Statin stupid

If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.

Fat Head: Tom Naughton's manifesto for low-carb eating

I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

Among the many interesting people I met on the cruise was the creator of the documentary film, Fat Head, Tom Naughton.

Tom brings both creative insights into low-carbohydrate eating as well as humor. Low-carb eating can be a pretty contentious issue, but Tom made it fun. He will make you laugh about many of the odd notions we have about diet.

Among the best parts of Fat Head is Tom's portrayal of the effects of carbohydrates on insulin and fat metabolism:






Fat Head joins the ranks of films like Food, Inc, that make nutrition information entertaining. For anyone interested in a unvarnished look at diet, weight loss, along with a few laughs along the way, Tom Naughton's Fat Head is worth viewing.

Oatmeal: Good or bad?


You've heard it before: oatmeal reduces cholesterol. Oatmeal producers have obtained permission from the FDA to use a cholesterol-reducing claim. The American Heart Association provides a (paid) endorsement of Quaker Oats.

I've lost count of the times I've asked someone whether they ate a healthy breakfast and the answer was "Sure. I had oatmeal."

Is this true? Is oatmeal heart healthy because it reduces LDL cholesterol?

I don't think so. Try this: Have a serving of slow-cooked (e.g., steel-cut, Irish, etc.) oatmeal. Most people will consume oatmeal with skim or 1% milk and some dried or fresh fruit. Wait an hour, then check your blood sugar.

If you are not diabetic and have a fasting blood sugar in the "normal" range (<100 mg/dl), you will typically have a 1-hour blood glucose of 150-180 mg/dl--very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Blood sugars this high, experienced repetitively, will damage the delicate insulin-producing beta cells of your pancreas (glucose toxicity). It also glycates proteins of the eyes and vascular walls. The blood glucose effects of oatmeal really don't differ much from a large Snickers bar or bowl of jelly beans.

If you are like most people, you too will show high blood sugars after oatmeal. It's easy to find out . . . check your postprandial blood sugar.

In past, I recommended oat products, specifically oat bran, to reduce LDL, especially small LDL. I've changed my mind: I now no longer recommend any oat product due to its blood sugar-increasing effects.

Better choices: eggs, ground flaxseed as a hot cereal, cheese (the one dairy product that does not excessively trigger insulin), raw nuts, salads, leftovers from last evening's dinner.

Mustard: Super health food?

Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


The vinegar slows gastric emptying, resulting in slower absorption of any carbohydrates and a reduced glucose area-under-the-curve. Of the little fats contained (about 3 grams per 1/4 cup), most are desirable monounsaturates. Mustards are relatively rich in selenium, with 20 mcg per 1/4 cup, helpful for protection against cancer and thyroid disease, and magnesium, 31 mg per 1/4 cup.

Turmeric is added to most mustards. One of the constituents of turmeric, curcumin, the substance that confers the bright yellow color, has been a focus of interest for its anti-inflammatory effects. Curcumin has been documented to reduce activity of the inflammatory enzymes cyclooxygenase-2 (COX-2), lipoxygenase, and reduce activity of inflammatory signal molecules, tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1,2,6,8, and 12, and monocyte chemoattractant protein (MCP). Curcumin also has been shown to reduce LDL oxidation, a potentially important step in atherosclerotic plaque formation. Turmeric is used as a tea by Okinawans. (Hmmmm . . . )

Turmeric content of mustard can vary, of course. Likewise, sugar content. Look for mustards that are not sweetened, so avoid honey mustard in particular. Look for hot, brown, horseradish, Dijon, etc. If there is a downside to mustard, it's sodium content, though the 709 mg per 1/4 cup should only be a problem for those who are sodium-sensitive (African Americans, in particular).

So perhaps mustard isn't exactly a super health food. But it may have some bona fide health effects and should be used generously especially if you are concerned about blood sugar and inflammatory phenomena.

Exercise and blood sugar

There is no doubt that exercise yields benefits across a spectrum of health: reduced blood pressure,  reduced inflammation, reduced blood coagulation, better weight control, stronger bones, less depression, reduced risk for heart attack.

Exercise also influences blood sugar. Diabetics understand this best: Exercise reduces blood sugar 20, 30, 50 or more milligrams. A starting blood sugar, for instance, of 160 mg/dl can be reduced to 80 mg/dl by jogging or riding a bicycle. (I recently had brunch at an Indian restaurant with my family. Blood sugar one-hour postprandial: 134 mg/dl. I was sleepy and foggy. I got on my stationary bike and pedalled at a moderate clip for 60 minutes. Blood sugar: 90 mg/dl.)

Could the reduction of blood sugar with exercise be THE reason that exercise and physical activity provide such substantial benefits?

Think about it. Reduced blood sugar:

1) Reduces risk for future cardiovascular events.
2) Reduces glycation of proteins, i.e., reduced glucose binding to proteins like the ones in artery walls and the lenses of your eyes.
3) Reduces blood coagulation
4) Reduces endothelial dysfunction (abnormal artery constriction that leads to atherosclerosis)

This might explain why it doesn't require high levels of aerobic activity to derive benefit from exercise, since even modest efforts (e.g., a 15-minute walk after eating) reduce blood sugar substantially.

