Thyroid: Be a perfectionist

If you'd like to reduce LDL cholesterol with nearly as much power as a statin drug, think thyroid.

When thyroid is corrected to ideal levels, LDL cholesterol drops 20, 30, 40 mg/dl or more, depending on how poor thyroid function and how high LDL are at the start. The poorer the thyroid function (the higher the TSH or the lower the T3 and T4) and the higher the LDL cholesterol, the more LDL drops with thyroid correction.

(For those of you minding LDL particle size, such as Track Your Plaque Members, the "dominant" LDL species will drop: If you are genetic small LDL, small LDL will drop. If you have mostly large LDL because of being wheat-free and sugar-free, then large LDL will drop.)

One of the problems is that many healthcare providers blindly follow what the laboratory says is "normal" or the "reference range," which is usually nothing more than a population average (actually the mean +/- 2 standard deviations, a common method of developing references ranges). In other words, a substantial degree of low thyroid function, or hypothyroidism, can be present when your doctor adheres to the reference range provided by the laboratory.

What does it mean to achieve ideal thyroid status? My list includes:

--Normal oral temperature of 97.3 F first upon arising. (The thyroid is the body's thermoregulatory organ.)
--TSH 1.0 mIU/L or less
--Free T3 upper half "normal" range
--Free T4 upper half "normal" range
--You feel good: mental clarity, energy, upbeat mood. You lose weight when you try.

Iodine replacement should be part of any thyroid health effort. Iodine is not an optional trace mineral, no more than vitamin C is optional (else your teeth fall out). The only dangers to iodine replacement are to those who have been starved of iodine for many years; increase iodine and the thyroid can over-respond. I've seen this happen in 2 of the last 300 people who have supplemented iodine.

In my view, neglecting T3 replacement is absurd. While it is not clear to me why many otherwise healthy people have low T3 at the low range of "normal" or even in the below-normal range, people feel better and have better health--faster weight loss, reduced LDL, reduced triglycerides, they are happier and enjoy more energy--when T3 is increased to the upper half of the reference range. (Crucial question: Why is the 5'-deiodinase enzyme that converts T4 to T3 inhibited, resulting in reduced free T3? What is in our diets or environment that is exerting this effect? I don't have answer, but we sorely need one.)

It pays to be a perfectionist when it comes to thyroid. Not only do you feel better, but LDL cholesterol can drop with a statin-like magnitude, but with none of the adverse effects.

If interested, Track Your Plaque offers fingerstick blood spot testing that you can perform in your own home. Each test kit will test for: TSH, free T3, free T4, along with a thyroid peroxidase antibody (a marker for Hashimoto's thyroiditis, an autoimmune inflammatory condition of the thyroid).

Nutrition Syllogism

What do you think of these chains of logic?

Cyanide is a potent lethal poison; carbon monoxide is a less lethal poison.
Therefore: plenty of carbon monoxide is good.




Having uterine cancer is a bad thing. Having uterine fibroids is a less bad thing.
Therefore: plenty of uterine fibroids are good.



These are obvious examples of seriously flawed logic. Students of logic and philosophy will recognize the above erroneous sequences as examples of the twisted arguments often used to persuade an argumentative opponent of the logic of a premise. As long ago as 335 B.C., Greek philosopher, Aristotle, recognized the pitfalls of thinking in such arguments. You think we’d know better by now.

Try this one:

White enriched flour is a bad for health; whole grains are less bad for health.
Therefore: plenty of whole grains are good for health.



Ouch!

In the 1960s, we all ate hot dogs on white buns, white flour Wonder Bread® sandwiches, Mom made cookies and cupcakes with white flour. Then, during the 1970s and 1980s, clinical studies were performed demonstrating that whole wheat and whole grains reduced colon cancer, high blood pressure, diabetes, and heart disease compared to white flour. In other words, add back fiber and B vitamins and health benefits develop: No argument here.

Therefore: whole grains must be good for health. Further, lots of whole grains?unlimited quantities of whole grains many times per day, every day?must be even better. Even the USDA says so on their nutrition pyramid, with 8-11 servings of grains per day, 4 of which should be whole grains, at the widest portion of the pyramid.

