dr. davis whats your take on brown rice? is it a good replacement for wheat? a cup full at mealtimes?

Dr Davis:  As you well know, not all of us can lower small LDL through carb restriction and wheat elimination to a level where small LDL is only say 30% of total LDL, a number low enough to perhaps get plaque regression. I have elimated all wheat, and eat low carb,have achieved HDL of 59, LDL of 45, NMR particle of 609, 57% of which remain small. Take Crestor and Zetia. Vitamin d measures at 60 and no thyroid issues.   My TRG's are only 28.  So, i think i am one that may have a CETP issue not responsive wholly to diet; if this drug works, it would most likely be of help to me and many others. The only way my particle count comes down is with drugs.  Not sure how i can go lower on the carb front given my only carbs now are veggies; no fruit or starch except teaspoon of Metamcuceil.  Any other natural ways to lower small LDL?

OK, I'm confused.  It sounds like this drug will increase the number of small LDL:

"This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S."

But then, maybe not:

"CETP inhibition is really a strategy to reduce small LDL particles"

Dear Dr Davis,
what is your commentary about this new investigation which represents decreasing properties of whole grain food to ldl levels
http://jn.nutrition.org/content/140/12/2153.short?rss=1
Thank you in advance for your opinion
George

Dr. D.

I love your Blog. Keep up the good work.

A few years ago I would have been very excited about this new class of drugs. I am however not so sure this drug will be the super star people think it will be (despite being able to raise HDL so much).

According to Chris Masterjohn @ The Daily Lipid Blog, he believes that much of the benefit of HDL is because HDL transfers vitamin E to the endothelial cells and that CETP inhibitors actually decrease the transfer of vitamin E from other lipoproteins to HDL by about half.  

http://blog.cholesterol-and-health.com/2009/03/wherefore-art-thy-protection-o-hdl.html

Another recent statin study, with null results: http://www.ncbi.nlm.nih.gov/pubmed/21067805

My experience on the Paleo diet plus psyllium plus guar gum equals this drug.  My HDLs went from 35 to 91.

@ JCarey:

Paleo diet + psyllium + guar gum raises HDL?
Glad you hdl's are up..got any references or links for this?

This is my take Chris.

Paleo diet = increases HDL as a result of an increase of dietary fats.

Psyllium husk = lowers LDL by stimulating the conversion of cholesterol into bile acid.  It may also lower small LDL by controlling glucose levels by slowing digestion.

Guar gum = lowers small LDL by controlling glucose levels by slowing digestion.

It amazes me to no end that people have forgotten what the longest long term study has shown us about LDL.  1998 final Framingham data.  Those with the lowest LDL levels died the soonest and those with the highest levels lived the longest and yet we are still trying to lower LDL small large or medium sized.  Its the oxLDL that matter. Dr. Davis keep fighting the battle.  

Dr. K

I notice from the Merck statement that this drug did not reduce CRP like most statins.

A few responses:

Anonymous--It depends on individual carb sensitivity. Most people can tolerate small quantities, e.g., 1/2 per serving. Others (like me) cannot even tolerate this much without triggering a surge in blood glucose and small LDL.

Steve--You likely have what I call "genetic" small LDL, meaning a CETP variant. Niacin can help. Beyond this, we struggle. I've seen variable effects with more fats, phosphatidylcholine, medium-chain triglycerides, and milk thistle. We also lack endpoint data to tell us what a desirable level is. I believe, however, it is somewhere around 300 nmol/L.

Jim--In the first paragraph, I was referring to the small LDL-yielding effects of CETP and triglyceride exchange. Blocking CETP prevents this exchange from occurring.

thanks for the response dr. davis.

What I saw from the study was no real difference after 76 weeks in mortality or cardiovascular events. In fact there were 11 deaths in the anacetrapib group and 8 deaths in the control group.