The incredible 33-year, 18,000-participant Whitehall study tells us that a postprandial (after-eating) blood sugar of an impossibly-difficult 83 mg/dl is required to erase the excess cardiovascular risk of blood sugar. Could this simply be telling us that physical activity or exercise is required to suppress blood sugars to these low levels?

It makes me wonder if an index of the adequacy of exercise is your post-exercise blood glucose.
The formula for aortic valve disease?

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Comments (60) -

  • Might-o'chondri-AL

    2/28/2011 1:03:38 AM |

    Aortic stenosis is +/- 2% once age 65 and +/-4% for those over
    85; but that's still
    +/-300,000 valve replacements done yearly for it. I'm not passing myself as the doctor here, so following is what I think is relevant science.

    The cytokine TGF-B1 (transforming growth factor beta)is seen in the blood progressively more as the aortic stenosis pathology worsens. Other elevated indicators
    are fibronectin, collagen I & II, plus sarcomeric protein myosin light-chain 2.

    All of the preceeding seem to be driven by TGF-B1 kinase-1 (TAK1) pathway, &/or TGF/SMAD transcription factors. The obstructive build up involves TGF-B1 inducing a pheno-type alteration of the local fibroblasts into more of a matix.

    It's altered the valvular cells' environment, so to speak, and so extra cellular matrix (ECM) components acrue. Calcium in circulation is capable of depositing in the aged valve matrix; which, scaffolding matrix, youth don't have to "trap" the calcium.

    The treatment of very high
    vitamin D would down-regulate the cytokine TGF-B1, high vitamin K2 encourage matrix solubility and restricted calcium mineral with it's ion dynamics take the load off valve.

  • Jim

    2/28/2011 1:16:04 AM |

    Doc, this is a phenomenal result!!  Thanks should be given to your keen medical insight and willingness to try alternative medicine in helping your patients!  You have what I consider to be probably the best website of its kind on the internet.  
         I live in a Chicago S/W suburb, which is really not that far, from your Milwaukee Office.  I have gone to your city a few times on business over the past couple of years and I regret not making an appointment in getting an exam.  One of these days I will make the trip to see you with or without an accompanying business trip.  Maybe this will spur more folks from the Chicago area to make the trip up North.

  • Ken

    2/28/2011 3:39:12 AM |

    Excellent work Dr.Davis.Vitamin K2 ensures that calcium ends up where we want it.The combination of vitamins D3
    and K2 has many benefits.

  • Anonymous

    2/28/2011 4:06:40 AM |

    I am thrilled to read this thread. I am a 64 y/o woman diagnosed w/"mild to moderate" aortic stenosis with some regurgitation as well as some mitral valve regurg. As a child I had several severe strep throats, had a total hysterectomy at 42, and subsequently have been diagnosed with hypothyroidism, all of which I have read might be causative.  My MGH cardiologist says I'm not "bad enough" for surgery,and of course I don't want it, but I feel really awful--very tired, some chest pain at times, and occasional feelings that I can't get my breath.
    I need a plan--and would appreciate any help.
    Laura

  • Anne

    2/28/2011 7:33:02 AM |

    Ever since I came across Dr Davis's heart scan blog four years ago I have been waiting for more more info on this. I have aortic valve stenosis - not due to degenerative changes but due to congenital aortic valve defect - a bicuspid aortic valve - and I have been supplementing with high dose vitamin D ever since.

  • Anonymous

    2/28/2011 9:52:57 AM |

    Maybe for those who have severe calcification, they should avoid calcium. However, for the rest of the population, ensuring enough K2+D3+retinol(natural form)+magnesium and other nutrients is probably a better approach. Calcium itself protects against the heavy metal burden the body has been shown to accumulate with age. Calcium has also been proven to result in lessened inflammation (CRP), less genomic damage, longer telomeres, and lessened mortality. In the end, I would say, don't avoid calcium. Just make sure you don't get too much ***in relation*** to the other nutrients you are getting.

  • Anonymous

    2/28/2011 11:17:02 AM |

    Echocardiograms can have substantial variability, certain assumptions are built into the mathematical formulas used to evaluate aortic valve stenosis. Was there any differences noted in the doppler velocity (Lvot, cw)or outflow tract dimension? Small differences in these measurements can yield large variability in aortic valve area. Just playing devils advocate here.......

  • Ken

    2/28/2011 2:01:33 PM |

    I read some comments by a doctor on a website.He said,"Vitamin K2 decreased calcium deposits in aortic valves.Some of my patients' stenotic aortic valve systolic gradients decreased by about 20mm mercury."

    Intestinal absorption of calcium can double or even quadruple when vitamin D levels approach desirable levels.Therefore, calcium supplements are not required.Hypercalcemia can lead to heart attacks, kidney stones , atherosclerosis and arthritis over long periods of time.There is plenty of calcium in food.