But what happens when you follow this logic through and fill your diet with whole grains?

Look around you and it’s easy to see: Appetite increases, people become obese, blood sugar increases, diabetes develops, HDL cholesterol plummets, triglycerides skyrocket, inflammatory patterns (e.g., c-reactive protein, or CRP) increase, small LDL (the number one cause for heart disease in the obese U.S.!) shoots through the roof.

I would no more fill my diet with “healthy whole grains” than I would close my garage door with the car running.

Is pomegranate juice healthy?


Pomegranate juice, 8 oz:

Sugars, total 31.50 g

Sucrose 0.00 g

Glucose (dextrose) 15.64 g

Fructose 15.86 g




In your quest to increase the flavonoids in your diet, do you overexpose yourself to fructose?

Remember: Fructose increases LDL cholesterol, apoprotein B, small LDL, triglycerides, and substantially increases deposition of visceral fat (fructose belly?). How about a slice of whole grain bread with that glass of pomegranate juice? The Heart Association says it's all low-fat!


(Coming on the Track Your Plaque website: A full in-depth Special Report on fructose in all its glorious forms and whether this is truly an issue for your health. Fructose tables and the scientific data to establish a safe "threshold" value will be included.)

Image courtesy Wikipedia

Honeydew melon


Honeydew melon:

Sugars, total 51.97 g

Sucrose 15.87 g

Glucose 17.15 g

Fructose 18.94 g

Because sucrose is half fructose (the other half is glucose), there are approximately 26 grams of fructose per one-half honeydew melon.



Image courtesy Wikipedia

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.
All posts by william-davis

Does high cholesterol cause heart disease?

How often does someone develop coronary heart disease from high cholesterol alone?

Believe drug industry propaganda and you'd think that everyone does. Physicians have bought into this concept also, driving the $27 billion annual sales in statin cholesterol drugs.

In my experience, I can count the number of people who develop coronary disease from high cholesterol alone on one hand. It happens--but rarely.

That's not to say that cholesterol is not an issue. That rant populates many of the kook websites and conversations on the internet that argue that high cholesterol is a surrogate for some other health issue, or that it is part of a medical conspiracy.

The problem with conventional measurement of cholesterol is that it ignores the particle size issue: whether particles are large or small. Small LDL are flagrant causes of coronary atherosclerotic plaque. Large LDL is a rather meager cause. Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

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

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

It is therefore an unfortunate oversimplification to say that high cholesterol causes heart disease or that it doesn't. It can--but not always, depending on size and other factors. In my view, it is therefore irreponsible to treat total or LDL cholesterol without knowledge of particle size. I've seen this play out many times: Someone with an LDL cholesterol of 150 mg/dl but all large still gets prescribed a statin drug by his/her doctor. Or someone with an LDL of 100 mg/dl--generally "favorable" by most standards--is not treated but it is all small and the person is truly at high risk. (Also, knowledge that all LDL particles are small does not mean that statins are the preferred agent. In my view, they are not.)

Are humans meant to be omnivores?

Are humans meant to be omnivores?

Does the ideal human diet include animal products like meat, fish, cheese, eggs, and dairy products?

Or should the ideal diet be devoid of all animal products?a vegetarian diet?

Though the argument is distorted by modern food processing methods (e.g., factory farming, long-term administration of antibiotics), convenience foods, and pseudo-foods crafted by food manufacturers, there are, obviously, proponents of both extremes.

The Atkins’ diet, for instance, advocates unrestricted intake of animal products, regardless of production methods or curing (sausage and bacon). At the opposite extreme are diets like Ornish (Dr. Dean Ornish’s Program for Reversal of Heart Disease) and the experiences of Dr. Colin Campbell, articulated in his studies and book, The China Study, in which he lambasts animal products, including dairy, as triggers for cancer and heart disease.

So which end of the spectrum is correct? Or ideal?

For the sake of argument, let's put aside philosophical questions (like not wanting eat animal products because of aversion to killing any living being) or ethical concerns (inhumane treatment of farm animals, cruel slaughtering practices, etc.). Does the inclusion of animal products provide advantage? Disadvantage?

