I am often disappointed with "experts" that you see being interviewed on tv. It makes you wonder where they get these people. Do you think they would ever interview you if you offered? Maybe you could get on their list of experts to refer to.

Dr. Davis, Thank you for this posting!  My vitamin D levels were tested in early April at 17.  I have been taking citrical with vit. D.  From your post, this sounds like a bad idea!  Can you recommend a good brand of oil-based D3 capsules?  Also, how long should it take for my vit. D levels to normalize?  Thank you!

Ortcloud--
Thanks for the vote of confidence.

We've used Carlson's and Vitamin Shoppe's 2000 unit vitamin D3 (cholecalciferol) capsules with great results. It takes about 4 weeks to fully reflect the dose.

How about co-administering an oil along with a powdered vitamin D tablet or capsule? I would be curious to see absorption rates using this method vs. oil-based vitamin D.

Also does this low absorption apply to all fat soluble vitamins? In other words, must vitamin A, E, and K also be in an oil or oil-based to maintain optimal bioavailability? Thanks.

Including oil with a powder form of D does enhance absorption though in my experience it remains erratic.

I'm uncertain about the E and A, though I suspect the same remains true. I would really like to know how important this phenomenon is with K2, but I am not unaware of any real data, nor do I have sufficient experience to say at this point. With time.

After taking Prescription Vitamin D ( oil ) capsule for
3 month my levels were up to 50.
Now I am taking 1ooooIU's daily and my levels are down to 29. Does fish oil capsule interfere with the asboprtion of Vitamin D?
   Maria

Hi, Maria--

No, in fact fish oil should do the opposite and can increase D absorption. It might therefore be variation in your preparation.

I live in Canada and am on a perpetual 50,000 iu/week dose of Vitamin D due to low blood levels.

AFAIK only D2 is available in Canada, and the endo dismissed any negative comparison with D3.

What can I do ?

I've had no success lowering my very high LDL(350), can't tolerate statins..supposedly have combination of large and small LDL, 20-40% blockages per cardiac cath.My HDL (80), Trig.(70)are good, but still concerned since already show athrosclerosis. I'm 55, 100 lbs., and have had high LDL since a teen. Any suggestions? Thanks!

Isn't inflammation the root cause of atherosclerosis ? Isn't cholesterol's role in heart disease only that it happens to be used as the material, with which the body repairs the lesions caused by inflammation ?

excellent post. 1. if statins not preferred way to go for small LDL, what is- Niacin and elimination of grains? 2. How is it possible that a VAP test showed large Pattern A(by small margin)and two years later NMR shows nearly 100% small dense Pattern B?  Is one test better than the other? 3. Do genetics overwhelmingly determine pattern size?  I have eliminated all grains,sugars, starchy veggies to see if i can get my LDL to be large and fluffy.  Thank you.

I am an example of someone with "normal" cholesterol and CAD. I was only 54 years old when my LAD blocked. I went on to bypass as I reblocked after each stent.

In the past few years I have been looking into many of the other factors may have contributed to my  health problems and trying to optimize my health. Yes, coromary heart disease is so much more than elevated cholesterol.

No it doesn't!

Hi Dr Davis,

Excellent post. The value of total cholesterol is irrelevant. While there is a VERY slightly higher cholesterol level in heart attack patients, the overlap with the normal population is such as to make total cholesterol level meaningless. Once it's meaningless and you can then look back to the initial work of Ancel Keys, who appears to have been the primary architect of the lipid hypothesis, and you can see it is based on this now clearly meaningless measurement.

The very slight increase in TC in cardiac patients is explicable by the fact that glycation of the apoA particle inhibits its attachment to the LDL receptor. I would expect this to produce a slight rise in TC. You then have to pose the question as to which does most damage: persisting apoA containing particles due to glycation of their surface protein, or glycation of all of the body proteins by the same hyperglycaemia that affected the apo A protein. Using HbA1c as a marker of hyperglycaemia there is a reasonable correlation with CVD even within "normal" HbA1c levels in the EPIC study. Whole grains = hyperglycaemia. Hyperglycaemia = apoptosis of vascular endothelium. What more do you need for vascular damage?

So, as the lipid hypothesis is based on TC and should have been stillborn or drowned at birth, where does particle size come in? We have the situation of good (HDL) cholesterol and bad (LDL) cholesterol to explain why TC is useless. Then we get good LDL (large fluffy) and bad LDL (small dense) to explain why total LDL (by calculation) is utterly useless too. We even now have good and bad HDL. Never mind good (small) VLDL and bad (large) VLDL to explain why some triglycerides are better/worse than others.