  • Anonymous

    2/28/2011 3:28:34 PM |

    So you're saying my knees won't get better?!

  • Anonymous

    2/28/2011 3:34:11 PM |

    1000 mcg per day!  Is that 1000 of MK-4 or MK-7.
    For about 6 months a while backmI ws taking 1000 of MK-7
    the-kid

  • PeterVermont

    2/28/2011 6:19:42 PM |

    I found out about K2 when my Dad was diagnosed with aortic stenosis. I tried to convince him to try Vitamin D and K2 but he went the conventional route and now has a cow's aortic valve.

    I have been taking 200mcg K2 every day along with my ~4000 IU/day Vitamin D. I have never had a scan and always wonder how blocked my arteries are and whether the vitamin k2 is regressing any blockage.

    A nice blog post from Nephropal on Vitamin K2

  • Anonymous

    2/28/2011 6:26:26 PM |

    Thanks again Dr. Davis, your dedication to your job is incredible!
    I have looked for K2 supplements containing both MK-4 and MK-7 but can't find them anywhere? They are not to be found in your own online shop at https://shop.trackyourplaque.com/ - where can I buy them in this proposed heavy duty dose (is's like 20 x 50mcg pills a day, quite a lot)? And what is the right balance between MK-4 and MK-7? Anyone?
    Thanks - The Viking.

  • Paul

    2/28/2011 9:45:42 PM |

    Viking,

    I have searched long and hard for such a supplement with no success.  My guess is it doesn't exist because these two forms of K2 come from two completely different sources.

    K2-MK4 (menatetrenone) is the animal form. The richest natural food source is found in green grass-fed cow's butter.  Supplements made from the natural source of menatetrenone are hard to find. The only one I'm aware of is a product called X-Factor Butter Oil made by Radiant Life.  There are less expensive synthetic forms of menatetrenone sold by Carlson Labs and Thorne Research.

    K2-MK7 (menaquinone-7) is the plant form. Its richest food source is fermented soy beans, also called "natto".  Supplements made from a natural source of menaquinone-7 are widely available.

  • Anonymous

    2/28/2011 10:37:38 PM |

    Life Extension's 'Super K' formula contains MK4 & MK7 and is available everywhere - try iherb.com

  • Might-o'chondri-AL

    2/28/2011 11:11:51 PM |

    Natto is fermenting here at home; it's remarkably easy and cheap. Doc's posted data is for each 100 grams Natto (3.5 oz., +/- 2 shot glasses volume) Mk-7 = 1,000 mcg, plus Mk-8 = 84 mcg.

    Home preparations won't exactly match commercial products analysis. Previously Doc stated that Natto raises serum Mk-4 & is active inside us for up to 4 hours; Mk-7 potent longer.

    G.E.M. Cultures (now in Washington state) sell pure Japanese Natto spores by mail order. I've no financial interest here, just their long term customer. (Natto's poly-glutamic acid was a melting stabilizer in a tropical dairy development project's ice cream manufacturing.)

    Buying the "commercial" size spore vial will let your learning curve be cheap. Online are plenty of variations on how to make Natto; G.E.M. ships with instructions in English and Japanese original.

    To make 1 pound soy bean batch you just need to incubate a dish +/- 10 inches by 10 inches and less than 2 inches deep. It'll last a person weeks refrigerated.

  • Ken

    2/28/2011 11:37:32 PM |

    I take one Life Extension Super K with Advanced K2 Complex softgel capsule per day.
    Each capsule contains 1000 micrograms Vitamin K2 as menaquinone-4, 100 micrograms
    Vitamin K2 as menaquinone-7 and 1000 micrograms of vitamin K1. I buy the capsules
    at iHerb.com but other places sell them including Life Extension.
    Invite K2 capsules contain 500mcg of MK-4,500mcg of MK7 and 1000mcg of vitamin K1.

  • Dr. William Davis

    2/28/2011 11:58:58 PM |

    Hi, Might'--

    Thanks, as always, for your incredibly insightful comments. I, too, suspect that there are discrete, identifiable pathways that would provide a plausible basis for a D3/K2 effect on aortic valve pathology.


    Anonymous with questions about the echo Doppler data--

    The aortic valve areas were obtained with 3 views on the maximal aortic supravalvular velocity, using both the standard transducer as well as the Pedoff. On both studies, the LV outflow tract diameter was 2.1 cm. The second aortic valve diameter was also confirmed with planimetry.

    Notably, peak aortic valve velocity dropped from 20 mmHg to 9 mmHg. I watched the echo tech (a very capable one, by the way) while he interrogated the valve. I am confident that we obtained the maximal peak velocity.

    All in all, I believe it is a real effect.

  • Dr. William Davis

    3/1/2011 12:00:15 AM |

    Anonymous and Paul--

    I have been advising the Life Extension "Super K."

    Super K contains 900 mcg MK-4, 100 mcg MK-7, as well as 1000 mcg vitamin K1.