The traditional argument against animal products has been saturated fat. If we accept that we’ve demoted the saturated fat question to a place far down the list of importance (though this is yet another argument to discuss another time), several questions emerge:

• If humans were meant to be vegetarian, why do omega-3 fatty acids (mostly from wild game and fish) yield such substantial health benefits, including dramatic reduction in sudden death from heart disease?

• Why would vitamin K2 (from meats and milk, as well as fermented foods like natto and cheese), obtainable in only the tiniest amounts on a vegetarian diet, provide such significant benefits on bone and cardiovascular health?

• Why would vitamin B12 (from meats) be necessary to maintain a normal blood count, prevent anemia, keep homocysteine at bay, and lead to profound neurologic dysfunction when deficient?


Omega-3 fatty acids and vitamins K2 and B12 cannot be obtained in satisfactory quantities from a pure vegetarian diet. The consequences of deficiency are not measured in decades, but in a few years. The conclusion is unavoidable: Evolutionarily, humans are meant to consume at least some foods from animal sources.

That's not to say that we should gorge ourselves on animal products. Gout (excessive uric acid) and kidney stones are among the unhealthy consequences of excessive quantities of meats in our diets.

It pains me to say this, since I’ve always favored a vegetarian lifestyle, mostly because of philosophical concerns, as well as worries about the safety of our factory farm-raised livestock and rampant inhumane practices.

But, stepping back and objectively examining what nutritional approach appears to stack the odds in favor of optimal health, I believe that only one conclusion is possible: Humans are meant to be omnivorous, meant to consume some quantity of animal products in addition to vegetables, fruits, nuts, and other non-animal products.

The question is how much?

Are you wheat-free?

According to the recent Heart Scan Blog poll, Are you wheat-free?, the 173 respondents said:

Yes, I am free of wheat products.
87 (50%)

No, I include wheat products in my diet.
73 (42%)

I'm not sure.
1 (0%)

I think you're nuts.
12 (6%)


That's kind of what I expected.

There are people who have eliminated wheat and experienced nothing except a feeling of deprivation. These people are in the minority. Though the poll was not set up to reflect this (i.e., asked who tried it and experienced no perceptible benefit), in my experience, this applies to about 20% of people. Little happens with elimination of wheat beyond modest weight loss. Those are the people who generally think I'm nuts.

Or, these people may have been brainwashed by "official" agencies like the USDA, the American Diabetes Association, and American Heart Association and the constant marketing of (high markup) grain products like Cheerios and Shredded Wheat . Some people are really uncomfortable going against the "grain" of popular public opinion.

Then there are the people who try to eliminate wheat and fail. They can't deal with the overwhelming fatigue, mental fog, and moodiness that comes with withdrawal from wheat, the phenomenon of converting from a sugar-burning metabolism to a fat-burning metabolism. Although wheat withdrawal usually runs its course in 2-5 days, some people find it intolerable. (That would be another fun poll to run: Have you experienced wheat-withdrawal?) Occasionally, the withdrawal is replaced by endless cravings, a phenomenon that applies to only about 10% of people. These are the true "wheat addicts." These are the people who eliminate wheat, lose 40 lbs, then regain it when they have one cracker and the floodgates of impulse control crumble.

Then there are the majority, 50% in the poll, though more like 70% in my face-to-face experience. Why is my experience skewed? Well, the people I deal with every day come because of coronary disease in some form (abnormal heart scan score, for instance) or because of lipid or lipoprotein abnormalities. So my experienced is skewed towards people who are likely to have something abnormal, such as high triglycerides or small LDL particles, both of which are created by including wheat in the diet.

This last group also shows unexpected effects of wheat elimination: substantial weight loss, dramatic reductions in blood sugar and triglycerides, increase in HDL, reductions in small LDL, reduction in c-reactive protein and other inflammatory measures. Appetite shrinks considerably. Not uncommonly, improved well-being, reduction in bowel complaints like cramping or "irritable bowel syndrome" is experienced, some rashes clear, occasionally arthritis will improve. See below for some of the testimonials to this experience.

