7 months ago I was dying. I was (still am) morbidly obese. I have GERD, hypertension,  sleep apnea, PCOS/insulin resistance, asthma, chronic back and skeletal pain. I could not walk across the room without severe pain and shortness of breath. I was afraid to do any testing or discuss this with my doctor because I knew that I would be prescribed a bunch of meds (statins, diuretics and BP meds) and sent to kaiser's group nutritional counseling to learn all about how six servings of whole grains and daily exercise would fix everything if I was "compliant".   I am not a compliant person . . .

I had amazing success with low carb 12 years ago--so successful that I conceived my second child despite PCOS (our first daughter was an in vitro).  But having a baby, working two jobs, and attending a doctoral program at night was a lot to handle, and gradually my diet fell by the wayside.

Returning to low carb was not as difficult as I imagined. I was still eating wheat and other grains, albeit in very small amounts within my 20 to 30 grams of carbs daily. While I felt better, I was still in a lot of pain and discomfort, still could not exercise.

I was reading everything I could get my hands on and eventually stumbled upon your blogs and Paleo and primal blogs to.   I decided to cut out grains, even my beloved oats. Even though I love baking bread, I was never a great bread eater, so wheat was actually easier to give up. And since I was already in low carb ketosis, it wasn't physically difficult at all.

I feel like a 1 ton cement jacket has been removed from my body!  My weightloss has stalled (looks like thyroid or IR is the culprit so I'm working on it) but I feel so energetic that on days I don't have time to exercise I feel restless to get moving. I can walk 2 1/2 miles and all of my chronic pain is gone. GERD is gone, I  haven't had an asthma exacerbation in since last winter, BP is normal. My post prandial blood sugars are good.

Most of all, LOOK AT THESE LABS!
Cholesterol  235  
Triglyceride  71  
HDL  79  
Low density lipoprotein calculated  142  

I know there's more work to be done (I'm going to get those triglycerides below 60!), but this is amazing to me considering I eat all the butter, cream, whole eggs,  animal fat, coconut oil, and olive oil I want.   I eat no grains or sugar, very occasional starchy vegetables, and a small serving of berries daily.  I feel like I have my life back. Thank you, thank you, thank you!

Very interesting stats and the controlled elements show their significance to the lipid profile. Wondering what the rest of your diet looks like. Are you primal or paleo, vegetarian, vegan? Do you drink fresh green juice daily?  Just curious....one concern I would have, in light of all the great things you are doing, eating out everyday with Asian-style foods leaves freshness, preparation, ingredients to someone else. I have found no matter how careful we are in our choice of a restaurant, eating out means eating off! I couldn't do it everyday.  It will be interesting to follow your diet changes and see what happens!  Happy 2012!

Hi Jan,
Context first:  my results may not translate to everyone, since weight is never a real problem as the 1st NMR results coincided with laboratory measured fasting serum blood glucose = 83 mg/dL & HbA1c = 5.4 (for comparison after 3rd NMR  HbA1c = 5.3 & then serum glucose = 88 mg/dL, probably a mild side effect from added high dose fish oil).
Asian restaurant lunch "specials" were chosen for  offering me a variety of affordable places &  menu variation to eat 7 days a week. It was to deliberately try to determine how well my lab results might hold up when have to partly yield responsibility &  dine in the world at large.
I  arranged all other meals to be one's that were nutritious,  yet  whose regularity could become factored around if the lab results from 1/2 year of  cheap lunches played havoc with my NMR  (or  glycation indicator HbA1c).  I  precisely wanted to avoid trying to micro-manage an unknown assortment of cooks who might be using a  bit of sugar, cheap cooking oil, starch for thickening &  flour to sometimes crust fish. The lunch meal's standard full cup of cooked white/brown rice was eaten to see if it made any difference to my metabolism (ie: fasting serum glucose).
I stuck with seafood dishes because I haven't eaten meat/chicken in over 40 years & have always had robust fortitude without those proteins. My breakfast & desert/snack protein preference is low/non-fat dairy casein (fermented milk solids with reduced whey - consistency of a pudding I can add anything to).
To establish a standard evening meal I found a olive oil based brand hummus to measure out as a known portion to make up into a nightly mixed vegetable salad (no additional bread/rice) that didn't whack my post-prandial blood sugar (tested once every 15 min. like Doc suggests & after 1 hour blood sugar just 2 units higher than pre-meal, with just 1 unit higher after 2nd hour of meal).
Green juice was not a part of these trials , so can't say if would affect NMR results. My budget for lab tests is empty so I am not experimenting to determine any other diet nuances now.