I don't find that encouraging, but maybe it was too short term.

thank you Dr Davis for your recommendations.  I have tried Slo-Niacin and had great difficulty tolerating it at 1500/1000 mg doses. Felt much better when not on it.  Have tightened up my diet even more, eliminating fruit and cheese and Greek Yogurt.  Will see what next NMR brings.  Might add Niacin at low dose to existing regime.  My small LDL particle size at 20.6 is type A and small particles not to far off from the 300 you suggest despite the proportion of small LDL to total LDL being larger than optimal

Dr. Davis - can you comment on an article that Shane Ellison has written entitled "Hidden Truth About Cholesterol-Lowering Drugs"?

Within the article, Mr. Ellison provides the statement that low cholesterol is a bad thing, not a good thing and people with higher cholesterol are living longer.

Can you place this in context with regard to small LDL particles?

Steve,
I'm not Dr. Davis, but I also have difficulty with Niacin.  I also have high homocysteine.  These 2 things can go hand in hand.  For me, it's a methylation problem.  I'm an undermethylator, which means I have to supplement with TMG and a few other things.  You should get your Homocysteine checked, and if it is elevated, be very careful with Niacin, since Niacin can make it worse unless you supplement with TMG etc...

thanks Tyson:  Homocysteine level is in normal range,but near the high end, ie 10 vs. 12 being top of the range.  My understanding is that it elevates with age and i am pushing 60.  I also hear that a B complex vitamin might make sense.

Perhaps Dr. Davis may weigh in on the homocysteine issue with regards to treatment and Niacin use.

Don't get your hopes up for anacetrapib. Despite the researchers best attempts to hide it, the anacetrapib group had higher cardiac mortality, and higher overall mortality. So, do you care that some numbers changed, or that the drug increases the risk of death? I wrote an article on the subject on my blog: http://clintoncpr.blogspot.com/2010/11/anacetrapib-scam-improve-your.html

Considering alledged 400% increase in cardiovascular mortality rate....

http://high-fat-nutrition.blogspot.com/2010/11/anacetrapib-giggle.html

...I think I'll pass on this new wonder drug.

Does this mean we shouldn't be taking calcium supplements? I've been taking 500 mg per day.

Hello Dr Davis, I've read recently that calcium supplements are a bad idea - they increase the risk of cardiovascular disease.

Does dietary calcium have a similar effect? I would value you opinion.

Thanks,

Richard

There is a lot of controversy in Canada currently for a treatment of MS; the opening of blocked or restricted neck veins.  Dr. D, you mentioned dementia, which, to my simple understanding, is either nerve damage or vascular dementia due to a series of small strokes. So my reason for this post is to ask the question; Is the tissue type of veins the same as arteries, and if so, would the same inflammation calcification cycle occur?  If the answer is yes, does that imply vitamin D3 /K2 and wheat elimination has potential for MS sufferers and people trying to avoid vascular dementia in old age?
thanks
Trev (recovering vegetarian)

http://www.cbc.ca/health/story/2010/11/18/multiple-sclerosis-vein-death-costa-rica-mostic.html

Mike and Richard--

I have been advising my patients to take no more than 500 mg calcium per day, given the potential for increased cardiovascular events with higher doses per the studies coming from New Zealand. Also, achieving healthy vitamin D blood levels easily doubles the intestinal absorption of calcium, making supplementation of additional calcium less necessary.

This research was published in 2005.
Any updates on this?

Thanks

Dr. Davis, I hear/read so much about 'inflamation' in the body and 'anti-inflammatory' diets, etc.  So I was wondering if the C-reactive protein test is a reliable way to measure this? If so what is the suggested limit or safe range in YOUR opinion?

