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.
All posts by william-davis

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Overweight, hungry, diabetic, and fat-free

Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Condition Afflicts Millions: Do you have “YBS”?

After one of the harshest winters, spring has finally arrived.  The welcomed warmer temperatures and longer daylight hours infuse us with a sense of renewal and new beginnings.   Low and behold we begin to come out of hibernation and start the mad dash to engage in positive lifestyle changes such as eating better, exercising, proper sleep and taking appropriate nutritional supplements.  But invariably, life happens.  

Yep, just when you were about to get started, it happens.  YBS sets in.   I see this “condition” all too often with clients attempting to enter or re-enter into any number of behavior changes.  I will go so far as to say we all have been afflicted at one point or another in our lives.  I call this condition Yeah But Syndrome, or “YBS”.    It is often paralyzing and prevents those afflicted from moving into action, instead remaining in a state of inertia.  

There are many symptoms of YBS but the following are some of the most common.  

• Yeah I planned to go to the gym today BUT, the kids needed a ride to practice.  
• Yeah I really want to eat better BUT I don’t have the time.   
• Yeah I didn’t plan to eat the cake BUT my husband wanted too, so I did also.   
• Yeah I really meant to go to the grocery shopping BUT I was too tired, so I hit the drive- thru.  
• Or this is a good one. Yeah I meant to start today BUT, I’ll start tomorrow.  

But tomorrow never comes.  You get the drift.  We can all come up with a million yeah buts, in other words, excuses.    The good news is the treatment for YBS is simple--just do it!  Take action.  The reality of today’s 24-7 planet is there will always be something.  The kids, work commitments, family obligations and various projects that need your attention will perpetually be present in some shape or form.  The difference to make the difference is to learn to dance in the rain, not wait for the rain to pass.  When will all the stars align so that your world will be “just right” to start?  If not NOW, WHEN will you begin?  

The key word here is begin.   Far too frequently, I coach clients that shoot themselves in the foot before they start.   Instead of consuming yourself with all the barriers to entry, select reasonable, low-hanging fruit that is “doable.”    The art of lifestyle change is to avoid all-or-nothing thinking and begin to appreciate what you CAN do, versus focusing energy on what you can’t do.  What is one action you can do TODAY to move toward your wellness goal(s)?  Start to focus on what you can do in the mist of your existing life demands. This mantra is a friendly reminder: BE-DO-HAVE.  Be committed.  Do what it takes.  And you will have results.  

Lastly, if you think removing cereal from your morning routine it is too difficult and you can’t do it. Guess what-- you’re likely right.   What you think is what you get!   But what if you think instead, “I can do this.  There are many truly healthy options for breakfast to replace cereal such as eggs and veggies that will help me look and feel my best.”  Then guess what--you will!  This simple change in mind-set can start a tidal wave of change and prevent you from abandoning ship when life tosses you into rough waters.  Ongoing support is hugely important to sustain lifestyle changes.  Join the conversations in the Cureality Forum to engage the support of health coaches and Cureality Members to stay on track. 

We Need More.....Kettlebell

You either love them or you hate them.

When you are in love with kettlebells, like I am, you enjoy the multi-muscle group movements.  Kettlebell workouts are fluid, like a dance, putting together a chain of movements that leave your heart pounding and sweat pouring.  Yes, there’s some sneaky cardio component to a kettlebell workout.   A great blend of aerobic and anaerobic conditioning.

If you hate kettlebells it’s because kettlebell exercises keep you honest with proper exercise execution.  Form is imperative to moves like the kettlebell swing or the kettlebell snatch.  Do it incorrectly and you’ll be either sore or have bruised wrists the next day.  But this is no reason to shy away from the kettlebell.  You have way too much to gain from this odd looking piece of exercise equipment.  

You will get a mega -caloric burn.  The American council on Exercise states that the average kettlebell workout burns 20 calories per minute.  That’s 1200 calories in just one hour.   Kettlebell workouts utilize many muscle groups to give you an efficient, total body conditioning workout.  

If you’re looking for a toned back side get a kettlebell.  The classic kettlebell swing works all the posterior muscles like your glutes, hamstrings, and lower back.  But only if you use correct form.  Otherwise you'll find yourself with nagging back pain, instead of a better butt.  