  • Anonymous

    3/1/2011 12:34:09 AM |

    Have you seen any results like this on any of the other heart valves?
    My Dad has severe mitral valve stenosis. I am taking D and K2 and trying to convince him to do the same.

  • Paul

    3/1/2011 1:27:34 AM |

    Thank you, Dr. Davis.

    Looks like I'm in need of sharpening my search skills.

    Super K looks like a good deal.  I'll have to check it out when my supply of K2 runs low.

  • Anonymous

    3/1/2011 1:44:15 AM |

    In the Life Extension Super K, is the 1000 mcg of K1 a problem as far as causing clotting?

    I always understood that K2 (both MK-4 & MK-7) do not cause clotting like K1 does.

    Would love to see some calcium scoring results (and/or angiogram) before and after K2 administration, as well as carotid ultrasound results.

    Thanks for this blog, I visit it often.

  • Davide

    3/1/2011 2:19:58 AM |

    I'm curious if the addition of large doses of fish oil to the formula would also help decrease stenosis.

  • AllanF

    3/1/2011 3:59:15 AM |

    FWIW, another source of K2: http://www.vitacost.com/NSI-Ultra-Vitamin-K-with-Advanced-K2-Complex/?ntt=844197013470

    I don't have the links at hand, but I remember reading second-hand a study that showed excess K1 does NOT up-regulate clotting. Unless you are on Warfarin, K1 is completely safe, even for stroke patients.

    Good luck.

  • Anonymous

    3/1/2011 5:28:12 AM |

    Off topic but amusing considering...

    http://www.sciencedaily.com/releases/2011/02/110223122425.htm

    High Vitamin-D Bread Could Help Solve Widespread Insufficiency Problem

    ScienceDaily (Feb. 24, 2011) — With most people unable to get enough vitamin D from sunlight or foods, scientists are suggesting that a new vitamin D-fortified food -- bread made with high-vitamin D yeast -- could fill that gap. Their study, confirming that the approach works in laboratory tests, appears in ACS' Journal of Agricultural and Food Chemistry.

  • Anonymous

    3/1/2011 5:40:59 AM |

    Wow, to any regular reader of this (wonderful) blog that (i.e., the vitamin D bread) is hilarious!!!

  • Might-o'chondri-AL

    3/1/2011 6:47:14 AM |

    Measured my just finished Natto yield from 1 pound dry soy beans. Digital scale here is down, so spring scale reading is ~ 875 grams Natto made.

    Spores cost $14 (plus shipping) and are enough to make +/- 86 pounds of finished Natto. That's 39,000 grams of Natto.

    If 100 grams Natto offering 1,000mcg Mk-7 is fine, then that's 390days worth. Dry soybean substrate for 390 days Natto is 45 pounds of soy (using my spring scale yield data).

    Elsewhere in this blog, Doc I think, stated 32.7 mcg K2 decreased aorta calcification. Maybe the decimal got misplaced in my notes. Or reversal, verses prevention, demands mega-dose vitamin K.

    I fork mash +/- 50 gr. Natto and blend it in with  +/- 50 gr. Hummus. That amount of Natto will fit on 2 rice cakes as well.

  • Anonymous

    3/1/2011 2:31:54 PM |

    Dr. Davis, my greatest respect for your work. Two questions to your groundbreaking observations on D3/K2:
    1) Did the patient in question have a biscupid or triscupid valve?
    2) Was the patient exposed to any other lifestyle changes apart from D3/K2 that could explain the remarkable change?
    3) I have seen some sites selling K2 warning against taking them together with high fibre meals. Why is that, and what is the best time/frequency to take D3/K2?
    Regards, Louis

  • Anonymous

    3/1/2011 6:05:12 PM |

    I'm curious if Dr. Davis has seen any improvements in his patients using vit D3 alone.

    I expect K2 (MK-7 to be exact) helped, but was just wondering how he knows what helps or doesn't, when his patients are doing several protocols at one time (D3, fish oil, no-wheat/low carbs, perhaps niacin)...

  • Paul

    3/1/2011 7:35:41 PM |

    Might-o'chondri-AL,

    Your notes are correct.  The 32.7 mcg K2 data point comes from the Rotterdam Heart Study.  It was the minimum dose in participants showing a lower risk of both heart attack and aortic calcification.

  • Diana

    3/1/2011 8:23:43 PM |

    I use Life Extension Super K with Advanced K2 Complex that I buy from iherb. You can also get K-2 (MK-4)from High vitamin butter oil from green pastures. (You can buy it alone or with Fermented Cod Liver Oil)
    Use this code to save $5.00 off your 1st order with iherb: ROV990

  • Dr. William Davis

    3/4/2011 3:01:31 PM |

    Hi, Louis--

    The fundamental problem with retrospective observations is that you never know with absolute certainty what was done to achieve the observed effect.

    However, everybody in the Track Your Plaque program and coming through my office do nearly the same thing, i.e., fish oil, vit D, diet, etc. I NEVER witnessed regression of aortic stenosis until we added vitamin D. I am speculating whether K2 adds yet another level of control over aortic valve disease.