Excellent blog! I eat an almost dairy free diet (grass-fed butter is the exception for vitamins K  and A and butyric acid etc and to add fat to overly lean protein)   that includes almonds, filberts, sardines and salmon with bones and greens for calcium. I also eat lots of very dark chocolate/cocoa.  I supplement with vitamin d.  I recently passed a calcium oxalate kidney stone and doc says my dairy free diet is far too rich in oxalates and phytic acid. I have also been plagued with calf and foot cramps. He suggests adding small amounts of cheese or a calcium supplement to block the oxalates.  Despite my magnesium rich diet -- he also says I need a magnesium supplement. It's only been a few days since I've added 2 calcium/mag tablets at night (only contain about 300mg calcium and 180 mag plus additional mag citrate powder in hot water) and my cramps seem to have subsided.  Anyone else get mineral deficiencies eating paleo style with nuts and bones but no supplements?

Anonymous, I take Mg supplements, too. I seem to have a hard time absorbing minerals.

The nuts you're eating contain phytic acid, which blocks mineral absorption. The Weston A. Price Foundation recommends soaking and roasting nuts and seeds to neutralize the phytic acid.

This is more complicated than the notion that high calcium intake=high "calcification" ...

...Blood Ca and its accumulation in soft tissues can increase (from bones) even though less is eaten. Ca metabolism is far more important than magnitude of intake.  It seems that Ca supplementation actually decreases intracellular amounts.

If the diet is acidic, calcium will be used to buffer this acid which will ultimately be excreted through the urine. On the other hand, if the diet is alkaline, then no calcium is needed for this purpose. So the question is, where does this un-needed calcium go?

Maybe an alkaline diet isn't such a good thing after all is all I'm saying.

Anon about MS--

I would be careful about extrapolating the wheat-dementia connection to MS. It would be deeply concerning if there were a connection, but I am not aware of such a connection.

The one truly compelling observation being made in MS is the vitamin D discussion. To my knowledge, that clinical trial is still underway in Toronto.

I too had lots of trouble with kidney stones but no more.  The only change I made was stopping calcium supplements and starting magnesium.  I take 500 mg of mag at bedtime and have not had a kidney stone pain in almost 2 years.

Dr. Davis,

Wondering how you explain the paradox that statins seems to significantly increase coronary calcium, but to lower coronary events?


Thanks,
David

Regarding magnesium supplementation - I've read that most magnesium supplements have little to no bio-availability, making it pointless to take them.  There are some on the market which address this concern and I've seen good reviews of them - but they do cost more.  I've also read at multiple nutrition sites that our foods have less and less magnesium as our soils are very depleted.  But almonds, pepitas and nut butters are good sources, as are some other foods, like black beans.  There are lists online.  I've also read that Epsom salt baths are a good source of magnesium.  So I take ES baths and I've made myself a magnesium skin lotion with ES.  Instructions for doing this can be found online.

Basic Ca phosphate crystal deposition disease: Most pathologic calcifications throughout the body contain mixtures of carbonate-substituted hydroxyapatite and octacalcium phosphate. Because these ultramicroscopic crystals are nonacidic Ca phosphates, the term “basic Ca phosphate” (BCP) is much more precise than “apatite.”

Nutritionally people eat hydroxyapatite not apatite  BCP

I guessing the moral of the story is to eat acidic calcium, calcium citrate or hydroxyapatite not apatite.

I have read that Vitamin K2 is very helpful in getting rid of the Calcium.

Martin Levac also raises a good point. I would think as long as the diet is balanced, then calcium will not stay in the arteries.

It could be that too alkaline diets might cause this problem. In India several very strict vegetarian (not vegan) societies do not eat onions and garlic. Both are very highly alkaline.

While Non-vegetarian societies eat a lot of them. I guess the difference may be due to the acid base theory. The over all diet should be very slightly alkaline to be best.

This ACID/BASE diet argument is a little odd sounding to me but even a quick Google leads to the simple explanation that it is the influence of minerals in the diet on blood pH

"The consumption of animal protein, grain, and high amounts of milk increases the acidity of the body, whereas foods rich in minerals such as green vegetables and fruit increase the alkalinity. Generally, the Western diet induces a chronic, low-grade metabolic acidosis.  This relates to the loss of calcium through excretion in urine.  Here is the link:-
http://jn.nutrition.org/content/136/9/2374.full#BIB7

cool, but is there any link to heart heath?