While Niacin is not a drug, 500 mg 3 times a day is excessive.

Recommend reducing Niacin supplementation to reasonable levels taking with everything else taken into consideration.

Mit:

So happy for you. I have recently found this site and been reading the info for a couple months now. Is the NMR that you get from ineedlabs the full NMR (beyond standards lipid test from local doctor) or is it a truncated version? Thank you for mentioning the site! Jim

Hi Andrew,
? How do  you attribute the rise in HDL those NMR demonstrated ?
My assessment of my carbohydrate intake during last 1/2 year was certainly not very low carb, but more like moderate . I tried to calculate daily carbs & figure a minimum of  100  to more commonly over 120 gr./day . But ,quite frankly , often as not  more likely at least 150 gr./day since ate couple lunches weekly of spicy asian food that chef's told me they  use some sugar as an ingredient (schechwan fish, 3 flavors fish, half a fortune cookie), starch for  cup of soup thickening& wheat for breading (outer fish crispy)  .
If I was moderate & not low carb I am at a loss to surmise how  that  made my HDL genetics  now re-programmed to going forward be able to provide me with (say) at least 60 mg/dL  if I cut back to 1,000 mg daily niacin.
Allow me to recapitulate this data:
NMR   with  zero (0)  niacin   HDL=45 mg/dL
next    taking     1,500 mg/d  HDL = 64 mg/dL
or   lastly           2,000 niacin HDL = 88 mg/dL  ( with no increase in fish oil, nor inc. in vit D supplement)
You echo Doc in cutting back the niacin & presumably this is to avoid over-taxing the liver - am I correct?
If  this orientates you opinion after 4 months on 1,500 mg daily Niacin I deliberately tested the standard liver enzymes;  showed  SGOT (AST) =  20 Iu/L & SGPT(ALT) = 17 IU/.  And, let me specify I think liver enzymes should  be checked by anyone regularly taking high  Niacin .
? Doesn't it seem that at least 1,500 mg/d Niacin is my individual safe dose ?

I'm a 38yo white male who experienced a nearly identical change to Mitochondri'Al's without reducing my carbs at all or changing my exercise routine. I'm taking 2,500mg/day of niacin with no side-effects apart from the flush (which I enjoy). My liver enzymes have remained stable and there has been no appreciable increase in homocysteine. Obviously Dr. Davis has infinitely more experience in this realm, but my suggestion would be to continue with the niacin. 1,500 is definitely a safe dose. Intuitively (and I STRESS "intuitively") I feel that it's better for me to take niacin and eat a moderately low-carb diet than to reduce my carb intake to the vanishingly small amount that Dr. Davis recommends. I have cut out wheat though and most grains. Really would love to reincorporate quinoa

September 2010
HDL 39
LDL 135
Triglycerides 149
These values had remained stable for 5 years, remaining unchanged in spite of diet and exercise changes. I won't go into all the VAP and NMR nuances (I've had both tests several times), but all the measures improved VERY dramatically...shifted from pattern B -->A LDL, more than quadrupled the "helpful" form of HDL (8 to 35), essentially eliminated IDL. CRP and Fibrinogen were fine to begin with and remained so after a year.

