Where do you find fructose?

Apple, 1 medium: Fructose 10.74 g




Honey: Fructose 17.19 grams per 2 tablespoons



Barbecue Sauce: HFCS number 1 ingredient
Ingredients: High Fructose Corn Syrup, Vinegar, Concentrated Tomato Juice (Water, Tomato Paste), Water, Modified Food Starch, Salt, Honey, Contains Less Than 2% of Molasses, Natural Flavor, Paprika, Spice, Mustard Flour, Guar Gum, Red 40.



A1 Steak Sauce: HFCS number 2 ingredient
Ingredients: Tomato puree (water, tomato paste), high fructose corn syrup, vinegar, salt, water dried onions, contains less than 2% of black pepper, modified food starch, citric acid, dried parsley, dried garlic, xanthan gum, caramel color, potassium sorbate and calcium disodium EDTA as preservatives, molasses, corn syrup, sugar, spices, tamarind, natural flavor

Do heart scans cause cancer?

Another in a series of data extrapolations that attempt to predict long-term cancer risk from medical radiation exposure was published in the July 13, 2009 Archives of Internal Medicine, viewable here.

Over the years, I've fussed about the radiation dose used by some centers for CT heart scans. (Note: I'm talking about CT heart scans, not CT coronary angiograms, an entirely different test with different radiation exposure.) In the "old" days, when electron-beam devices (EBT) were the best on the block, the old single-slice CT scanners (the predecessor of the current 64-slice MDCT scanners) exposed patients to ungodly quantities of radiation, while the EBT devices required very small quantities (0.5 mSv or about the equivalent of 4 standard chest x-rays or one mammogram).

But CT technology has advanced considerably. While EBT has been phased out (although it was an exceptional technology, GE acquired the small California manufacturer, then promptly scrapped the operation; you can guess why), multi-detector CT (MDCT) technology has improved in speed, image quality, and radiation exposure.

While it has improved, radiation exposure still remains an issue. The authors of the study applied the scanning protocols used at three hospitals and those in several CT heart scan studies, then calculated radiation exposure. They found a more than ten-fold range of exposure, from 0.8 mSv to 10.5 mSv. (All scanners were MDCT, none EBT.)

That's precisely what I've been worrying about: In the rapid rush to develop new devices, radiation exposure has often been a neglected issue. While some scan centers do an excellent job and take steps to minimize exposure, others barely lift a finger and consequently expose their patients to unnecessary radiation.

However, it's not as bad as it sounds. For one, the study included 16-slice MDCT scanners, a scanner type that I warned people to not use because of radiation. On the current most popular 64-slice devices, much lower radiation exposure is possible, on the order of 0.8-1.2 mSv routinely--if the center takes the effort.

This study, while eye-opening, will achieve some good: CT heart scans are here to stay. But the day-to-day practice of heart scanning should be:

1) standardized
2) conducted with radiation exposure as low as possible, preferably <0.8 mSv


To read more about this issue, below I've reprinted a 2007 full Track Your Plaque Special Report, CT Heart Scans and Radiation: The Real Story.




CT heart scans and radiation: The real story

“My personal opinion is that many patients today who are receiving multiple CT scans may well be getting at least comparable doses to subjects that have now developed malignancies from x-ray radiation received in the 1930s and '40s. And, similar to those days when the doses were unknown, the dose that patients receive today over a course of years of multiple CT scans is also completely unknown . . .

“I recommend that all healthcare providers become familiar with the concept that 1 in 1000 CT studies of the chest, abdomen, or pelvis may result in cancer.”


Richard C. Semelka, MD
Professor and Vice Chairman, Department of Radiology
University of North Carolina–Chapel Hill



Is this just hype to generate headlines? Or is the truth buried in the enormous marketing clout of the medical device industry, among which the imaging device manufacturers reign supreme?

It’s been over 110 years since radiation was first used for medical imaging. Over those years, it has had its share of misadventures.

In the 1930s and 1940s, before the dangers of radiation were recognized, shoe shoppers had shoes fitted using an x-ray device of the foot to assess fit. High doses of radiation were used to shrink enlarged tonsils and extinguish overactive thyroid glands. Attitudes towards radiation were so lax that doctors commonly permitted themselves to be exposed without protection day after day, year after year, until an unexpected rise in blood cancers like leukemia was observed. As recently as the 1970s and 1980s, cancers like Hodgkins’ disease were treated with high doses of radiation, also leading to radiation-induced diseases decades later.

Not all radiation is bad. Radiation can also be used as a therapeutic tool and even today remains a useful and reasonably effective method to reduce the size, sometimes eliminate, certain types of cancer. Forty percent of people with cancer now receive some form of radiation as part of their treatment (Ron E 2003).


Just how much does medical radiation add to our exposure?

Estimates vary, but most experts estimate that medical imaging provides approximately 15% of total lifetime exposure. In other words, radiation exposure from medical imaging is simply a small portion of total exposure that develops over the years of life. Exposure can be much higher, however, in a specific individual who undergoes repeated radiation imaging or treatment of one sort or another.

