if you disagree with any of the above.

It is a sad testament to cardiac care in the U.S., but I  completely agree with everything you commented on. I would be willing to bet that at his last check-up he was told he was doing  well and everything was fine.

I wish you could do a Q&A session with his cardiologist and we could see just what had been done or not done.

Thanks for posting this. I'll print it and show it to my father.

Slightly off topic, but I took advantage of Porter Hospital's $99 CT scan special since four generations of my family have had strokes. They seemed confused because I didn't have a doctor's order for the scan.

I bet he trusted his heart to Lipitor, or some such statin, and presented with a nice low LDL-C of 105.  That is the average LDL-C of people hospitalized for heart issues (see G. Fonarow et al).  (I am not saying the statin didn't help him, but it ain't the be-all and end-all, and neither is low LDL-C.)

Further in the direction pointed by Dr. Davis, I bet bubba's triglycerides are consistently well over 100, suggesting issues with carbs.  So, eating low fat would lead him (like others) to higher carbs, leading to where he ended up.  Probably wheat -- "healthy" whole wheat -- in particular.

I hope he was taking niacin to do what help he could to HDL.

I'd be interested in your thoughts on this recent article in The New York Times, particularly regarding calcification in blood vessels:

excerpt: "The scientific community continues to debate the optimum level of vitamin D. In general, people are considered to be deficient if they have blood levels below 15 or 20 nanograms per milliliter. But many doctors now believe vitamin D levels should be above 30. The ideal level isn’t known, nor is it known at what point a person is getting too much vitamin D, which can lead to kidney stones, calcification in blood vessels and other problems."

Celebrity medicine -- a celebrity gets the most esteemed doctors, but they may not be the best.

April 14, 1865 -- Lincoln was shot in the head with a low velocity bullet.  His celebrity doctors then went probing around in the wound.  He died.  The case has been made that Civil War battlefield doctors had learned not to probe a head wound, and if Lincoln had been treated by one of those doctors there was a decent chance he could have survived.

Dr. Davis and other preventative cardiologists are the battlefield doctors of the current generation, desperately seeking that which works and rejecting that which doesn't as fast as possible, in the midst of the carnage of heart disease.

An old article of Clinton's health report just before the 1992 election:

TC: 184
TG: 59
Normal BP
Normal treadmill ECG

http://www.nytimes.com/1992/10/15/us/1992-campaign-candidate-s-health-doctors-call-clinton-healthy-campaign-offers.html?pagewanted=1

Tell us more about thyroid normalization, please?

"Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. "

Mr. Clinton, like me, has very pale skin that is not well-suited to the tropical sun.  I recall reading that either the Norwegians or the Swedes had very high levels of D owing to fish consumption.  I supplement with D, but my Irish ancestors did not, and they didn't get much sun either.

MAGNESIUM. Thats what fmr prsident did not do. Did not take 500mg of Magnesium Oxide daily. With all the above he would have had his heart problem anyway. But not with Magnesium. Wigh is the mineral that his metabolic Type does not handle well. Cops of GENETICS.
www.ludwigjohnson.blogspot.com

MAGNESIUM. Thats what fmr prsident did not do. Did not take 500mg of Magnesium Oxide daily. With all the above he would have had his heart problem anyway. But not with Magnesium. Wigh is the mineral that his metabolic Type does not handle well. Cops of GENETICS.
www.ludwigjohnson.blogspot.com

Today the PMRI (Preventive Medicine Research Institute) announced:

"Dr. Dean Ornish will appear on the Larry King Live show on CNN tonight to discuss new findings in heart disease."

No doubt that he will be asked about his take on Mr. Clinton's situation.  I would hazard a guess that it will probably involve advocating an extremely low fat diet, liberal amounts of grains, but perhaps there will be new input from the Doctor, i.e. those "new findings".

Hi Guys - Clinton's diet doctor is non else than "ultra low fat" Dr. Dean Ornish!

A couple of years ago, the pastry chef at the White House published a book about his 25 year experience. I have heard that in the book he said Pres. Clinton was allergic to wheat and chocolate. I wonder if he has been sticking to a wheat/gluten free diet? Of course if you have a pastry chef, sugar intake is probably very high.

I am working hard to make my bypass my last heart procedure. I am 10 yrs out and doing great...I hope.

A Simple Health-Care Fix Fizzles Out

http://online.wsj.com/article/SB10001424052748703652104574652401818092212.html

Dr. Davis, did you get a chance to read this article?
http://www.cortlandtforum.com/Healthday-Article/section/955/?CID=8D70113C&NFID=P&articleId=635663

What is Clinton's homocysteine level??  That molecule, as opposed to cholesterol that is essential for health, is universally accepted as an artery structure corrosive and underlying cause of slowly building heart disease.