November 2011
HDL 87
LDL 89
LDL-P 700
sdLDL <90
Triglycerdes 40

My regime included:
* 2,500 mg/day nicotinic acid
* Vitamin K2
* Lovaza, 2 caps/day (I know Dr. Davis hates Lovaza because of the exorbitant price, but my insurance pays for it and I'm not going to shell out $$$ for a nonprescription fish oil of equivalent dosage)
* Metformin, 500 mg/day (I'm not remotely diabetic. My NMR IR score was 4. However, I wanted to take it as a general antiaging drug and to offset any possible blood sugar increases from the niacin.)
* D-3, 4000 mcg (or is it IU?)/day
* Deplin, 7.5 mg/day (to methylate any extra homocysteine from the niacin and metformin and to provide precursors for monoamine neurotransmitters)
* TMG (same reason as Deplin)
* Methyl B12 (same as Deplin and TMG; also I'm vegan and don't get much from my diet)
* 1 tablespoon extra virgin coconut oil / day
* I purchased a blood glucose meter and test strips. There's more postprandial fluctuation than I would like to see, but my glycated hemoglobin remains at a respectable 5.1. I'd like to get that down to 4.9.
* Had the battery of cardiovascular-related genetic tests. I'll only mention one: I'm an ApoE 2/3, meaning that moderate fat intake is indicated (versus low fat for 3/4s and 4/4s).

Hi Jim,
I think  ineedlabs authorized NMR is now sent through the  Labcorp system & so I got whatever Labcorp's NMR details; namely: "LDL-P,  LDL-C,  HDL-P , HDL-C, Triglycerride, Total Cholesterol, small-LDL, LDL size" & also some suggested interpretations Doc says he ignores. Standard old type of lipid test is not  the same as NMR lipo-protein profile , nor  is the  VAP type of lipid test some get.

@ Mitochondri'Al

I had my liver enzymes tested pre-niacin and have repeated the test 7 times. There has been no change. From what I've read it's people taking the extended- and sustained-release formulations who develop liver issues. Immediate-release niacin doesn't seem to affect the liver much.

Hi Jacob,
I daily eat a good cooked handful  (trying to get beyond need to micro-manage all  portions of ingredients)  of low salt canned red beets into my night time hummus salad.  So, maybe that betaine has been enough to neutralize the homocysteine  you just informed me arises from high dose niacin. I have split niacin in 1,000 mg with morning dairy quark & 1,000mg  with evening meal; flushing has long been minor, aside from reddened face I splash with cold water if think anyone will freak out.

Since you are the first to suggest blood sugar may elevate from taking high dose niacin this is also intriguingly new to me. My understanding is that it is high dose fish oil that Doc's protocol leads to higher blood sugar. When I introduced high dose EPA/DHA fasting serum glucose went from 1st 83 mg/dL  without fish oil after 4 months on fish oil to 88 mg/dL. Of course I  did start fish oil at the same time as  the niacin, but when I kept fish oil constant and varied upward the niacin (from 1,550 to 2,000 daily) for that last 1/2 year  experimentation my fasting serum glucose stayed at 88 mg/dL. Which  implicates fish oil is the controlled factor provoking 3 mg/dL more fasting blood sugar.

Doc recently trashed the NMR's derivative chat; but  if  other's have noticed the category "IR score" I'll mention lab 1st gave me an "Insulin Resistance Score " (IR) of 45, 2nd test rated an IR score of 4 and then last NMR put me at 1.  But I am inclined to think many other readers may be more prone to overweight & they  may find it extremely helpful to go with Doc's  "very" low carb to see  lab results he aims for them to achieve if their genetics of blood glucose and lipo-protein are not as favorably responsive as mine seem to be.

@Mitochondri'Al...