For all of us, exposure to medical radiation is part of lifetime exposure from multiple sources, added to the radiation we receive from the world around us. Just by living on earth, we are exposed to radiation from space and naturally-occurring radioactive compounds, and receive somewhere around 3.0 mSv per year (U.S. Nuclear Regulatory Commission). (Doses for radiation exposure are commonly expressed in milliSieverts, mSv, a measure that reflects whole-body radiation exposure.) People living in high-altitude locales like Colorado get exposed to an additional 30–50% ambient radiation (1.0–1.5 mSv more per year).

Much of the information on radiation exposure comes from studies like the Life Span Study that, since 1961, has tracked 120,000 Japanese exposed to radiation from the atomic bombs dropped in 1945 (Preston DL et al 2003). Although regarded as a high-dose exposure study for obvious reasons, there are actually thousands of people in this study who were exposed to lesser quantities of radiation (because of distance from the bomb sites) who still display a “dose-response” increased risk for cancer many years later in life. Radiation exposures of as little as 5–20 mSv showed a slight increase in lifetime risk.

Occupational and excessive medical exposure to radiation also provides a “laboratory” to examine radiation risk. Miners exposed to radon gas; patients exposed to the imaging agent, Thorotrast, containing radioactive isotope thorium dioxide and used as an x-ray contrast agent in the 1930s and 1940s and possesses the curious property of lingering in the body for over 30 years after administration; radium injections administered between 1945 and 1955 to treat diseases like ankylosing spondylitis and tuberculosis, all provide researchers an opportunity to study the long-term effects of various types of radiation exposure over many years (Harrison JD et al 2003).

The excess exposure of workers and several hundred thousand nearby residents to the Mayak nuclear plant in Russia has also revealed a “dose-response” relationship, with increasing exposure leading to more cancers, including leukemia and solid cancers of the bone, liver, and lung (Shilnikova NS et al 2003). Nuclear waste released into the Techa river between 1948 and 1956 contaminated drinking water used by over 100,000 Russians. A plant explosion in 1957 also released an excess of radiation into the atmosphere, yielding exposure via inhalation. Some sources estimate that at least 272,000 people have been affected by radiation from the Mayak plant. This unfortunate situation has, however, yielded plenty of data on radiation exposure and its long-term effects.

It’s also been known for several decades that people who receive therapeutic radiation for treatment of cancer, even with the reduced doses now employed, are subject to increased risk of a second cancer consequent to the radiation treatment.

From experiences like this, radiation experts estimate that an exposure of 10 mSv increases a population’s risk for cancer by 1 in 1000 (Semelka RC et al 2007).

This question was recently thrust into the spotlight with publication of a study from Columbia University in New York suggesting that a 20-year old woman would be exposed to a lifetime risk of cancer as high as 1 in 143 consequent to the radiation received during a CT coronary angiogram. (Important note: This was estimated risk from a CT coronary angiogram, not a simple heart scan that we advocate for the Track Your Plaque program.) The risk at the low end of the spectrum would be in an 80-year old man (because of the shorter period of time to develop cancer), with a risk of 1 in 5017. If “gating” to the EKG is added (which many scan centers do indeed perform nowadays), risk for a 60-year old woman is estimated at 1 in 715; risk for a 60-year old male, 1 in 1911 (Einstein AJ et al 2007). This study generated some criticism, since it did not directly involve human subjects, but used “phantoms” or x-ray dummies to simulate x-ray exposure. Nonetheless, the point was made: CT coronary angiograms in current practice do indeed expose the patient to substantial quantities of radiation, sufficient to pose a lifetime risk of cancer.


The media frenzy

The NY Times ran an article called With Rise in Radiation Exposure, Experts Urge Caution on Tests in which they stated:

"According to a new study, the per-capita dose of ionizing radiation from clinical imaging exams in the United States increased almost 600 percent from 1980 to 2006. In the past, natural background radiation was the leading source of human exposure; that has been displaced by diagnostic imaging procedures, the authors said."

“This is an absolutely sentinel event, a wake-up call,” said Dr. Fred A. Mettler Jr., principal investigator for the study, by the National Council on Radiation Protection. “Medical exposure now dwarfs that of all other sources.”

Radiation is a widely used imaging tool in medicine. Although CT scans of the brain, bones, chest, abdomen, and pelvis account for only 5% of all medical radiation procedures, they are responsible for nearly 50% of medical radiation used. It’s been known for years that increasing radiation exposure increases cancer risk over many years, but the boom of newer, faster devices that provide more detailed images has opened the floodgates to expanded use of CT scanners.