When I first set out to advise people to eliminate wheat, I did it because I reasoned that it would be a quick and simple way to get people to reduce blood sugars and help correct the ubiquitous metabolic syndrome that afflicts nearly 50 million Americans now. And it did indeed accomplish that simple goal. But I did not expect all the other benefits to develop, the dramatic weight loss, improved well-being, reduction in hunger, etc.

I view wheat elimination as an easy-to-remember, digestible way to obtain enormous health benefits in a coronary plaque-control program, one that works for most--but not all--people. And I relate this experience not to sell you something, but to simply relate what I see as the truth, a way that is contrary to conventional advice yet works enormously well.



Unsolicited testimonials of people who have successfully been wheat-free:

Barbara W said:

It's true! We've done it. My husband and I stopped eating all grains and sugar in February. At this point, we really don't miss them any more. It was a huge change, but it's worth the effort. I've lost over 20 pounds (10 to go)and my husband has lost 45 pounds (20 to go). On top of it, our body shapes have changed drastically. It is really amazing. I've got my waist back (and a whole wardrobe of clothes) - I'm thrilled.

I'm also very happy to be eating foods that I always loved like eggs, avocados, and meats - without feeling guilty that they're not good for me.

With the extremely hot weather this week in our area, we thought we'd "treat" ourselves to small ice cream cones. To our surprise, it wasn't that much of a treat. Didn't even taste as good as we'd anticipated. I know I would have been much more satisfied with a snack of smoked salmon with fresh dill, capers, chopped onion and drizzled with lemon juice.

Aside from weight changes, we both feel so much better in general - feel much more alert and move around with much greater flexibility, sleep well, never have any indigestion. We're really enjoying this. It's like feeling younger.

It's not a diet for us. This will be the way we eat from now on. Actually, we think our food has become more interesting and varied since giving up all the "white stuff". I guess we felt compelled to get a little more creative.

Eating out (or at other peoples' places) has probably been the hardest part of this adjustment. But now we're getting pretty comfortable saying what we won't eat. I'm starting to enjoy the reactions it produces.


Weight loss, increased energy, less abdominal bloating, better sleep--I've seen it many times, as well.


Dotslady said:

I was a victim of the '80s lowfat diet craze - doc told me I was obese, gave me the Standard American Diet and said to watch my fat (I'm not a big meat eater, didn't like mayo ... couldn't figure out where my fat was coming from! maybe the fries - I will admit I liked fries). I looked to the USDA food pyramid and to increase my fiber for the constipation I was experiencing. Bread with 3 grams of fiber wasn't good enough; I turned to Kashi cereals for 11 years. My constipation turned to steattorrhea and a celiac disease diagnosis! *No gut pains!* My PCP sent me to the gastroenterologist for a colonscopy because my ferritin was a 5 (20 is low range). Good thing I googled around and asked him to do an endoscopy or I'd be a zombie by now.

My symptoms were depression & anxiety, eczema, GERD, hypothyroidism, mild dizziness, tripping, Alzheimer's-like memory problems, insomnia, heart palpitations, fibromyalgia, worsening eyesight, mild cardiomyopathy, to name a few.

After six months gluten-free, I asked my gastroenterologist about feeling full early ... he said he didn't know what I was talking about! *shrug*

But *I* knew -- it was the gluten/starches! My satiety level has totally changed, and for the first time in my life I feel NORMAL!



Feeling satisfied with less is a prominent effect in my experience, too. You need to eat less, you're driven to snack less, less likely to give in to those evil little bedtime or middle-of-the-night impulses that make you feel ashamed and guilty.



An anonymous (female) commenter said:

My life changed when I cut not only all wheat, but all grains from my diet.

For the first time in my life, I was no longer hungry -no hunger pangs between meals; no overwhelming desire to snack. Now I eat at mealtimes without even thinking about food in between.

I've dropped 70 pounds, effortlessly, come off high blood pressure meds and control my blood sugar without medication.