    This is still in the world of anecdotal observation. This is, of course, nothing even close to a clinical trial. But this can be how new ideas get their start.

  • C.J. Bahnsen

    3/4/2011 10:25:31 PM |

    Hi Doctor Davis,

    I am new to your HS blog and, after reading a few, I'm glad I signed on. Great info. Quick question regarding this idea of "cleaning" or adding flexibility to the arteries: Do you put any value in Chelation therapy? I took oral chelation supplements for a time and it seemed to lower my triglyceride and cholesterol levels. Any thoughts on this, especially as it pertains to the oral version versus the IV method?

    Thanks,  Chris

  • bodylift

    3/5/2011 9:43:55 AM |

    This is been amazing. I am take it seriously. Thanks for this information.

  • Jack

    3/9/2011 6:55:39 PM |

    Chances are the calcium supplement you are taking now is a rock source of calcium. The label will say "calcium carbonate", which is nothing more than limestone. AlgaeCal Plus contains an organic, plant-sourced calcium form derived from a unique South American marine algae called Algas Calcareasâ„¢.

  • Karen

    6/5/2011 8:18:39 PM |

    Dear Dr. Davis,

    Thank you for your website.  I am a 68-yr female with AS.  My aortic valve area is 0.69.  I weigh 118, and fast-walk/jog for an hour 4 days/wk.  I am asymptomatic, and my cardiologist advises watchful waiting.  

    How much Vit.D would you advise.  Is the amount weight related?

    Thanks again.  

    Karen

  • nose surgery

    7/6/2011 5:33:09 PM |

    Intestinal absorption of calcium can double or even quadruple, when vitamin D levels levels.Therefore desirable approach, calcium can not required.Hypercalcemia to heart attacks, kidney stones, atherosclerosis and arthritis over a long period have lead tours is a lot of calcium in food.

  • varicose veins

    7/6/2011 6:06:28 PM |

    Dr. Davis's heart scan blog ever since I met four years ago, I have been waiting for more information on this. I have aortic stenosis - not because of degenerative changes, but because of congenital aortic valve defect - bicuspid aortic valve - I have been using high doses of vitamin D supplements since.

  • Eric

    8/16/2011 6:49:42 PM |

    Dr. Davis,

    Do you mean to say that you put him on 1,000mcg of K2 MK-7 per day? (or was the 1,000mcg a combined total of all forms?)

  • Adam

    10/8/2011 4:28:38 PM |

    Dear Dr. Davis, a Final Guidance question.....

    I know Life extensions Super K is a good supplement, but the question that seems to have been asked a few times on this blog is..."what is a good & ideal target daily does combination of both MK-4 and MK-7" ?

    We have heard you say that 1000 mg a day of mk4 & mk7 is a good target...but in what ratio?  Just like Omega3 has good target ratio of EPA/DHA....can you suggest some guidance as to what a good target ratio
    of mk4 & mk7 would be ?

    Thank you!

    Adam

  • Dr. William Davis

    10/9/2011 11:00:50 PM |

    HI, Adam--

    I wish I knew! This is the difficulty with K2: too little known.

    Sure, there are plenty of opinions, but little fact. You and I can only continue to follow the emerging evidence and make our decisions as the evidence unfolds. Right now, it is simply not clear what the ideal regimen is.

  • Tom

    12/8/2011 4:33:42 PM |

    Dear Dr,

    I just came across your blog. Mind-blowing stuff. Especially because I have mild-moderate stenosis. Moderately calcified and bi-cusped. I wanted to know if any of your patients had bicusped aortic stenosis and your treatment with D3 and K2 might have seen reversals?

    also, do you suggest K2 with Mk-4 and Mk-7 or is just MK-7 sufficient?
    I am taking just about 2000 IU D3 and 100 MK-7 K2, fish oil and veggies, fruits, walking.

    Hope you can respond.

    As always, thank you for all the good work you do.

    Tom.

  • Sandra Broussard

    12/20/2011 9:00:24 PM |

    life extention vitmin k2 is from GMO soy.  Shame on them for trying to poison us.

  • Rita

    1/25/2012 5:08:47 PM |

    Can you tell me how you found out that Super K contain GMO soy?

  • jane cook atkins

    3/5/2012 4:06:52 AM |

    My father was just diagnosed with aortic stenosis and I had to go to a friend who is a biochemist to discuss some nutritional options for an 83 year old man.  I have used Isotonix supplements or the Nutrametrix line of same product since 1995.  Personally I wanted to go in that direction with a scientific mind to talk with. My Dad''s doctor told me he personally uses supplements but was not allowed to direct my father on them.  He is basically following a check list.  My Dad is a player and I have him on a great regimen.  After finding your blog, I am looking to add d with k2 in Isotonix.  I have him on an Isotonix Calcium supplement that has d3 in it.   Not junk calcium or tums.  
    http://dwithk2.blogspot.com/
    this is my blog and you can go to the bottom of it to see label on the product.
    Our next stop is the cardio doc who we were advised would want to replace his aortic valve.  I really think that should be a very last resort.  
    Really, I believe some lifestyle changes and bumping some Isotonix supplements to heavy dosing is a better option.