But before we join in the hysteria, let's first take a look at exposure measured for different sorts of tests:


Typical effective radiation dose values for common tests

Computed Tomography

Head CT 1 – 2 mSv
Pelvis CT 3 – 4 mSv
Chest CT 5 – 7 mSv
Abdomen CT 5 – 7 mSv
Abdomen/pelvis CT 8 – 11 mSv
Coronary CT angiography 5 – 12 mSv


Non-CT

Hand radiograph Less than 0.1 mSv
Chest radiograph Less than 0.1 mSv
Mammogram 0.3 – 0.6 mSv
Barium enema exam 3 – 6 mSv
Coronary angiogram 5 – 10 mSv
Sestamibi myocardial perfusion (per injection) 6 – 9 mSv
Thallium myocardial perfusion (per injection) 26 – 35 mSv

Source: Cynthia H. McCullough, Ph.D., Mayo Clinic, Rochester, MN


A plain, everyday chest x-ray, providing less than 0.1 mSv exposure, provides about the same quantity of radiation exposure as flying in an airplane for four hours, or the same amount of radiation from exposure to our surroundings for 11–12 days. Similar exposure arises from dental x-rays.

If you have a heart scan on an EBT device, then your exposure is 0.5-0.6 mSv, roughly the same as a mammogram or several standard chest x-rays.

With a heart scan on a 16- or 64-slice multidetector device, exposure is ideally around 1.0-2.0 mSv, about the same as 2-3 mammograms, though dose can vary with this technology depending on how it is performed (gated to the EKG, device settings, etc.)

CT coronary angiography presents a different story. This is where radiation really escalates and puts the radiation exposure issue in the spotlight. As Dr. Cynthia McCullough's chart shows above, the radiation exposure with CT coronary angiograms is 5-12 mSv, the equivalent of 100 or more chest x-rays or 20 mammograms. Now, that's a problem.

The exposure is about the same for a pelvic or abdominal CT. The problem is that some centers are using CT coronary angiograms as screening procedures and even advocating their use annually. This is where the alarm needs to be sounded. These tests, as wonderful as the information and image quality can be, are not screening tests. Just like a pelvic CT, they are diagnostic tests done for legitimate medical questions. They are not screening tests to be applied broadly and used year after year.

It’s also worth giving second thought to any full body scan you might be considering. These screening studies include scans of the chest, abdomen, and pelvis. These scans, performed for screening, expose the recipient to approximately 10 mSv of radiation (Radiological Society of North American, 2007). Debate continues on whether the radiation exposure is justified, given the generally asymptomatic people who generally undergo these tests.

Always be mindful of your radiation exposure, as the NY Times article rightly advises. However, don't be so frightened that you are kept from obtaining truly useful information from, for instance, a CT heart scan (not angiography) at a modest radiation cost.


Heart scans, CT coronary angiograms and the future

Unfortunately, practicing physicians and those involved in providing CT scans are generally unconcerned with radiation exposure. The majority, in fact, are entirely unaware of the dose of radiation required for most CT scan studies and unaware of the cancer risk involved. It is therefore up to the individual to insist on a discussion of the type of scanner being used, the radiation dose delivered (at least in general terms), the necessity of the test, alternative methods to obtain the same diagnostic information, all in the context of lifetime radiation exposure.

Our concerns about radiation exposure all boil down to concern over lifetime risk for cancer, a disease that strikes approximately 20% of all Americans. Many factors contribute to cancer risk, including obesity, excessive saturated fat intake, low fiber intake, lack of vitamin D, repeated sunburns, excessive alcohol use, smoking, exposure to pesticides and other organochemicals, asbestos and other industrial exposures, electromagnetic wave exposure, and genetics. Radiation is just one source of risk, though to some degree a controllable one.

Some people, on hearing this somewhat disturbing discussion, refuse to ever have another medical test requiring radiation. That’s the wrong attitude. It makes no more sense than wearing lead shielding on your body 24 hours a day to reduce exposure from the atmosphere. Taken in the larger context of life, radiation exposure is just one item on a list of potentially harmful factors.

It is, however, worth some effort to minimize radiation exposure over your lifetime, particularly before age 60, and by submitting to high-dose testing only when truly necessary, or when the potential benefits outweigh the risks. Thus, with heart scans and CT coronary angiography, some thought to the potential benefits of knowing your score or the information gained from the CT angiogram need to be considered before undergoing the test. Often the practical difficulty, of course, is that your risk for heart disease simply cannot be known until after the test.

In our view, in the vast majority of instances a simple CT heart scan can serve the simple but crucial role of quantifying risk for heart attack and atherosclerotic plaque. CT heart scans yield this information with less than a tenth of the radiation exposure of a CT coronary angiogram. In people without symptoms and a normal stress test, there is rarely a need for CT coronary angiography with present day levels of radiation exposure. Perhaps as technology advances and the radiation required to generate images is reduced, then we should reconsider.

Early experiences are suggesting that the newest 256-slice scanners, now being developed but not yet available, will cut the dose exposure of 64-slice CT angiograms in half (from 27.8 mSv to 14.1 mSv in a recent Japanese study). The 256-slice scanners will allow scanning that is faster over a larger area in a given period of time.