Kettlebell exercises are functional movements that will allow you to play hard without getting injured.  If you are an athlete, a nature enthusiast, or just want to keep up with the kids then you need to give kettlebells a try.  During a workout, the exercises will target movements that will make getting up and down off the floor easier, as well as bending over to pick something up.

If you are interested in doing kettlebell workouts start with a coach or take class.  You can’t fake form with kettlebell exercises or you could end up hurt.  I’m not trying to scare anyone away because good form is easy to learn.   Your body will memorize the correct movement pattern and you’ll be on your way to a successful kettlebell workout.  

Thyroid and the gut: Hidden health partners

Though I have personally dealt with both auto-immune thyroiditis (Hashomoto’s) and several gut issues (wheat sensitivity, gastritis, etc.), it was not until recently that I discovered how close the thyroid and gut work together to keep you healthy – and how problems with one can affect the other along with your overall health.
 
Most of us understand that the primary function of the gut, that 25 to 30 feet of “tubing” that includes everything from your stomach to your large intestines, is to process the food we eat and allow the “good stuff” (essential nutrients) to pass into our blood stream while keeping the “bad stuff” (harmful proteins) out. However, it may surprise some that the gut also holds as much as 70% of all the immune tissue in the body.
 
Now, imagine all the health havoc that could ensue if, suddenly, the gut stopped doing its job – particularly if it failed to stop toxic proteins from entering the blood stream and then mounted an overzealous immune response against them.  Sometimes, those overzealous immune responses reach beyond their intended targets to attack otherwise healthy tissues and organs – like the thyroid gland.
 
Recent studies indicate that thyroid hormones play a significant role in maintaining gut integrity, preventing leaky gut that can, in some cases, lead to auto-immune attacks against the thyroid.  A properly functioning gut also aids the production of thyroid hormones by converting some of the inactive “T4” thyroid hormone into the functional “T3” hormone.  Failure to simultaneously maintain both a healthy gut and a healthy thyroid can create a vicious cycle leading to chronic health problems and declining vitality.
 
What it all means is that to enjoy optimal health, you must promote good thyroid health to promote good gut health and vice versa.  Unfortunately, traditional medicine tends to focus on one issue to the exclusion of others.  A typical endocrinologist may treat your under active thyroid without spending a moment to address underlying gut issues.  A gastroenterologist will work alleviate a gut problem but will rarely address a potential thyroid problem.
 
This illustrates, once again, how our bodies work as a system and why it is necessary to bridge the “healthcare gaps” in traditional medicine by becoming personally responsible for your health.  I encourage everyone to consult the Cureality Program Guide and online Cureality Diet and Thyroid Health Tracks to learn more about how to optimize both your gut and thyroid health on your journey to realizing complete, whole-body health.

Omega-3 fatty acids likely NOT associated with prostate cancer

A weakly constructed study was reported recently that purportedly associated higher levels of omega-3 fatty acid blood levels and prostate cancer. See this CBS News report, for instance.

Lipid and omega-3 fat expert, Dr. William Harris, posted this concise critique of the study, exposing some fundamental problems:

First, the reported EPA+DHA level in the plasma phospholipids in this study was 3.62% in the no-cancer control group, 3.66% in the total cancer group, 3.67% in the low grade cancer group, and 3.74% in the high-grade group. These differences between cases and controls are very small and would have no meaning clinically as they are within the normal variation. Based on experiments in our lab, the lowest quartile would correspond to an HS-Omega-3 Index of <3.16% and the highest to an Index of >4.77%). These values are obviously low, and virtually none of the subjects was in “danger” of having an HS-Omega-3 Index of >8%. So to conclude that regular consumption of 2 oily fish meals a week or taking fish oil supplements (both of which would result in an Index above the observed range) would increase risk for prostate cancer is extrapolating beyond the data.

This study did not test the question of whether giving fish oil supplements (or eating more oily fish) increased PC risk; it looked only a blood levels of omega-3 which are determined by intake, other dietary factors, metabolism and genetics.