I don't know whether it was just the elimination of grain, especially wheat, or whether it was a combination of grain elimnation along with a number of other changes, but I do know that mere reduction of grain consumption still left me hungry. It wasn't until I elimnated it that the overwhelming redution in appetite kicked in.

As a former wheat-addicted vegetarian, who thought she was eating healthily according to all the expert advice out there at the time, I can only shake my head at how mistaken I was.




Stan said:

It's worth it and you won't look back!

Many things will improve, not just weight reduction: you will think clearer, your reflexes will improve, your breathing rate will go down, your blood pressure will normalize. You will never or rarely have a fever or viral infections like cold or flu. You will become more resistant to cold temperature and you will rarely feel tired, ever!



Ortcloud said:

Whenever I go out to breakfast I look around and I am in shock at what people eat for breakfast. Big stack of pancakes, fruit, fruit juice syrup, just like you said. This is not breakfast, this is dessert ! It has the same sugar and nutrition as a birthday cake, would anyone think cake is ok for breakfast ? No, but that is exactly the equivalent of what they are eating. Somehow we have been duped to think this is ok. For me, I typically eat an omelette when I go out, low carb and no sugar. I dont eat wheat but invariably it comes with the meal and I try to tell the waitress no thanks, they are stunned. They try to push some other type of wheat or sugar product on me instead, finally I have to tell them I dont eat wheat and they are doubly stunned. They cant comprehend it. We have a long way to go in terms of re-education.

Yes. Don't be surprised at the incomprehension, the rolled eyes, even the anger that can sometimes result. Imagine that told you that the food you've come to rely on and love is killing you!



Anne said:

I was overweight by only about 15lbs and I was having pitting edema in my legs and shortness of breath. My cardiologist and I were discussing the possible need of an angiogram. I was three years out from heart bypass surgery.

Before we could schedule the procedure, I tested positive for gluten sensitivity through www.enterolab.com. I eliminated not only wheat but also barley and rye and oats(very contaminated with wheat) from my diet. Within a few weeks my edema was gone, my energy was up and I was no longer short of breath. I lost about 10 lbs. The main reason I gave up gluten was to see if I could stop the progression of my peripheral neuropathy. Getting off wheat and other gluten grains has given me back my life. I have been gluten free for 4 years and feel younger than I have in many years.

There are many gluten free processed foods, but I have found I feel my best when I stick with whole foods.



Ann has a different reason (gluten enteropathy, or celiac disease) for wanting to be wheat-free. But I've seen similar improvements that go beyond just relief of the symptoms attributable to the inflammatory intestinal effects of gluten elimination.



Wccaguy said:

I have relatively successfully cut carbs and grains from my diet thus far.

Because I've got some weight to lose, I have tried to keep the carb count low and I've lost 15 pounds since then.

I have also been very surprised at the significant reduction in my appetite. I've read about the experience of others with regard to appetite reduction and couldn't really imagine that it could happen for me too. But it has.

A few weeks ago, I attended a party catered by one of my favorite italian restaurants and got myself offtrack for two days. Then it took me a couple of days to get back on track because my appetite returned.

Check out Jimmy Moore's website for lots of ideas about variations of foods to try. The latest thing I picked up from Jimmy is the good old-fashioned hard boiled egg. Two or three eggs with some spicy hot sauce for breakfast and a handful of almonds mid-morning plus a couple glasses of water and I'm good for the morning no problem.

I find myself thinking about lunch not because I'm really hungry but out of habit.

The cool thing too now is that the more I do this, the more I'm just not tempted much to do anything but this diet.

No more canned foods

If you haven't already caught the news, it's time to eliminate canned foods and exposure to plastics that contain the chemical, bisphenol A (BPA). A worrisome and unexpected association with heart disease and diabetes has been found.

This issue has been debated for some years ever since scientists at the NIH detected BPA in the blood samples of 93-95% of Americans, with consumer protection advocates calling for more research or even the outright banning of BPA , while industry representatives have argued that the data fail to conclusively prove adverse health effects.