Thankfully, the scanner manufacturers are increasingly sensitive to the radiation issue and have been working on methods to reduce radiation exposure. However, it still remains substantial.


References:
Einstein AJ, Henzlova MJ, Rajagopalan S. Estimating risk of cancer associated with radiation exposure from 64-slice computed tomography coronary angiography. JAMA 2007 Jul 18;298(3):317–323.

Harrison JD, Muirhead CR. Quantitative comparisons of cancer induction in humans by internally deposited radionuclides and external radiation. Int J Radiat Biol 2003 Jan;79(1):1–13.

Hausleiter J, Meyer T, Hadamitzyky M et al. Radiation Dose Estimates From Cardiac Multislice Computed Tomography in Daily Practice: Impact of Different Scanning Protocols on Effective Dose Estimates. Circulation 2006;113:1305–1310.

Kalra MK, Maher MM, Toth TL, Hamberg LM, Blake MA, Shepard J, Saini S. Strategies for CT radiation dose optimization. Radiology 2004;230:619–628.

Mayo JR, Aldrich J, Müller NL. Radiation exposure at chest CT: A statement of the Fleischner Society. Radiology 2003; 228:15–21.

Mori S, Nishizawa K, Kondo C, Ohno M, Akahane K, Endo M. Effective doses in subjects undergoing computed tomography cardiac imaging with the 256-multislice CT scanner. Eur J Radiol 2007 Jul 10; [Epub ahead of print].

Preston DL, Pierce DA, Shimizu Y, Ron E, Mabuchi K. Dose response and temporal patterns of radiation-associated solid cancer risks. Health Phys 2003 Jul;85(1):43–46.

Ron E. Cancer risks from medical radiation. Health Phys 2003 Jul;85(1):47–59.

Shilnikova NS, Preston DL, Ron E et al. Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Res 2003 Jun;159(6):787–798.

Semelka RC, Armao DM, Elias J Jr, Huda W. Imaging strategies to reduce the risk of radiation in CT studies, including selective substitution with MRI. J Magn Reson Imaging 2007 May;25(5):900–9090.


Copyright 2007, Track Your Plaque.

Goodbye, fructose

A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects.

The study is published in its entirety here.

Compared to glucose, fructose induced:

1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)

2) 13.9% increase in LDL cholesterol but double the increase for Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).

3) 44.9% increase in small LDL, compared to 13.3% with glucose.

4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC), fructose increased postprandial triglycerides 99.2%.


The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.

Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.

Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).

Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.

When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says.

The statin-free life

Matt came to me because his doctor couldn't reduce his LDL cholesterol.

His doctor had prescribed Zocor (simvastatin), Lipitor, Crestor, even pravastatin, all of which resulted in incapacitating muscle aches and weakness within a week of starting. No surprise, Matt had a jaundiced view of statin drugs.

We started out by characterizing his lipoprotein patterns:

--LDL 155 mg/dl

--72% of LDL was small LDL, a moderately severe pattern. (This means that small LDL comprised 112 mg/dl of the total 155 mg/dl LDL; large LDL comprised 43 mg/dl--small LDL was the problem.)

--HDL 42 mg/dl --Triglycerides 133 mg/dl

--No lipoprotein(a)

Beyond lipoproteins, Matt proved severely deficient in vitamin D with a starting level of 18 ng/ml.

Matt's doctor had advised that he avoid salt, as his blood pressure had been borderline high. His thyroid assessment disclosed a TSH of 3.89 mIU/ml with thyroid hormones free T3 and free T4 in the lower half of the normal range.

I therefore asked Matt to:

--Eliminate wheat, cornstarch, and sugars to reduce small LDL
--Add iodine
--Supplement 6000 units of an oil-based vitamin D preparation
--Take fish oil to provide at least 1800 mg EPA + DHA per day
--Take Armour Thyroid 1 grain per day


Several months later on this program, Matt had a repeat basic lipid panel:

--LDL 82 mg/dl--a 47% reduction

--HDL 52 mg/dl a 24% increase

--Triglycerides 60 mg/dl--a 55% decrease

In addition, vitamin D was 66 ng/ml, TSH was <1.0 mIU/ml with free T3 and free T4 in the upper half of the "reference range." Matt also felt great.

While the numbers could be slightly better, Matt had made tremendous progress towards achieving perfect values.

There you have it: Marked correction of cholesterol values, no statin drugs involved.

Creatine: Not just for muscle heads

Even if you’re not interested in building big muscles like a bodybuilder, there are health benefits to increasing muscle mass: increased bone density, better balance, and fewer injuries. Greater muscle mass means higher metabolic rate, improved insulin responsiveness, lower blood sugar. The inevitable loss of muscle mass of aging can lead to frailty, an increasingly common situation for the elderly. Muscle loss be reversed, health improved as a result.

Since its introduction in 1994, creatine has exploded in popularity, particularly among bodybuilders and athletes interested in gaining muscle mass and strength. But creatine is not just for young weight lifters. If you are just interested in increasing muscle mass for its health benefits, then creatine is something to consider.