The hyperglycemic effect of high-dose niacin is very well documented, though in my case I don't think it had much of an effect. Even in diabetics, the consensus seems to be that the benefits of niacin outweight any associated blood sugar increase. Like you, I didn't go into this with a weight issue. I'm ~5 pounds lighter than when I began this regimen (5'10'' 152 pounds now), a change attributable entirely to the Metformin.

The rise in homocysteine from high-dose niacin has something to with niacin's action depleting the available methyl donors. I don't think beets will provide anything approaching the amount of TMG necessary to methylate excess homocysteine back to methionine (which is a SAM-E precursor...oh happy day). I take about 3,000 mg/day of TMG. It's an inexpensive supplement, and I'd rather be safe than sorry, as homocysteine can make some major mischief over time in the vascular endothelium.

I didn't know about the fish oil / blood sugar connection.

FYI, I don't know if you're familiar with the study in which participants taking vitamins A and C with niacin showed a much-reduced--in fact, practically negated--effect of niacin on blood lipis versus those not taking A and C. No further investigation took place, and the mechanism (assuming this finding is valid) remains unknown. As a precautionary measure, I drink my vitamin A - rich green juices and take my C supplements at least a few hours before or after taking niacin.

BTW, I've read in several places that effects of niacin can become MORE robust over time, which squares with the steady increase in HDL and the HDL-2 subfraction I've observed over the last year, as well as a decreasing LDL value and increase in mean LDL size.

One anomalous thing I've noticed is that my lp(a) reading on VAP tests has increased from 4 to 17, but the test for lp(a) alone has remained at the minimum value. I had a VAP today and will be getting the lp(a) monoassay on Wednesday. If this strange discrepancy shows up again, I'm going to call Atherotech and LabCorp and ask them what's up. I did recently read a study in which blood samples from one or more patients were sent to Atherotech, Liposcience, Berkeley Heartlab, and one other company; there were striking discrepancies among the reported results from the four labs. Interestingly, of the four, Atherotech's VAP test was the least likely to characterize a patient as having Pattern A LDL; although, now that I think about it, Liposcience (NMR) doesn't even use the Pattern A, AB, B terminology, do they? Anyway, it's fun to share these observations with a group that actually is thinking about this stuff! I've posted all my blood panels to my facebook account along with what I did to achieve the dramatic changes reflected in the data. My friends found it all very interesting but only one has initiated a similar experiment.

outweight = outweigh

Why Doc's low carb may be more important for some more than others is these after meal events. He's pointed out that high after meal (post-prandial) blood sugar (glucose) are a problem because the liver will make that excess glucose into triglycerides (trigs). Some of us may also trend toward low trigs, despite any  post-prandial  glucose spikes, because of our constellation of genetic quirks in how the sequential triglyceride synthesizing enzymes play out their essential esterifying and hydrolyzing ( enzymes = glycerol-3 phosphate acyl-transferase1, 1-acyl-glycerol-3-phosphate-O-acyl-transfe​rase5 & 9, plus di-acyl-glycerol acyl-transferase2). I should stress that my non-low carb lunches were always followed by me walking around extensively on errands - so any contradiction inferred from my lab results (above)  with Doc's low carb preference may be explained by my immediate use of the post-prandial glucose in real time skeletal muscle activity  & not just my genetics.

Doc insists excess post-prandial trigs should be avoided because those trigs get cobbled into VLDL cholesterol and sent out from the liver. It is when the VLDL comes back to the liver without giving up most of it's trigs that confuses many people. This is because, in the specific context of post-prandial  VLDL, the molecule that brokers recycling entry into the  liver of that VLDL (whatever it's residual trig load) does so in accord with ApoE. (note: it is  not the same type of dynamic that happens with clearing our LDL.)

Curiously, it is the isoform variant of ApoE4 which can help get the most VLDL quickest into the liver cells; so ApoE4 individuals are shunting plenty of  VLDL in, for recycling, but at the same time plenty of  ApoE4 is also coming into that liver cell. Conversely, ApoE3 will be relatively slower clearing VLDL out of circulation & ApoE2 conformation is slowest in helping get returning VLDL into liver cells; which means, for ApoE2 there's more of a backlog going on in the blood stream of VLDL (& any of those post-prandial trigs our skeletal muscles didn't take up when trigs circulated by).