  • Dr. William Davis

    3/6/2012 3:52:23 AM |

    The key, in my view, for control over aortic stenosis (thought I have not YET published the observations) is:

    1) Supplement vitamin D to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml, and
    2) Vitamin K2 supplementation to provide 1000 mcg MK-4 or at least 100 mcg MK-7, and
    3) Take NO supplemental calcium, as calcium is passive "mortar" that will calcify the aortic valve.

  • Dr. J. Edwards

    3/16/2012 6:18:32 PM |

    Pertaining to myself (aortic valve stenosis and stenosis of the spine) and my wine (parathyroid adenoma (non malignant) on Sinsipar to control without surgery.

    If we eliminate calcium  supplements (which this  makes me consider), can I forget about getting too much in food (I also take buffered Vitamin C, which will be a problem, since I have gastritis).

    Also wonder if magnesium, boron & strontium are good or bad to take??????

    Last, can you give me a link for natural treatment of parathyroid adenoma. My wife also refuses to take Boniva and her bone density is bad.

    Thanks in advance.

  • Dr. Davis

    3/26/2012 4:52:09 PM |

    Dr. Edwards--

    Unfortunately, no data.

    You are venturing further into the world of "normalizing" calcium metabolism. I'd like to believe that all this makes sense, as they tend to benefit osteoporosis/osteopenia, and removal of calcium as a supplement is likely a good thing, given its contribution to cardiovascular risk.

    But we lack real data on the effects. I will tell you that the vitamin D, however, is very real, having now done this in around 60+ patients.

  • Rita C.

    5/3/2012 7:38:41 PM |

    Dr. Davis,
         I'm 67, female with CAVD.  Heart murmur, dizziness, exhaustion since holidays led to apt with cardiologist resulting in mild aortic stenosis diagnosis in early April.
         I have taken Vitamin D3 over last two years after Welcome to Medicare physical showed low levels.  I have now added CoQ10.  After stumbling upon your blog, I'm now adding 135 mcg K-2 Mk7.  
         Despite the fact that I'm symptomatic, I'm hoping to avoid heart surgery until the new trans-vascular technique is approved for a wider range of patients.  I return to my cardiologist in early August and I will be most interested in comparing new test results against my April numbers--call it a personal clinical trial of one.
         A few years ago I observed open heart surgery at a major surgical center in Houston.  I vowed I would never have it myself, but here I am now, staring it squarely in the face.  I can't thank you enough for your website. It's given me a small measure of hope.

  • John Wilsonf

    5/25/2012 9:22:58 PM |

    Dr Davis:
    I am a 70 year old slim athletic male with a bicuspid aortic valve that has been stable for about 6 years with echo area measurements showing 1.2 to 1.3 sq cm.  When I got my first echo 6 yrs ago I searched published literature and decided to start 200mg MK-7 daily and I take quite a few supplements, including vit D, niacin, and about 3 gms fish oil (EPA+DHA).  My cardiologist is surprised to not see a reduction in area, and valve replacement seems to have been put off successfully.  This year, however, my ascending aorta was measured at  48 mm by echo, up from 44 (MRI measurement) a year ago.  Surgery was recommended, based on the aneurysm, not the valve, but of course both would be done at the same time.  A cardiac CT scan was ordered by the potential surgeon and the radiologist report indicated a maximum ascending aortic diameter of 45mm, but the surgeon said he looked at the 3-D CT images and it looked more like 47-48 mm to him.  Search for coronary artery plaque indicated all arteries "normal" except for the "1st Obtuse marginal: Tiny focal calcified plaque causing no luminal narrowing" .Beginning January, 2012, I have eliminated wheat and calcium supplements and have actually gone low-carb, high fat, adequate protein to the extent to be in "nutritional ketosis".  Ketones range from 0.5 to 1.9, depending on time of day and whether it is before or after exercize, etc.  I feel great!  Given that I am "on the boarder line" where surgery is recommended, I have thought about giving this more stringent diet a year to see if the aneurysm shrinks.

    My question is this:  Some time ago you posted your experience of seeing patients ("Jake") where diet/supplements contributed to reducing the size of an aneurysm, but I cannot find any follow-up information in your excellent blog (or publications).  What is the best diet/supplement regime that would optimize reduction of an aneurysm?  If the mechanism for the aortic wall degredation is the same as for artery plaque, then I know your answer because of your writings on this subject.  My interest in writing is to determine if there are other dietary or supplement changes I should make that would optimize my chances of improvement in my one-year trial, should I decide to do it.  Also, do you agree that nutritional ketosis (which I have no problem staying on) should be advantageous?

  • Gaurav

    8/17/2012 11:23:56 PM |

    Dr. Davis,
    I chanced upon your blog while searching for content of MK7 in natto! What a fortuitous discovery for me.