A study of creatine supplementation in men, average age 70 years, demonstrated that, when creatine was combined with strength training, it increased muscle mass 250% better than placebo (7.26 lb muscle vs 2.86 lb muscle), along with improved leg strength and endurance. The same group also demonstrated 3.2% increased bone density (measured using dual energy X-ray absorptiometry) after 12 weeks in participants taking creatine with strength training, while the control (no strength training, no creatine) group decreased by 1.0%.

Benefits are not confined to men. Similar results were observed in another study that included women (age 65 and older), with outcomes in females comparable to males. This is especially important for females, given the common development of osteopenia and osteoporosis in postmenopausal females.

Other studies have shown that benefits are maintained after stopping creatine supplementation.

The most popular form of creatine is the monohydrate, generally taken as a “loading” phase of 15-20 grams per day (generally split into 3-4 doses of 5 grams) for 5-7 days, followed by weeks to months of 2-5 grams per day.

An alternative form, polyethylene glycosylated creatine (PEG-creatine) provides similar effects at one-fourth to one-half the dose of creatine, i.e., 1.25-2.5 grams per day.

Despite previous concerns about kidney toxicity with prolonged use, another study showed that athletes taking creatine for up to 21 months have shown no adverse effects on kidney function, lipid (cholesterol) values, or other basic health measures.

Having healthy muscle mass doesn't make you bulge like a bodybuilder. With modest efforts at strength training, augmented with creatine supplementation, you have a wonderful tool to feel better, reduce injury, increase bone density, and combat abnormal insulin resistance, not to mention accelerate weight loss, since lean muscle mass consumes energy.

The ultimate “bioidentical” hormone

There has been a lot of debate over whether or not “bio-identical” hormones, i.e., hormones identical to the human form, are superior to non-human forms dispensed by the drug industry.

The FDA is currently taking steps to clamp down on availability of bioidentical hormones and their claims of superiority, despite a groundswell of grassroot support for them. The argument has pitted anti-aging practitioners and the public, as well as the likes of Oprah and Suzanne Somers, against Big Pharma and the FDA, the two forces trying to squash the bioidentical hormone movement.

Regardless of what heavy-handed approach the FDA takes, we already have access to hormones identical to the original human form. It requires no prescription and yields downstream hormones that the human body recognizes as human.

That "bioidentical" hormone is pregnenolone.

Pregnenolone is the first biochemical step in the conversion of dietary cholesterol (yes-cholesterol!) to numerous other hormones. Pregnenolone is the source of the hormones that lie at the center of the bioidentical hormone controversy: estrogens, progesterone, and testosterone. We therefore already have our own over-the-counter, non-prescription form of bioidentical hormones.

Supplemental pregnenolone increases estrogens (mildly), progesterone, and testosterone. Prenenonlone supplementation simply provide more of the basic substrate for hormone production. The increase in hormones is usually modest, not as vigorous as direct hormone replacement like, say, testosterone or progesterone topical creams. But pregnenolone can be useful when small to moderate increases are desired, such as for reduction of Lp(a). A theoretical downside is that pregnenonlone can also convert to cortisol, the adrenal gland hormone that regulates fluid and blood pressure. However, I've not seen any measurable increase in cortisol with low doses of pregnenonlone and limited data suggest that it does not. Pregnenolone also converts to the other adrenal gland hormone, DHEA; I call DHEA "the hormone of assertiveness," since some people who take too much pregnenolone (or direct DHEA) acquire excessive assertiveness.

The key to pregnenolone supplementation is to proceed gradually and begin with a small dose, e.g., 5 mg every morning. Hormonal assessment is best conducted periodically to assess the effects and to determine whether a dose adjustment is in order.

Roger's near-miss CT angiogram experience

Heart Scan Blog reader, Roger, described his near-miss experience with CT coronary angiograms.

Hoping to obtain just a simple CT heart scan, he was bullied to get a CT coronary angiogram instead. Roger held strong and just asked for the test that we all should be having, a CT heart scan.


I posted yesterday that I was about to have my first CT heart scan...well, it was an interesting experience for reasons I coudn't possibly have anticipated. Dr. Davis has commented in the past on the confusion in the media about the difference between a CT calcium score scan, and a CT angiography, the latter requiring a far higher dose of radiation. I assumed this was a source of confusion only among patients and lay folks, but, lo and behold, I discovered today that doctors--or at least their helpers--can be just as confused.

Here's my story:

After checking in, I asked the receptionist to see if she had any information on whether my medical insurance was covering the scan. She called someone, and I heard her say over the phone, "He's here for a CT angiogram." At that point my ears perked up. I explained I wasn't here for a CT angiogram, only a regular CT scan. "Well, do you want to call your doctor and talk about this?" she asked. No, I said, I would like to ask one of their folks to verify exactly what test my doctor had ordered. As luck would have it, the technician was walking by at that point. "Is this a CT angiogram?" the receptionist asked. "No, it's just a CT calcium score scan" was the reply. But apparently the technician had been unclear herself, and had called my doctor just to verify. In other words, the "default" procedure they were accustomed to doing at this august Houston vascular clinic was a CT angiogram.