Once an individual VLDL complex is inside a liver cell it is subjected to an initial processing in a specialized compartment  (endo-some) of the cell that naturally lowers the pH in that intra-cellular compartment to break the VLDL complex apart for recycling. In response to that normal processing pH drop the ApoE4 molecule (as opposed to other ApoE isoforms) becomes more fickle; basicly  it's (ApoE4) molecular configuration is vulnerable to undergo changes like become globular gel, truncated in some sectors and open up it's hydro-phobic surfaces. In simple terms this means that re-cycling truncated ApoE4 won't move well in the liver cell's interior fluid matrix and hug the lipids it finds closest there more so than recylcled ApoE3 & ApoE2 does.

VLDL, thus will shed it's ApoE  and that ApoE will ideally move to another compartment inside the same liver cell to tag up with an HDL that has been taken up by that liver cell. One of the things this does for us is hold that ApoE molecule nearby, but where pH isn't going to drop. In this phase until the ApoE gets incorporated, as a component, into on of two cholesterol components. One is to put the recycled ApoE into fledgeling HDL that then becomes "mature" HDL sent out of the liver into circulation.. The other, less understood function (and purpose of this long explanation) is of stashing our VLDL recycled ApoE temporarily bound close by to an HDL (inside the liver cell) is to take & re-use it  (ApoE) reformulated with a VLDL molecule when the liver needs to send out any post-prandial trigs.

Doc's paradigm is preventative, meaning avoid lingering high blood glucose (hyper-glycemia) due to excessive single meal carbs and thus put less demand for ApoE to be cycled into trig loaded VLDL that might just come back again & again demanding the liver engage in futility. For those with degrees of ApoE4 variants there is slower teaming up of it to that helpful HDL inside the liver cell that normally pulls ApoE away from the cell's low pH compartment. Explicitly it is HDL itself that activates this key stage; it is an additional specialized function of HDL. I don't know if one aspect of having low blood level's of HDL is from when a person's stuck with high trigs driving them to cobble it (trigs) into VLDL  with ApoE and this stalls too much HDL inside liver cells performing an HDL function in there & not out as circulating.HDL.

Some theorize that by diverting so much ApoE  into post-prandial trig loaded  VLDL there is then going to be "mature" HDL going out of the liver that doesn't carry the ideal amount of  ApoE  to fully perform a cholesterol pick-up function for the HDL molecule while HDL is out in circulation. And  if one has ApoE4 being recycled, which is relatively slower to get over to any HDL in the liver cell, then the "mature" HDL will also go out with less ApoE to snatch back cholesterol.

Lost? ....We essentially don't want "fat" (lipid, like trigs) we may have made to build up in the liver. So,  if we can't get all the "fat" lipids we made out of our excess blood sugar (glucose) get sent out  of the liver as trigs tied to VLDL there is a backlog of trigs always hanging around in the liver . And then, because the process of  us making trigs potentially stalls at a transitional molecule involved called di-acyl-glycerol (please note, don't let this long word make you confused now: this is just being two "fats", since "di" =2 in a formation that is one step short of the well known  tri =3 "fats"  formation  of tri-acyl-glycerol , that everybody  calls tri-glyceride for short & I  lazily type as  "trigs" ). Anyway ending simply,  it is this intermediate "fat" lipid of di-acyl-glycerol  subsequently building up in the liver that triggers a cascade  (for geeks: protein kinase C ), which ends up involving  the receptor for insulin in that liver cell. This unwanted downstream phase of bonding to that insulin receptor blunts the next cascade (4 geeks: tyrosine kinase) and  then that step is more directly what contributes to liver insulin resistance over time (ie: insulin comes to liver cell but more & more insulin receptors being kept too busy) . This is the problem played out by  our "fat" lipids in a chain of events that individuals with excessive trigs risk getting stuck with. Doc warns us to  beware of carbs making you synthesize lots of after meal trigs from prolonged high blood glucose which then forces you to put out VLDL (ie: to try to reliably take trig load off your liver). Elsewhere he stated, in accord with current science, that it is post-prandial trigs that are the most insidious trigs.