Ultimately small dense LDL, large VLDL and HDL3 are strong markers of the metabolic syndrome. Hyperinsulinaemia and insulin resistance are the cornerstones of metabolic syndrome according to Reaven, who largely popularised the concept. The lipid changes are easily viewed as a consequence, not a cause, of metabolic syndrome. It is undoubtedly believable that sdLDL is stickier/more oxidisable than other lipoproteins, but that becomes unimportant if it's not there in the first place, ie no metabolic syndrome. This would, simply, explain why reducing wheat products works to reduce sdLDL, unless they are replaced by equally insulinogenic "wheat free" comparable junk foods based on non wheat sugar sources. If it turned out that purple spotted LDL, induced by eating blackberries, was stickier than sdLDL we would no doubt have a drive to eliminate blackberries or (more likely) develop a drug to remove the purple spots.

Following your blog gives me the distinct impression that one day you really could become a cholesterol skeptic. Stranger things have happened.

Peter

Anonymous and Steve - I stronly believe in a propper low carb (note that I say LOW carb, and not NO Carb) way of eating. I would really like to suggest some awesome reading material. It is from dr. James E Carslon who wrote the book "Genocide. How your doctors dietary ignorance will kill you!!!". In the book he explains amongst other things the actual benefits of dietary cholesterol and how a low-carb way of eating will increase the ldl-particle sizes and bring down the triglycerides and dangerous VLDL.

From a recent personal answer I got from him, he explained to me the benefits of adding dietary cholesterol from a biochemical point of view. I hope this helps in understanding that a correct dietary change can help.

Here is what he said :

OK, so what are the benefits of adding cholesterol to the diet? It's not only fascinating, it'll blow your mind. When we eat cholesterol containing foods, the cholesterol in the food we consume actually binds to an enzyme called HMG CoA reductase and inhibits its function. This enzyme is what's known as the rate limiting enzyme in cholesterol biosynthesis. This means that once this enzyme does what it's supposed to do, cholesterol will be made no matter what. By inhibiting the enzyme's function, choilesterol cannot be made. So eating cholesterol actually inhibts its own production.
But wait, it gets even better.

The cholesterol in the foods we eat is what's referred to as fat soluble, or lipophilic (or fat loving). Since cholesterol is lipophilic, it diffuses through not only the outer cell membrane, but the cell's=2 0nucleus membrane and attaches the the DNA. Guess where it attaches to on the DNA? It attaches to the sites on DNA WHERE HMG Co A IS MADE!!!!! That's right, so not only does the cholesterol in the food we eat attache and inhibit the function of the enzyme already present to make cholesterol; the cholesterol in the foods we eat also prevents the production of the enzymes needed to make itself. In biochemical speak, this is known as negative biofeedback.

Eat more cholesterol, make less cholesterol. By the way, the only thing I've seen in eighteen years considerably raise the good cholesterol known as the HDL, is the consumption of more cholesterol. So EAT MORE CHOLESTEROL IT"S GOOD FOR YOU!

Inflammation is essentially the cause of heart disease isn't it?
I'm not medically trained, but I assume small particle LDL is a signifier of crammed, broken up large particles - perhaps a long time accumulation of what was once sent to the skin hoping to be converted to D by UVB but didn't(there is a study that says British gardeners have lower cholesterol in the Summer which seems very interesting).
The fact that statins work (albeit with alarming side effects), and that according to a Spanish study, that atorvastatin raises vitamin D some degree shows the problem isn't really cholesterol. That is erroneous cholesterol readings are the 'symptom' of either vitamin D deficiency or associated things that domino on to the ability for the heart to succomb to heart disease. As a rule I still think the general cholesterol hypothesis is a farce, not just because of the way the products are marketed but because it's only looking at one station on the tube system. 'High cholesterol causing heart disease' might be better termed as 'low vitamin D causes heart disease' because that's perhaps the root, or at least one root.

Dr. Davis,

First let me say a big thank you for your blog.  I follow your's, Jimmy Moore's and the Drs. Eades' blogs closely.  As a result of reading your book and blot, I just had my first heart scan at age 50, and was vert happy to hear zero calcium score.

I do low carb nutrition (~50g/day), so my triglycerides were very low (28).  I've read that all LDL will be large with triglycerides that low (below 70).  Can you confirm that?  Would I be wasting my money on blood work to determine particle size?  HDL is 62, LDL 136.

Steve L.

Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.

I'm looking for heart disease info that isn't related to cholesterol OR grain intake, because my cat has it--cats are obligate carnivores, and therefore do not take in grains unless fed commercially-prepared foods.  Mine do not--I make their food from scratch, using a UC Davis vet-designed diet recipe.  Cholesterol levels aren't a concern either, although I now know to have the SIZE of cells examined, as well as vitamin D levels checked.  As for anti-inflammatories, fish oil is part of the diet recipe.