In fact, my appointment was even listed on their calendar as a "CT angiogram." For all I know, my insurance will be billed for the same. Later, during the procedure, the technician acted surprised I wasn't doing the "full test." I explained I had minimal risk factors (actually only one, an HDL of 34 a couple of years ago, which has since been raised to 50 partly as a result of taking advice from this site), but that my doctor was progressive (he is an MD for the Houston Astros) and thought it was a good idea since there is heart disease in my immediate family. My doctor did indeed prescribe only a CT calcium score scan, but it seems to have been an order that this clinic, at least, wasn't all that used to seeing.

So, I guess the message is: we have a lot of educating to do. Had I not been a faithful reader of these pages, I certainly wouldn't have known what kind of test I was about to get, or what questions to ask!

As for the heart scan itself, a piece of cake. If you can hold your breath, you can take this test. Just be sure it is the right one!



Why the "push" towards CT coronary angiograms and not "just" a CT heart scan? Well, I know it's shocking but it's . . . money!

CT coronary angiograms yield around $1800-$4000 per test. CT heart scans yield somewhere around $200. Though the scan center support staff might not care too much about the money themselves, their administrators likely make the cost distinctions clear to them.

Another reason: Most scan center staff, ironically, don't understand what a heart scan means, nor do they understand how it might serve to launch a program of prevention. They do understand that severe blockage by CT angiogram "needs" to be stented or bypassed. So they push patients towards things they understand.

Nobody makes money from CT heart scans, just as nobody makes money from a mammogram. Heart scans also don't lead to heroic, "lifesaving" procedures. They just lead to this sleepy, unexciting, inexpensive thing called prevention.

The Myth of Prevention: Letter to the Wall Street Journal





The June 20-21, 2009 Wall Street Journal Weekend Journal featured a provocative front page article written by physician, Dr. Abraham Verghese:

The Myth of Prevention

While eloquently written, I took issue with a few crucial points. Here is the letter I sent to the Editor at Wall Street Journal:


Dear Wall Street Journal Editor,

Re: Dr. Abraham Verghese’s article, The Myth of Prevention in the June 20-21, 2009 Weekend Journal.


I believe a more suitable title for Dr. Verghese’s article would be: “The Myth of What Passes as Prevention.”

As a practicing cardiologist, I, too, have witnessed firsthand the systemic “corruption” described by Dr. Verghese, the doing things “to” people rather than “for” them. Heart care, in particular, is rife with this form of profit-driven health delivery.

There is a fundamental flaw in Dr. Verghese’s otherwise admirable analysis: He assumes that what is called “prevention” in mainstream medicine is truly preventive.

Dr. Verghese makes issue of the apparent minor differences between preventing a condition and just allowing a condition to run its course. Prostate cancer screening is one example: Men subjected to repeated screenings have little length-of-life advantage over men who just allow their prostate to suffer the expected course of disease.

What if, instead, “prevention” as practiced today is nothing more than a solution that has been adopted in mainstream practice to suit yet another doing “to” strategy than doing “for”? In the prostate cancer example, PSA and prostate exam screenings often serve as little more than a means of harvesting procedures for the local urologist.

That’s not prevention. It is a prototypical example of “prevention” being subverted into the cause of revenue-generating procedures.

I submit that Dr. Verghese has fallen victim to the very same system he criticizes. His views have unwittingly been corrupted by the corrupt profit-driven system he describes.

What if, instead, prevention were just that: prevention or elimination of the condition. What if “prevention” of prostate cancer eliminated prostate cancer? What if heart disease “prevention” prevented all heart disease? What if this all proceeded without regard for profit or revenue-generating procedures, but just on results?

Dr. Verghese specifically targets heart scans or coronary calcium scoring, a test he likens to “miracle glow-in-the-dark minnow lures,” calling them “moneymakers.” Yes, when subverted into a corrupt algorithm of stress test, heart catheterization, stent, or bypass, heart scans are indeed a test used wrongly to “prevent” heart disease.

But what if the risk insights provided by heart scans prompt the start of a benign yet effective “prevention” program that inexpensively, safely, and assuredly prevents--in the true sense of the word--or eliminates heart disease? Then I believe the differences in mortality, quality of life, and costs would be substantial. Such strategies exist, yet do not necessarily include prescription drugs and certainly do not include the aftermath of heart catheterization and bypass surgery. Yet such programs fail to seize the limelight of media attention with no new high-tech lifesaving headline nor a big marketing budget to broadcast its message.

The problem in medicine is not prevention and its failure to yield cost- and life-saving results. It is the pervasively profit-driven mindset that keeps true preventive strategies from entering mainstream conversation. It is a repeat of Dr. Ignaz Semmelweis’ late 19th-century pleads for physicians to wash their hands before delivering babies to reduce puerperal sepsis, ignominious advice that earned him life and death in an asylum. We are essentially continuing to deliver children with unwashed hands because there is no revenue-generating procedure to clean them.