The authors also failed to present the fuller story taught by the literature. The same team reported in 2010 that the use of fish oil supplements was not associated with any increased risk for prostate cancer. A 2010 meta-analysis of fish consumption and prostate cancer reported a reduction in late stage or fatal cancer among cohort studies, but no overall relationship between prostate cancer and fish intake. Terry et al. in 2001 reported higher fish intake was associated with lower risk for prostate cancer incidence and death, and Leitzmann et al. in 2004 reported similar findings. Higher intakes of canned, preserved fish were reported to be associated with reduced risk for prostate cancer. Epstein et al found that a higher omega-3 fatty acid intake predicted better survival for men who already had prostate cancer, and increased fish intake was associated with a 63% reduction in risk for aggressive prostate cancer in a case-control study by Fradet et al). So there is considerable evidence actually FAVORING an increase in fish intake for prostate cancer risk reduction.

Another piece of the picture is to compare prostate cancer rates in Japan vs the US. Here is a quote from the World Foundation of Urology:


"[Prostate cancer] incidence is really high in North America and Northern Europe (e.g., 63 X 100,000 white men and 102 X 100,000 Afro-Americans in the United States), but very low in Asia (e.g., 10 X 100,000 men in Japan).”

Since the Japanese typically eat about 8x more omega-3 fatty acids than Americans do and their
blood levels are twice as high, you’d think their prostate cancer risk would be much higher...
but the opposite is the case.


Omega-3 fatty acids are physiologically necessary, normalizing multiple metabolic phenomena including augmentation of parasympathetic tone, reductions of postprandial (after-meal) lipoprotein excursions, and endothelial function. It would indeed make no sense that nutrients that are necessary for life and health exert an adverse effect such as prostate cancer at such low blood levels. (Recall that an omega-3 RBC index of 6.0% or greater is associated with reduced potential for sudden cardiac death.)

I personally take 3600 mg per day of EPA + DHA in highly-purified, non-oxidized triglyceride form (Ascenta Nutrasea liquid) that yields an RBC omega-3 index of just over 10%, the level that I believe the overwhelming bulk of data suggest is the ideal level for humans.

Are statins and omega-3s incompatible?

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association's advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

--Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)
--Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)
--Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don't have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.



DHA: the crucial omega-3

Of the two omega-3 fatty acids that are best explored, EPA and DHA, it is likely DHA that exerts the most blood pressure- and heart rate-reducing effects. Here are the data of Mori et al in which 4000 mg of olive oil, purified EPA only, or purified DHA only were administered over 6 weeks:



□ indicates baseline SBP; ▪, postintervention SBP; ○, baseline DBP; •, postintervention DBP; ⋄, baseline HR; and ♦, postintervention HR.

In this group of 56 overweight men with normal starting blood pressures, only DHA reduced systolic BP by 5.8 mmHg, diastolic by 3.3 mmHg.

While each omega-3 fatty acid has important effects, it may be DHA that has an outsized benefit. So how can you get more DHA? Well, this observation from Schuchardt et al is important:

DHA in the triglyceride and phospholipid forms are 3-fold better absorbed, as compared to the ethyl ester form (compared by area-under-the-curve). In other words, fish oil that has been reconstituted to the naturally-occurring triglyceride form (i.e., the form found in fresh fish) provides 3-fold greater blood levels of DHA than the more common ethyl ester form found in most capsules. (The phospholipid form of DHA found in krill is also well-absorbed, but occurs in such small quantities that it is not a practical means of obtaining omega-3 fatty acids, putting aside the astaxanthin issue.)

So if the superior health effects of DHA are desired in a form that is absorbed, the ideal way to do this is either to eat fish or to supplement fish oil in the triglyceride, not ethyl ester, form. The most common and popular forms of fish oil sold are ethyl esters, including Sam's Club Triple-Strength, Costco, Nature Made, Nature's Bounty, as well as prescription Lovaza. (That's right: prescription fish oil, from this and several other perspectives, is an inferior product.)

What sources of triglyceride fish oil with greater DHA content/absorption are available to us? My favorites are, in this order:

Ascenta NutraSea
CEO and founder, Marc St. Onge, is a friend. Having visited his production facility in Nova Scotia, I was impressed with the meticulous methods of preparation. At every step of the way, every effort was made to limit any potential oxidation, including packaging in a vacuum environment. The Ascenta line of triglyceride fish oils are also richer in DHA content. Their NutraSea High DHA liquid, for instance, contains 500 mg EPA and 1000 mg DHA per teaspoon, a 1:2 EPA:DHA ratio, rather than the more typical 3:2 EPA:DHA ratio of ethyl ester forms.

Pharmax (now Seroyal) also has a fine product with a 1.4:1 EPA:DHA ratio.