Well, the argument has been tilted heavily in favor of increased consumer protection with the publication of a study in the Journal of the American Medical Association by Dr. Iain Lang and associates at the University of Exeter, UK, and the University of Iowa. Their study, released Sept. 17, 2008, Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults, persuasively demonstrated a 40% increased incidence of coronary heart disease, heart attack, and diabetes with increasing exposure to BPA (as judged by urine levels) among the nearly 1500 adults aged 18-74 years. People with coronary heart disease had double the blood level of BPA compared to those without.

In addition, higher urine levels of BPA were associated with abnormalities of two liver tests, GGT and alkaline phosphatase.

Interestingly, although much of the debate over adverse health effects of BPA have centered around concern over cancer and reproductive risks, an association with cancer did not hold. (No analysis for reproductive issues was conducted in these adults, since most of the concern is for children exposed through polycarbonate baby bottle use. Some BPA critics have raised questions like low birth weight developing from exposure.) No relationship to thyroid disease was identified, also.

The editorial accompanying the study added some sharp commentary:

"Subsequent to an unexpected observation in 1997, numerous laboratory animal studies have identified low-dose drug-like effects of BPA at levels less than the dose used by the US Food and Drug Administration and the Environmental Protection Agency to estimate the current human acceptable daily intake dose (ADI) deemed safe for humans. These studies have shown adverse effects of BPA on the brain, reproductive system, and--most relevant to the findings of Lang et al--metabolic processes, including alterations in insulin homeostasis and liver enzymes. . . For example, when adults rats were fed a 0.2 microgram/kg per day dose of BPA for 1 month (a dose 250 times lower than the current ADI), BPA significantly decreased the activities of antioxidant enzymes and increased lipid peroxidation, thereby increasing oxidative stress. When adult mice were administered a 10 microgram/kg dose of BPA once a day for 2 days ( a dose 5 times lower than the ADI), BPA stimulated pancreatic beta cells to release insulin."

This study, piled on top of the worrisome literature that precede it, are enough for me: No more tin cans (which are lined with BPA), no more hard plastics labeled with recycling code #7 or #3, no more polycarbonate water bottles (the hard ones, often brightly colored). Microwaveable-safe may also mean human-unsafe, as highlighted by this damning assurance from the Tupperware people that BPA is not a health hazard.

The National Toxicology Program also issued these advice in response to the Lang study to reduce BPA exposure (reported by the Washington Post) :

· Don't microwave polycarbonate plastic food containers. Polycarbonate may break down from overuse at high temperatures and release BPA. (Manufacturers are not required to disclose whether an item contains BPA, but polycarbonate containers that do usually have a No. 7 on the bottom.)

· Reduce use of canned foods, especially acidic foods such as tomatoes that can accelerate leaching of BPA from plastic can linings. Opt for soups, vegetables and other items packaged in cardboard "brick" cartons, made of safer layers of aluminum and polyethylene plastic (labeled No. 2).

· Switch to glass, porcelain or stainless-steel containers, particularly for hot food or liquids.

· Use baby bottles that are BPA-free; in the past year, most major manufacturers have developed bottles made without BPA.

Add Boston Globe to the list of heart scan blunders

Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe.

In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states:

". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."

As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of.


The story goes on to say:

. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said.

"Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital."

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.

And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.



It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch.

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:




You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get?

The most recent addition to this literature is the PREDICT study which concluded:

Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001).

In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values.

How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:

There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):

"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)."

Calcium score provided additional information even after factoring in the Framingham risk score.

That's just a sample of the studies. There are a number more.

Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe.



Contary to the above statements, the data are clear:

--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold.

--A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline.

--Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that.

--Heart scans are not the same as CT coronary angiography.

--The lack of "need" for a procedure does not equate to the absence of disease.

The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened.

Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.

What's worse than sugar?

There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods.

One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving.

Table sugar has a GI of 65, a GL of 65.

Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.)

What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.

How about Corn Flakes? GI 81, GL 70--also both higher than sugar.

How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64.

How about Shredded Wheat cereal? GI 75, GL 62.

All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.

Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human.

Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:

“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ??

Are sterols the new trans fat?

By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.

Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century.

Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods.

Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them.

But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters.


Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods.

Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol.