No, Dr. Verghese, the economic and medical failings of preventive strategies are not at fault. The failure of the medical system, in which everyone is bent on seizing a piece of the financial action for himself, has resulted in the failure to support the propagation of true preventive strategies that could genuinely save money and lives.

President Obama’s goal of cultivating preventive practices in medicine can work, but only if the profit-motive for “prevention” does not serve as the primary determinant of practice. Results-driven practices that are applied without regard to profit have the potential to yield the sorts of cost-saving and life-saving results that can reduce healthcare costs.


William Davis, MD
Milwaukee, Wisconsin
Medical Director, The Track Your Plaque Program (www.cureality.com)
Blog: http://heartscanblog.blogspot.com

A victory for SHAPE, CT heart scans, and doing what is RIGHT

The efforts of Texas House of Representatives Rep. Rene Oliveira and the SHAPE Guidelines committee have paid off: The Texas legislature passed a bill that requires health insurers to cover CT heart scans.

(NOTE: Don't make the same mistake that the media often makes and confuse CT heart scans with CT coronary angiography: two different tests, two different results, two different levels of radiation exposure. The difference is discussed here.)

Track Your Plaque previously reported the release of the SHAPE Guidelines, an ambitious effort to open CT heart scanning to people who would benefit from a simple screening test for coronary disease. Rep. Rene Oliveira initially introduced the bill in 2006, after having a heart scan uncovered extensive coronary plaque that resulted in coronary bypass surgery.

The bill requires that health-benefit providers cover the cost of CT heart scans (and carotid ultrasound) in men between the ages of 45-76, women 55-76, as well as anyone with diabetes or at "intermediate-risk" or higher for coronary disease by Framingham risk score.

The usual panel of cardiology knuckleheads stepped to the media podium, expressing their incredulity that something as "unvalidated" as heart scans could gain the backing of legislative mandate. Heartwire carried this comment:

"Contacted by heartwire, Dr Amit Khera (University of Texas Southwestern Medical Center, Dallas) confirmed there are still no comprehensive, adequately powered studies showing that these screening tests lead to better outcomes. In a phone interview, Khera said he has major concerns about how physicians will use these tests, particularly primary-care physicians. "I gave a talk last week to primary-care doctors, and there were probably 250 people in the room, and when I asked how many people had ordered a calcium scan, just one person raised a hand. . . . Most people don't even know what to do with the Framingham risk score, so they're going to follow an algorithm that they don't know how to follow to order a test result that they don't know what to do with."

It's the same criticisms hurled at heart scans over the years despite literally thousands of studies validating their application.

Studies have conclusively shown that:

--Coronary calcium scores generated by a CT heart scan outperform any other risk measure for coronary disease, including LDL cholesterol, c-reactive protein, total cholesterol, HDL cholesterol, blood pressure.
--Coronary calcium scores yield a graded, trackable index of coronary risk. Scores that increase correlate with increased risk of cardiovascular events; scores that remain unchanged correlate with much reduced risk.
--A coronary calcium score of zero--no detectable calcium--correlates with extremely low 5-year risk for cardiovascular events.
--Coronary calcium scores correlate with other measures of coronary disease. Heart scans correlate with coronary angiography, quantitative coronary angiography, carotid ultrasound (intimal-medial thickness and plaque severity), ankle-brachial index, and stress tests, including radionuclide (nuclear) perfusion imaging.

The reluctance of my colleagues to embrace heart scans stems from two issues, for the most part:

1) No study has yet been performed showing that knowing what the score is vs. not knowing what the score is changes prognosis. That's true. But it is also true of the great majority of practices in medicine. While many wrongs don't make a right, the miserable and widespread failure of other coronary risk measures, like LDL cholesterol or c-reactive protein, to readily and reliably detect hidden coronary disease creates a gaping void for improved efforts at early detection. If your LDL cholesterol is 140 mg/dl, do you or don't you have coronary disease? If your doctor's response is "Just take a statin drug anyway" you've been done a great disservice. (If and when this sort of study gets done, its huge cost--outcome studies have to be large and last many years--it will likely be a statin study. It is unlikely it will include such Track Your Plaque strategies that help reduce heart scan scores, like vitamin D and correction of small LDL particles.)

2) Fears over overuse of hospital procedures triggered by heart scans. This is a legitimate concern--if the information provided by a heart scan is misused. Heart scans should never--NEVER--lead directly to heart catheterization, stents, bypass surgery. Heart scans do not change the indications for performing revascularization (angioplasty, stents, bypass). Just because 20% of my cardiology colleagues are more concerned with profit rather than patient welfare does not invalidate the value of the test. Just because the mechanic at the local garage gouged you by replacing a carburetor for $800 when all you need was a new spark plug does not mean that we should outlaw all auto mechanics. Abuse is the fault of the abuser, not of the tool used to exercise the abuse.