    I started taking a Vitamin D3 supplement last year when my level was diagnosed at 20 ng/ml. I took about 3000 IU per day for 9 months and my level rose to 27 ng/ml. I did so using a D3 spray in coconut oil sprayed under my tongue.

    Recently, I came across research that D3 supplementation, even in the 2000-3000 IUs a day dosage, without K2 supplementation will cause calcification of arteries and soft-tissues.

    Wanted to ask for your input on this:
    - How much K2 should I take, especially to reverse calcification? Seems like 100 mcg of MK7 and 1000 mcg of MK4 are common doses.
    - Can I take K2 just 2-3 times a week, just to be conservative. How about if I just eat Natto for MK7 and stay away from the supplements?
    - Would you still recommend D3 along with K2? If so, what is a safe D3 dose to go with 100 mcg of MK7?
    - Is calcification observed in those who were taking Calcium with D3 or it can be seen even without Calcium supplementation? I eat a pretty low-carb, high-fat, decent amount of proteins, less red meat diet. Also, I take no dairy, calcium supplement or calcium fortified foods.

    Thanks so much for your time.

  • Rita C..

    9/16/2012 4:35:50 PM |

    Update to my first comment after six months.  

    After six months of K2/D3, CoQ10, and Niacin supplements, I had my first nuclear stress test at my cardiologist's office.  Photos were picture perfect--strong, well functioning heart.  Efficiency percentage was mid 60s in March, but went to 87% in late August.  Primary Care physician had difficulty locating murmur that was pronounced in March.  I'm now scheduled for a second echocardiogram in early February.  That will be the acid test.  

    Despite excellent test results, I'm still experiencing some fatigue and dizziness, but not nearly so much as when first diagnosed.  I remain hopeful that with continued supplement therapy and good eating habits, I'll be one of the lucky ten percent who experience remission from AS with K2/D3 therapy.

  • Mel

    10/12/2012 9:29:25 AM |

    Hi Rita I thought to mention that I've been going through the comments here and really appreciate that you are giving us updates of your progress. Hoping for good results for you next round!

  • Holly

    12/18/2012 4:39:24 PM |

    Dear Dr.Davis,
    I came across your blog by chance and very interested in your opinion regarding valve problems. I would be most grateful if you can advice me on my situation:
    I always believed that I have a strong heart as I excercised a lot--swimming and hiking, never expected that the first thing knocked me down is my heart. Starting this year from January, I went to Hospital Emergency 8 times, 4 in Jan, 2 in Feb and 1 in April and anthor 1 in Nov, all because of very fast heartbeat. The first 4 made me hard to breath and thought I was dying. All the blood tests at the hopsital came out normal. However, the ecogram showed that I had moderate aortic valve regurgitation. As meantime I was suffering from gastric problems of not being able to eat much, my heart condition gave me scaring experience of being extreme fatigue, dizzy, chest pain, neck and should pain.  Doctors said I do not need to do anything.
    Even the fast beat of my heart is getting better recently, constant fatigue and dizziness and neck pain prevents from living a normal life.

    I am also scared to see my 4 year ecogram with only "traces of aortic valve regurgitation," now changed to moderate.

    I would likfe to know why my valve degenerate so fast? what can I do to stop the process. After seeing your blog, I bought vitamin D (my level is 43) and K2 (both mk4 and 7), how much dose should I take, will these vitamins alone help stop the degeneration process?

    I also considering coming down to see you if you give appointments for consultation.

    Thanks for your help!

    Holly

  • Holly

    12/18/2012 4:43:39 PM |

    by the way, I am 50 years old and have a stressful job.
    HOlly

  • Karen

    2/10/2013 9:47:04 PM |

    Dr Davis,

    Any research on a wheat less diet and lipoproteins and their affects on Aeortic stenosis? If elemenating them will prevent or reverse this condition?

    Thank you,

    Karen

  • John Wagner

    5/11/2013 6:16:00 PM |

    There are several different causes of aortic stenosis. Congenital (ie bicuspid aortic valve) and rheumatic fever start at younger ages. ASc or sclerosis is a disease of older people, same age risk as ASHD or coronary disease (atherosclerosis) and is nothing more than a variant manisfectation of the same risk factors that causes myocardial infractions., high blood pressure, smoking, obesity, diabetes and lipid disorders from high carb diets or a combination commonly called Metabolic syndrome. All of these risk factors cause coronary artery disease and/or ASc, it is just a crap shoot as to which one may show up first...but, treat both the same. Does that mean Vit D doesn't work? Of course not, newer studies beginning to show high Vit D levels are Importent in atherosclerosis Ann cancer prevention.

  • Courtney Janak

    7/31/2013 3:08:56 PM |

    My husband has a coronary calcium score of over 900. His cholesterol levels were: total:217, HDL:44, LDL:147, trigyclerides:167. His cardiologist wanted to put him on Provastatin and scheduled him for an echo-cardiogram stress test. He has chosen to put off taking the statins and has started taking K2 and magnesium supplements. Is this ok? Should statins be recommended for his score?