Interesting about the postprandial trigs. I was unaware of their significance. Makes sense, though, given the relatively greater importance of the magnitude of postprandial blood glucose excursions versus fasting levels.

Your post conjured up images from long-ago courses on enzyme mechanisms, except without the fun electron pushing.

2011 Post-prandial trigs relation to cardio-vascular details at the link below will give abstract but click at box where says "The full text is free" in pdf. if inclined.
http://www.ingentaconnect.com/content/ben/cvp/2011/00000009/00000003/art00001
(titled) "Free Content Assessment and Clinical Relevance of Non-Fasting and Postprandial Triglycerides: An Expert Panel Statement"
Current Vascular Pharmacology, Volume 9, Number 3, May 2011 , pp. 258-270(13)

While not directly related to this thread I wanted to get this request out there. I am hoping that  some one can help me find a doctor that is following a similar or the same protocol wtih vitamin K2 etc. and diet as Dr. Davis'.
I was recently diagnosed with aortic stenosis and am looking for an alternative to valve replacement. I am looking for a cardiologist in the Greater Toronto ON  - Buffalo NY area.
Thanks in advance for any suggestions given.

@ Might
Sorry, it my comment is out of tangent, but as a long-time fan of you, I want to share a Russian recipe of a beet salad with you. It contains cooked (or canned) chopped beets, chopped raw onion, chopped  fermented pickles or sauerkraut, some potatoes cooked and cut in small cubes (it is possible to skip), salad is seasoned with mix of brine and olive oil (in Russia an unrefined sunflower oil is used).  Other things may be added like cooked cubed or shredded raw carrots, fresh cucumber ,celery, some herbs, maybe garlic.  It is often consumed instead of a potatoes salad, especially at winter time..

The lp(a)  measurement truly puzzles me. When I get the lp(a) monoassay it always comes back <2 (the minimum measurable) , but the VAP is all over the place (up to 17).

Hi GalinaL,
Thank you. Beets' nitrate are converted into nitrite in us to do all kinds of good things, as medical news reports.

Galina,
How about a Russian borscht (a beet soup, for those who are not familiar with it)? We had it at home recently, but I neglected to take my BG after eating, so will do it next time. It is hard to give up beets, but Might's comment about it is encouraging. I also surprised Dr Davis that such dish existed, when I saw him not long ago.

Borscht is a cabbage soup , with two main features - first of all it contains beets(obviously), second, very important  secret difference,  that it is seasoned , when it is almost ready,  with the bacon (fatty part) crashed together with some salt and couple garlic gloves. I use mortar and pestle, but it is possible to do crashing between wax paper sheets, plastic sheets, just make sure it looks more or less like a paste. There several recipes,
here is an example - use broth or  water, may be 3 - 4 cups, bring it to a boil, while water is getting into a  boiling, make sauteed veggies , fist put on a pan chopped carrots (1 big or 2 small) and parsley , then bell pepper, then chopped onions, when onions are ready - add  1 -2 tomatoes. Prepare garlic+bacon paste. Put 1/2 head of shredded cabbage into boiling salted water, when cabbage is almost ready, add sauteed veggies, let is quickly boil, add  the chopped content of one can of beets(beets must be added only after sour ingredient - tomato in that recipe) with the liquid and the paste, then  take it  from the heat, close with a lid.. Taste is better next day. I didn't mention herbs, possible vegetables to add, when to put salt. It taste very good with sour cream, chopped chives, even slice of a lemon in your plate..