The ONLY therapy to reduce it is a multivitamin pill with high levels of  the B vitamins.  Nobody argues this, nobody.

So, they "bypassed" the problem areas but the disease process continues unabated.  This is the medical equivalent of bypassing Bin Laden by invading Iraq.

Clearly, the amount and the diameter of LDL are not the problem; it is what you put INSIDE the LDL emulsion globules that matters: omega-3 or trans fat, good or evil.  Also, LDL is a Trojan Horse for homocysteine.  

Clinton may be taking a statin to reduce the amount of LDL but that does not alter its composition or homocysteine level.  My independent take on cholesterol and homocysteine are here:
http://www.health-heart.org/cholesterol.htm and
http://www.health-heart.org/why.htm

Did Clinton take such multivitamin? Agree: a multi does not quickly repair existing damage but it slows the process of decline while some repair [first seen in fewer strokes] DOES take place.

Very opportune post Dr. Davis. I would like to have an idea to how much fish oil you have to take per day in order to keep your omega 3 Index above 10%. Just a practical example.

Some years ago, Clinton said he was following Dean Ornish's plan. He isn't much of an advertisment for the success of that.

Jeanne S

I wasn't aware that Dean Ornish was part of the Clinton picture.

It will be interesting to see what his comments will be.

Just as lungs would be removed to treat tuberculosis, or heart disease treated with removal of the thyroid gland, so low-fat diets like Dr. Ornish's need to be sent to the junk heap of failed practices.

The iodine suggestion makes me wonder if the push to eliminate table salt from diets is resulting in abnormally low iodine levels. Putting iodine in table salt was done to fix the problem of low iodine levels in the food that most Americans were eating. Eating lots of seafood will fix the iodine and omega-3 deficiencies.

Nice summary of things to do for a really healthy cardiovascular life style.   Specifically for Billy, I'm suggesting that his chronic is Wheat Allergies [beer and bagles].  All chronic inflamation is cause for any degenerative disease, certainlly cancer, cardiovascular, arthritis etc.  

Each person has to address their chronic inflammation--often it comes from the dirtiest part of the body, the mouth [some say the brain] both need to be well.

John McDougall, MD has written an open letter to Bill Clinton (one of a series over the years) regarding the care he receives from his intervention-oriented cardiologists.

I was absolutely right there with Dr. McDougall... well until the last two paragraphs, where Dr. McDougall gets to the point of his letter and advocates a "healthy low-fat diet" like Pritikin, McDougall, Ornish, or Esselstyn.

OHHHHH... I thought Mr. Clinton HAS BEEN on such a program... under the tutelage of Dr. Ornish, who as much as said so on the Larry King program the other evening.

Dr. McDougall makes some very strong points regarding the interventional care Mr. Clinton has received and will continue to receive... it's just that extremely low-fat, vegetarian to veganish focus where we diverge.

http://www.drmcdougall.com/misc/2010other/news/clinton.htm

Happy Valentines Day... may all our hearts be strong and healthy!

madcook

Interesting comments, thank you for including the homocysteine and B vitamin perspective, and usually the allergy to chocolate is milk not the bean.    Bill should definitely eat more fish and more curry foods for the Turmeric, COX-2inhibitor.  Mag Oxide is great diarrhea, does it even absorb?   Chlorophyll is a chelated Mg and rebuilds the mitochondria.  Concerned about Abd. fats and Metabolic syndrome--get you Free Testosterone normalized!

Re: wheat, it's curious to me that in northern India where people eat lots of wheat they have a fraction of the heart disease that they do in southern India, where people eat rice.  If anybody understands this, please reply.

Dr. Davis: Your comment about a possible link between higher Lp(a) and higher intelligence sent me on a very brief ego trip, as tests showed that I do have both, but a more rational explanation may be that those of higher intelligence are more likely to get engaged in their own health, search for answers (as the readers here do) and find out that they have a elevated Lp(a), while others may never know they have it. Also, the March 2010 issue of Men's Health has a positive article about a pro-cycling team's switch to a gluten free diet, a favorite subject of yours, thanks for the blog.

I would like to know more information regarding this statement;

"Lp(a) tends to be the province of people with greater than average intelligence."

Can you point me in a direction that would explain more about this?

Thank you,
JenE

Re North India:  They do use quite a bit of mustard seed oil in N. Indian cuisine.

http://www.ajcn.org/cgi/content/full/79/4/582

Mustard seed oil has antiarrhythmic omega-3  It is in that respect like canola/rapeseed .. or any brassica family seed oil [turnip, et al].

The northeners may also get more vitamin B12, allowing homocysteine to be lower, a MASSIVE problem in India, massive.  In New Delhi in early 20 year olds, homocysteine is about 3x higher than currently in Americans youth in their teens.

I second JenE's question re lp(a) - correlation with IQ. Thanks!

It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.