I see that some readers asked the same question I was thinking related to calcium supplements. For instance, I hear quite a bit how much coral calcium is good for people. I would assume based on what you have said to take no more than 500 mg of that as well per day?

HI, David--

While statins do not have much effect on slowing the progression of coronary calcium, I know of no data suggesting that they increase coronary calcium.


Hi, Pat--

While absorption of magnesium products varies widely, magnesium "salts" like the malate and glycinate are absorbed quite well.

Basicly, calcium concentrated outside a cell has a safe bio-chemical role to perform & magnesium inside that same cell has it's major bio-chemical role. They both have vital cellular functions.

When calcium "lingers" inside a cell it keeps over-stimulating things; building up in there is even worse. This inflammatory mechanism occurs in many tissues, not just blood vessels.


Dietary deficiencies of calcium & magnesium naturally trigger a para-thyroid hormone activation. This hormone signal is for getting more calcium available to the body's tissue cells.

As you get older there is commonly more para-thyroid hormone circulating in your blood. It can form a negative feedback loop with pro-inflammatory factors (like cytokines); as the inflammation keeps calcium inside the cell.

Cause or effect of calcium being where it's not supposed to be may involve a vicious circle. Rare youngsters with coronary calcium would suggest uncommon genetics.

The preceding paragraph to the above-quoted passage is probably also very relevant to this discussion:

"It is not clear how or why the claims for high vitamin D levels started, medical experts say. First there were two studies, which turned out to be incorrect, that said people needed 30 nanograms of vitamin D per milliliter of blood, the upper end of what the committee says is a normal range. They were followed by articles and claims and books saying much higher levels — 40 to 50 nanograms or even higher — were needed."

Can you point us to other studies that point to the efficacy of 30 ng+ concentrations?  

I am not attempting to be adversarial at all to your views -- I have been following them closely following my own research.  But given that I havea  data-driven bent, this report has given me a reason to reconsider, and I would love your guidance.

I doubt anyone needs calcium or magnesium supplementation. Calcium and magnesium are virtually impossible to avoid - I believe they're in every plant food. I'll stick with D3, MK-7 and hormones.

"Less calcium, less plaque to rupture, less risk."
It is well known that ethylesterized omega-3 fatty acids, e.g., E-EPA, stabilize arterial plaques. This explains at least partly how these omega-3´s protect the heart and arteries. See for instance J Atheroscler Thromb. Epub ahead of print 2010 Nov 17

http://www.jstage.jst.go.jp/article/jat/advpub/0/1011160316/_pdf

Minä suosittelen K2-vitam.  Se poistaa kalkkia ja ehkäiseen sen kertymistä verisuoniin !!!

Are all OTC omega 3 products ethylesterized? If not, which ones are?

I want to thank for your work. I am a big fan of the site. As a Nephrologist, unfortunately, not only do I see many patients under going a cardiac cath but they may also receive "drive by" angiograms of the renal arteries with stenting. A recent study in the Annals of Interal Medicine, July 16, 2009 showed no difference in medical management and stenting of the renal arteries. Moreover, 2 patients in the stenting arm of the study died within 30 days of stenting. From a Renal prospective, there are complications of renal angiograms and stenting which are aneurysms, bleeding, infections and the possibility of worsening kidney failure which can be permanent. I fear that more patients are under going this procedure than necessary. I will be commenting more about this study in my blog:
www.nephropal.blogspot.com.

Thank you for your hard work.

Kenneth Tourgeman, MD

Dr. Davis-

What are your recommendations for females under 30?  I was told that I am not eligible for a heart scan due to my age, but I have a strong family Hx of CVD (father had bypass at age 50).

rom a Renal prospective, there are complications of renal angiograms and stenting which are aneurysms, bleeding, infections and the possibility of worsening kidney failure which can be permanent. I fear that more patients are under going this procedure than necessary.