There many variations, important thing - don't let it boil again after it  isready - it will change color and flavor.

Hi Jacob,
Lp(a) is a molecule with an Apo-lipo-protein B100 core like an LDL with protein ApoA bonded on it. The gene LPA encodes for the Apo-lipo-protein A & there are many genetic variations of LPA.

When the LPA copy # if greater the amount of gene driven expression going on is less. This is apart from  any SNP (polymorphism) of LPA & involves the number of reating domain(s), called  "kringles" (kringle IV domain). Basicly the more kringles the less genetic induced protein to build up into a full Apo-lipo-protein A. In Europeans +/- 60% of the variation in circulating Lp(a) is due to the peculiarity of kringle copy #.

The SNP variants (of LPA) have more relationship to the way that particular conformation of  Lp(a) might uniquely degrade and give off metabolic by-products that potentially can act against organ tissue promoting enough new blood supply (angio-genesis). If the heart can readily make new blood supply routes that is ideal & thus a specific genetic Lp(a) variant that doesn't stymie angio-genesis is not a cardio-vascular problem  - irregardless of that Lp(a) level.

You take supplements to restore homocysteine back into methionine. There is a specific LPA polymorphism giving one a SNP allele 4399 methionine (in substitution for the standard isoleucine amino) inclining those people to make +/- 6 times more Lp(a) than otherwise. I don't know if you carry that particular SNP, but if your rise in Lp(a) coincides with your protocol against homocysteine you may (?) be feeding  into
the LPA4399Met hand . Admittedly far fetched, yet methionine boosting is not always benign for longevity according to some investigators.

Vitamin A converts to retinoic acid in the body & this may ( ?) be more relevant. The Retinoic acid-related orphan receptor alpha (RORalpha) has 4 different variant iso-forms. It (RORalpha) is found in the nucleus of liver cells and responds to melatonin if you supplement with  melatonin as well.

Your RORalpha iso-form may also be prone to receiving activation when there is  excess vitamin A's retinoic acid reaching the liver. RORalpha activation gets it's  nuclear response element ( Rev-erba) to bind to DNA & this engages several genes. In other words liver RORalpha up-regulation greatly influences Apo-lipo-proteins A, as well as A"V"(5), & C"III" (3) put out by the liver - among other things (ex: carb processes).

Which, coincidentally, leads back to heart as per 3rd paragraph above....Hypoxia (oxygen low) also activates RORalpha, and thus Lp(a);  but one's LPA variant iso-form can give an Lp(a) degradation that acts anti(against)-angio-geneic. Then that heart's ability to get alternate blood supply  of oxygen to fall back on is limited; meaning the degree of  hypoxia damage done to any of that heart's cells becomes more problematic. Hypoxia isn't an all at once state of an all over or nothing organ-wide event.

Cardio-vascular problems are said to be an "inflammation" problem & the more pro-inflammatory Il-6 (interleukin 6) the greater upregulation of Lp(a) going into circulation. Doc expounds his low carb protocol cuts down inflammation marker CRP (C-reactive protein) & Il-6 is a big part of CRP dynamic.  By blunting  Il-6 (or if  fortunately genetically don't make or even receptor  much) there is less Apo-lipo-protein B being made that is an important part of  liver's VLDL formation. Consider, as an example,  that the drug "Mipomersin" acts to block ApoB synthesis with a side effect of lowering Lp(a).

Unfortunately too, high Il-6 is associated with lots of  triglycerides being made in the liver .  Having high Il-6 instigating lots of ApoB to cobble the excess trigs it (Il-6) provoked into VLDL  favors getting those Il-6 hyped trigs get sent out into circulation. Then too high Il-6 makes for lower rates of liver trig clearance from the trigs brought back by various lipo-proteins. D ue to the inflammatory  settting when the VLDL (with it's remaining load of trigs) comes back to a liver cell for VLDL re-cycling (detailed in earlier comment here)  it can't unload  & clear it's trigs  due to the co-existing high levels of Lp(a).