So far, so good.

The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels.

They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short.

In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.)

Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people.

There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption.

Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase?

Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%.

Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels.

Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known.

Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.

The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program.

(The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.)

The Diabetes Gold Rush

Lou came into the office. Clearly, his program had gone sour.

Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency).

But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios.

Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").

Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!"




To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:

The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development.

Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly.

The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:

Diabetes revenue of $269 million grew 12 percent driven by sales
of consumables, the accessories required by insulin pump users, and
continuous glucose monitoring products. Revenue from international
sales grew 31 percent over the same quarter last year.


That's what I call a growth industry.

The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others.

When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.

So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade.

To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place.

What else is there?

This question comes up frequently:

Aren't there any alternatives to heart scans performed on a CT or EBT device?

Yes, there are.

First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase.

Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation.

Among the other ways to uncover hidden coronary plaque:

--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms.

--Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater.

Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking.

How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes.

Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis.

CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it.

--Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms.

Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only.

--Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms.

Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal.


Outside of experimental settings, that's it.

You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers).

The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed.

Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque.

Let's gamble with your health

Let's play a game.

I'm going to list some lipid patterns and you tell me whether or not the person with these values has heart disease.

Patient 1

Total cholesterol 150 mg/dl
LDL cholesterol 75 mg/dl
HDL 50 mg/dl
Triglycerides 125 mg/dl


Patient 2

Total cholesterol 300 mg/dl
LDL cholesterol 200 mg/dl
HDL cholesterol 35 mg/dl
Triglycerides 325


Patient 3

Total cholesterol 300 mg/dl
LDL cholesterol 100 mg/dl
HDL cholesterol 25 mg/dl
Triglycerides 875 mg/dl



Let's say that any one of these profiles is yours. Should you be getting your affairs in order, preparing for your cardiac catastrophe? Should you demand a stress test from your doctor, hoping that it will shed some light on your dilemma? Should you go ahead and go to the all-you-can-eat rib restaurant, content that you will be attending your granddaughger's wedding in 2020 in full health?

If you can tell, you're a lot better at this than I am.

I provide consultation to other physicians and patients on complex hyperlipidemias in my area. In other words, if someone has a difficulty to manage lipid disorder, the doctor sends the patient to me.

Managing these wildly variable values is the easy part. Deciding whether or not heart disease is concealed within the patient . . . well, that's the hard part.

Let's take it a step further: Suppose all three profiles also have 50% of all LDL particles as the abnormal small particles. And they all have a lipoprotein(a) level of 50 mg/dl, an abnormally high level.

How about now: Can you tell whether any or all of these people have hidden heart disease?

What if they are 20 years old? Does that make a difference?

What if they are all females over 65 years--how about now?

If the only tool you have to divine the presence of hidden heart disease is a lipid panel, or even a lipoprotein panel, then the best you can manage is to hazard a guess based on statistical probability. You also assume that this "snapshot" represents the sorts of values someone has had for their entire lives. You cannot factor in the fact that the first person gained 60 lbs in the last three years since completing menopause. You can't factor in that patient 2 smoked two packs of cigarettes a day for 25 years, but quit 10 years ago.

It's also foolhardy to believe that every known cause of heart disease is currently identifiable and revealed by modern-day blood testing.

A heart scan is simply a means to quantify the sum-total of risk factors--causes--that have exerted an effect up until the moment of your scan. It will reveal the quantity of coronary atherosclerotic plaque present, regardless of whether you stopped smoking 20 years ago or lost 30 lbs last year.

For these reasons, nothing can replace the value of quantifying plaque: not cholesterol, not the Framingham risk calculation, not measures of small LDL or lipoprotein(a), not the presence or absence of symptoms. In 2008, the method of choice for measuring plaque remains a CT heart scan. Perhaps in 10 years it will be some other method.

As always, let me remind Heart Scan Blog viewers that I make this point NOT to sell heart scans, which I have no reason whatsoever to do. I say this because we require a tool to track this potentially fatal disease. We require a yardstick for tracking progression or regression. The only tool that suits these purposes in 2008 is a CT heart scan.