    Is there a cardiologist in or near Santa Fe, NM, who has an understanding of nutrient issues similar to yours?

  • Lisa D

    7/31/2013 5:15:57 PM |

    I stumbled upon your blog a year ago when researching how to reverse aortic valve calcification.  At the time I was 49 and had just gotten my echo results.  I was told that I had abnormal relaxation of my left ventricle consistent with diastolic dysfunction, a trileaflet aortic valve with a trace of regurgitation and mild calcification.  My aortic root is borderline in size.  Well that was a heck of a blow because my echo the previous year was normal.  (I have echos done because I had chest pain several years ago that turned out to be esophageal spasm.  However, everyone in my family died from heart disease and my father had his major MI at age 47.  My grandmother died from aortic stenosis... so they do yearly echos on me.  I also have hypothyroidism, polycystic ovary syndrome and my ApoE genotype is 3/4)

    After I read your blog, I went out and bought Life Extension Super K.  I have been taking it for over one year--since last July.  I found in my research that people with the ApoE4 allele don't hold on to vitamin K2 as well as those who do not have this genotype, so I didn't know if one pill a day was enough.  After a gigantic hassle trying to find a lab that runs the undercarboxylated osteocalcin test, I finally had my level drawn.  It came back at 3.8.  (Normal was anything below 12.1).  The results provided a graph which showed I am in the low normal end of the spectrum.  It showed that 80% of the population is lower than me--which surprises me because I bet most of the population doesn't take vitamin K2.  Maybe the only people having this test done are those who do supplement with vitamin K...   In any case, that lab was drawn in mid May, and since that time I doubled my dose to 2 capsules per day.  What should my undercarboxylated osteocalcin level be?  I can't find any data about what level is acceptable to reverse calcification.  I have also been taking vitamin D for several years--my level was originally 9.  I take 50,000 units once a week.  My last D level was 87.4, so I'm pretty close to the 70 that you suggest.  I also throw in about 8,000 u of vitamin A twice a month because I read that it's necessary to downregulate the D.  My D had gotten as high as 115 last year but has been in the mid 60s-80s since.  I also take CoQ10 200mg per day and fish oil. (I was taking it daily, but what do you think about the new study out saying it increases the incidence of prostate cancer?  I didn't want to increase my possibility of any kind of cancer, so I'm only taking it twice a week now... thoughts?)

    I had an echo and a Lexiscan (because I couldn't walk on the treadmill due to foot problems and foot surgery 1.5 yrs ago) done last week.  I get my results tomorrow and am hoping that the calcification is gone... When I had my echo done last year I was overweight (BMI 38.8) with some sleep apnea.  After that appointment, I walked out of that office and changed my life.  I have been on basically a "no white" diet--no sugar, flour, pasta, rice, bread, sweets, etc.  Because of my PCOS, I can't even eat complex carbs without gaining weight.  (I have done strict Atkins before but couldn't sustain it because it was so strict.  This is working for me.  My carbs come from low glycemic fruits and vegetables primarily.  I do eat meat, dairy and nuts).  I went back to the gym and go every other day.  I lift weights (my son is a personal trainer), climb the stair master for 20 minutes and then go home to ride my exercise bike for 45 minutes every day.  I ride my exercise bike every day for at least 45 minutes and sometimes do double cardio days on weekends.  I have lost 63 pounds in the last year.  I would like to lose another 20 pounds.  I have an oral appliance for the sleep apnea and will have another sleep study done after I lose the last 20 lbs.  I know that I didn't used to snore when I was thin (pre-pregnancy).  I'm only 11 lbs above my pre-pregnant weight now.  I know that the sleep apnea can lead to diastolic dysfunction.  I'm hoping I'm reversing that!

    Any other suggestions for me?  I'm especially interested to know how much vitamin K2 I need to take to potentially reverse this darn calcification.  I've mentioned the K2 to my other doctors and so far they're all in the dark and don't even seem to care about it... I'm shocked, because there are big studies out there that back it up.  I don't know about my cardiologist because I don't see him until tomorrow.  I'm shocked that my endocrinologist didn't seem to care because he does bone density scans in his office.  I'm getting one done in a couple months.  In my past 2 scans, I was dropping towards osteopenia.  I'm hoping with the vitamin K2 that I show dramatic improvement so that I can show him I was right about the K.

    Thank you for any help,
    Lisa D. RN

  • Marsha

    8/25/2013 12:40:59 AM |

    Oh come on Jim, try google every once in awhile.  This isn't Dr. Davis' discovery...it's been studied and written about for at least 8 years now.

  • Michael

    8/25/2013 12:51:35 AM |

    Isn't that the brand that everyone over on the Inspire.com site is having problems with?  Seriously, there's been quite a discussion about it.  Many found that once they switched to Carlson's K2 only, that their palpitations, etc., went away.

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All posts by william-davis

Cholesterol follies

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD

Risks for coronary disease 2008

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2



Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.











Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.