All in all, while I am not a fan of legislating behavior in healthcare, the blatant and extreme ignorance of this simple tool for uncovering hidden heart disease makes the Texas action a huge success for heart disease prevention. I hope that this success will raise awareness, not just in Texas, but in other states and cities in which similar systemic neglect is the rule.

Remember: CT heart scans are tools for prevention, not to uncover "need" for procedures. They serve as a starting point to decide whether or not an intensive program of prevention is in order, and I don't mean statin vs. no statin.

Though not a multi-million dollar statin drug study, I have NEVER seen a heart attack or "need" for procedure in any person who has stopped progression or reduced their heart scan score. A small cohort from my practice was reported:

Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of >/= 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides /=60 mg/dL; and vitamin D3 supplementation to achieve serum levels of >/=50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Sleep: A to Zzzzzzzzzz

Take a look at the results from the Heart Scan Blog's most recent reader poll (399 respondents):

How many hours do you sleep per night (on average)?


9 or more hours per night
15 (3.7%)

8-9 hours per night
72 (18%)

7-8 hours per night
152 (38.1%)

6-7 hours per night
111 (27.8%)

5-6 hours per night
38 (9.5%)

Less than 5 hours per night
11 (2.8%)


Like many issues in health, too much or too little of a good thing can present undesirable consequences.

Too much sleep: While psychologists and sleep researchers advise us that at least 9 hours are required to fully eliminate sleep "debt" and achieve optimal vigilance and mental performance, epidemiologic studies have shown increased mortality with this quantity of sleep.

Too little sleep: Getting less than 7 hours habituallly increases blood sugar, appetite, inflammatory measures, and encourages weight gain. Mortality is also increased, just as with sleeping too much. It is also associated with increased likelihood of a positive heart scan score.

7-8 hours per night from a health viewpoint is that Goldlilocks "just right" value: just enough to not erode mental performance substantially, but not so little that inflammatory, insulin-disrupting, and appetite-increasing effects develop.

Of our 399 respondents in the poll, 56.1% (38% + 18%) slept what appears to be an optimal amount for health. While only 3.7% slept too much (9 hours or more), the remaining 40.1% slept too little.

Our informal poll confirms what most of us observe in everyday life: The majority of people shortchange sleep in order to meet the demands of their high-pressure, squeeze-as-much-as-possible-into-every-day lives. But not paying off your sleep "debt" is like not paying the mortgage for a couple of months. You wouldn't expect your friendly neighborhood bank to say, "Oh, you forgot to pay your mortgage? Forget about it. Just pay next month's." Sure, fat chance. But if you don't pay off your sleep "debt," you will pay it back with health.
Diet is superior to drugs

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Comments (27) -

  • Janknitz

    1/7/2012 6:24:17 PM |

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

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

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

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

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

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

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

  • Jan

    1/7/2012 6:52:31 PM |

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

  • Might-o'chondri-AL

    1/7/2012 11:46:08 PM |

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

  • Andrew

    1/9/2012 1:04:15 PM |

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

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

  • Jim

    1/9/2012 5:54:03 PM |

    Mit:

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

  • Might-o'chondri-AL

    1/9/2012 6:30:07 PM |

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

  • Jacob

    1/9/2012 10:37:21 PM |

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

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

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

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

  • Might-o'chondri-AL

    1/9/2012 10:42:21 PM |

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

  • Jacob

    1/9/2012 11:00:15 PM |

    @ Mitochondri'Al

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

  • Might-o'chondri-AL

    1/10/2012 1:20:11 AM |

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

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

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

  • Jacob

    1/10/2012 3:33:50 AM |

    @Mitochondri'Al...

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

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

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

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

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

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

  • Jacob

    1/10/2012 3:34:45 AM |

    outweight = outweigh

  • Might-o'chondri-AL

    1/10/2012 7:59:56 AM |

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

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

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

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

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

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

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

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

  • Jacob

    1/10/2012 8:58:03 AM |

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

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

  • Might-o'chondri-AL

    1/11/2012 3:44:15 AM |

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

  • Taking Charge

    1/11/2012 3:55:46 PM |

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

  • Galina L.

    1/11/2012 7:14:38 PM |

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

  • Jacob

    1/13/2012 4:50:46 AM |

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

  • Might-o'chondri-AL

    1/13/2012 3:31:55 PM |

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

  • Gene K

    1/13/2012 6:15:53 PM |

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

  • Galina L

    1/14/2012 3:32:19 AM |

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

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

  • Might-o'chondri-AL

    1/14/2012 4:39:38 AM |

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

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

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

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

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

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

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

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

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

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

  • Might-o'chondri-AL

    1/14/2012 6:23:11 AM |

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

  • Gene K

    1/14/2012 9:32:24 PM |

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

  • Jacob

    1/16/2012 1:52:02 AM |

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

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

  • Jacob

    1/16/2012 1:58:50 AM |

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

  • Dennis

    1/23/2012 6:47:58 PM |

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

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