I'm going back to the vet for more blood work (now that I have more clues).

Statins Do Not Decrease Small, Dense Low-Density Lipoprotein
Free full text at link.
In an observational study, we examined the effect of statins on low-density-lipoprotein (LDL) subfractions.
Using density-gradient ultracentrifugation, we measured small, dense LDL density in 612 patients (mean age, 61.7 ± 12.6 yr), some with and some without coronary artery disease, who were placed in a statin-treated group (n=172) or a control group (n=440) and subdivided on the basis of coronary artery disease status.
Total cholesterol, LDL cholesterol, apolipoprotein B, and the LDL cholesterol/apolipoprotein B ratio were significantly lower in the statin group. However, the proportion of small, dense LDL was higher in the statin group (42.9% ± 9.5% vs 41.3% ± 8.5%; P=0.046) and the proportion of large, buoyant LDL was lower (23.6% ± 7.5% vs 25.4% ± 7.9%; P=0.011). In the statin group, persons without coronary artery disease had higher proportions of small, dense LDL, and persons with coronary artery disease tended to have higher proportions of small, dense LDL.
Our study suggests that statin therapy—whether or not recipients have coronary artery disease—does not decrease the proportion of small, dense LDL among total LDL particles, but in fact increases it, while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL. If and when our observation proves to be reproducible in subsequent large-scale studies, it should provide new insights into small, dense LDL and its actual role in atherogenesis or the progression of atherosclerosis.

The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

For years I suffered from high cholesterol and was almost permanently on statin medication. I come for a family with a strong history of heart disease and I personally believe that high cholesterol can cause heart disease. Thankfully I now have my cholesterol under control but it has been hard work, and I done it the natural way, as I suffered from the side effects statins cause.

How To Lower Cholesterol Without Medication

About eighty percent of our cholesterol is produced by the liver and the rest depends on our diet. Foods such as red meat and butter are rich in cholesterol where as those from plant origin have very little or no cholesterol at all. The control of cholesterol in our body is done by the liver. I think,more can be found out from:
http://www.heart-consult.com/articles/how-cholesterol-affects-heart

exactly!!!!!

Dr. Davis:
doctors including most in your specialty use statins as their first line of defense in treating heart disease. Perhaps because it is easy; perhaps because of the drug company sponsored tests.  In any event, it may be that it makes sense in some cases, only we the public do not know when they should be prescribed.  Perhaps you can enlighten us on when and for what reasons you would prescribe statins, if at all.
Excellent post.

Why didn't you tell her that it's now been proven that no woman should ever be on statins (and very few men should be.)

My mom now has to walk with a cane after six months on statins, at her idiot doctor's insistence.

At least I'm sure her doc enjoyed his free lunches (paid for by hot, nubile drug reps, just a year or two out of the sorority.)

Sometimes this country makes me want to VOMIT!

Dr. Eades keeps repeating it's never been proven that statins do any good to women of any age - what do you think about it, maybe that patient should just stop taking statins and increase fish oil?

http://www.lipidworld.com/content/pdf/1476-511x-7-37.pdf
In this paper Das proposes that a rational combination of -3 and -6 fatty acids and the co-factors that are necessary for their appropriate action/metabolism is as beneficial as that of the combined use of a statin, thiazide,a  blocker, and an angiotensin converting enzyme (ACE) inhibitor, folic acid, and aspirin.
Furthermore, appropriate  combination of -3 and -6 fatty acids may even show additional
benefits in the form of protection from depression, schizophrenia, Alzheimer’s disease, and enhances cognitive function; and serve as endogenous anti-inflammatory molecules; and could be administered from childhood for life long.

But I suspect that such an approach would not be as profitable as the use of a polypill.

RCT's have demonstrated that Omega 3 fatty acid supplements can reduce
cardiac events like death,non fatal MI and non fatal stroke.

I like Omega3 fatty acid supplement from Neurovi.It has many benefits related with Heart disease.Check out the website of Neurovi.

www.neurovi.com

There's a relatively new (rat) study on krill oil.

If you're interested, you can access the abstract here:

http://www.ncbi.nlm.nih.gov/pubmed/18755044?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Is this true? If someone takes a statin drug, like Crestor, Lipitor, Zocor (simvastatin), pravachol, or lovastatin, they don't need to take anything else because the statin drug is so powerful that it eliminates risk?

We must first gather some informations bbelieving that when we take statin, we should not take any other like fish oil.

We must first gather some informations before believing that when we take statin, we should not take any other like fish oil.