Nordic Naturals has a fine liquid triglyceride product, though it is 2:1 EPA:DHA.





Krill oil: Do the math

The manufacturers of krill oil claim that the phospholipid form of omega-3 fatty acids, EPA and DHA, enhance their absorption. There are indeed some data to that effect:


Here are some representative krill oil preparations available on the market:


MegaRed Krill Oil:
EPA 50 mg
DHA 24 mg
Total omega-3s (EPA + DHA + other forms) 90 mg
Price: $28.99 for 60 softgels

Source Naturals (a fine company otherwise, by the way):

EPA 150 mg
DHA 90 mg
Total omega-3 fatty acids 300 mg
Price: $24.99 for 60 softgels

Alright, let's do some simple math:

Average volume of blood in the human body (all components): 5000 cc
Percentage of red blood cells (RBCs) by volume: 45%
Total volume RBCs: 2250 cc
Percentage of total volume RBCs occupied by fatty acids:

What tests are MORE important than cholesterol?

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Cranberry Sauce

Happy Thanksgiving 2012, everyone, from all the staff at Track Your Plaque!

Here’s a zesty version of traditional cranberry sauce, minus the sugar. The orange, cinnamon, and other spices, along with the crunch of walnuts, make this one of my favorite holiday side dishes.

There are 31.5 grams total “net” carbohydrates in this entire recipe, or 5.25 grams per serving (serves 6). To further reduce carbs, you can leave out the orange juice and, optionally, use more zest.

1 cup water
12 ounces fresh whole cranberries
Sweetener equivalent to 1 cup sugar (I used 6 tablespoons Truvía)
1 tablespoon orange zest + juice of half an orange
½ cup chopped walnuts
1 teaspoon ground cinnamon
½ teaspoon ground nutmeg
¼ teaspoon ground cloves

In small to medium saucepan, bring water to boil. Turn heat down and add cranberries. Cover and cook at low-heat for 10 minutes or until all cranberries have popped. Stir in sweetener. Remove from heat.

Stir in orange zest and juice, walnuts, cinnamon, nutmeg, and cloves.

Transfer mixture to bowl, cool, and serve.


Apple Cranberry Crumble

Apple, cranberry, and cinnamon: the perfect combination of tastes and scents for winter holidays!

I took a bit of carbohydrate liberties with this recipe. The entire recipe yields a delicious cheesecake-like crumble with 59 “net” grams carbohydrates (total carbs – fiber); divided among 10 slices, that’s 5.9 grams net carbs per serving, a quantity most tolerate just fine. (To reduce carbohydrates, the molasses in the crumble is optional, reducing total carbohydrate by 11 grams.)

Other good choices for sweeteners include liquid stevia, stevia glycerite, powdered stevia (pure or inulin-based, not maltodextrin-based), Truvía, Swerve, and erythritol. And always taste your batter to test sweetness, since sweeteners vary in sweetness from brand to brand and your individual sensitivity to sweetness depends on how long you’ve been wheat-free. (The longer you’ve been wheat-free, the less sweetness you desire.)


Crust and crumble topping
3 cups almond meal
1 stick (8 tablespoons) butter, softened
1 cup xylitol (or other sweetener equivalent to 1 cup sugar)
1½ teaspoons ground cinnamon
1 tablespoon molasses
1½ teaspoons vanilla extract
Dash sea salt

Filling
16 ounces cream cheese, softened
2 large eggs
½ cup xylitol (or other sweetener equivalent to ½ cup sugar)
1 Granny Smith apple (or other variety)
1 teaspoon ground cinnamon
1 cup fresh cranberries

Preheat oven to 350° F.

In large bowl, combine almond meal, butter, sweetener, cinnamon, molasses, vanilla, and salt and mix.

Grease a 9½-inch tart or pie pan. Using approximately 1 cup of the almond meal mixture, form a thin bottom crust with your hands or spoon.

In another bowl, combine cream cheese, eggs, and sweetener and mix with spoon or mixer at low-speed. Pour into tart or pie pan.

Core apple and slice into very thin sections. Arrange in circles around the edge of the cream cheese mixture, working inwards. Distribute cranberries over top, then sprinkle cinnamon over entire mixture.

Gently layer remaining almond meal crumble evenly over top. Bake for 30 minutes or until topping lightly browned.

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