In other words,  induced to make lots of Lp(a) overactivated LPA gene means excessive ApoA. Since ApoA can also go where ApoE  can , the  molecule of ApoE that is normally designed to get free from the VLDL risks getting out-competed. Then HDL inside that liver cell doesn't mediate the movement of  stale VLDL's  ApoE as much (because busy with ApoA),  which creates a backlog of  freed ApoE in that  cell's endosome  forcing other returning VLDL ( with it's trigs & ApoE) stalled in a traffic jam.  And that HDL doesn't rush to leave the liver cell because it isn't getting normal ApoE chain of events making it a "mature" HDL; so circulating HDL level is paradoxically lessened despite plenty of  ApoA  around.

IL-6 meant by Il-6 (among other proof reading  mistakes )

Galina,
Thank you for this extensive recipe. I am tempted to continue, but it is not my blog. Maybe Dr Davis will find these Russian recipes good for the TYP program...

". There is a specific LPA polymorphism giving one a SNP allele 4399 methionine (in substitution for the standard isoleucine amino) inclining those people to make +/- 6 times more Lp(a) than otherwise. I don’t know if you carry that particular SNP..."

I don't. I'm 4399 Ile/Ile homozygous.

Also LPA-Intron 25: tt homozygous.
KIF6: 719 Trp/Arg heterozygous :-(  [[I don't want to take statins though]]
9p21: ag heterozygous at rs10757278 and gc heterozygous at rs1222049 [[I read a recent study indicating that a diet primarily composed of vegetables and fruits (and maybe nuts) almost negates the associated risk here, and that's how I eat. So, fingers crossed.]]

While Dr. Davis' website & blogs got me started on the path of getting off the statins, etc (thank you 1000 times!!!)...I believe we are over-thinking this and making it way too complicated.
Look at it from an evolutionary biology perspective (I just finished Food and Western Disease by Staffan Lindeberg, http://www.amazon.com/Food-Western-Disease-evolutionary-perspective/dp/1405197714) Our metabolic processes developed over the course of millions of years, being optimized by evolution all along the way. We ate meat, eggs, fruit, veges, nuts and did just fine. Then about 10,000 years ago we figured out we could stay put, not follow the wild herds and dig up food as much, and grow our food where we lived. Big problem...the food we decided to grow makes us sick (wheat, corn, rice). Not falling down, vomiting sick, but just a little at a time sick. We get fat, have strokes, heartattacks, high BP, diabetes, cancer, etc... aka Western Disease. But don't all the experts tell us to eat whole grain, and drink milk, and eat cheese, and use olive oil??? That's where the next problem arises...we don't know what we don't know. All the "science" behind good nutrition today is based on studies with many, many flaws. And, our metabolic systems are so enourmously complex, that we don't really understand how it works. If you look at people today, who still maintain a paleolithic diet (hunter / gatherer) you find that they do not suffer from Western Diseases. When they move from their ancestral ways to "modern" diets, they suffer like we do.
I've gone from a Mediterranean diet to a Paleo diet, lost 15 lbs in 7 wks without changing my exercise routine, stopped taking my statin, am eating less, sleeping better, and feel really good. And this coming from a lifelong semi-hardcore athlete, who at 45 got a stent in a coronary artery, and prescriptions for Plavix and Simvastatin. Two years later i felt like crap and decided it was time to do something different. First stop was DR. Davis' sites, then others. The blood work is coming in mid Feb to establish the first real data points.
Bottom line...eat what the cave man ate, get plenty of sleep, go outside in the sun, do some strenuous excercise, and quit letting your doctor feed you the Big Pharma line of BS. It's not easy. Nothing worth while is. But, as your body changes, so will your resolve to save your own life!
//DM9