I've noticed a point of confusion recently, something I hadn't noticed in my patients before: Because of the public health advice from the FDA, American Heart Association, and Surgeon General's office to reduce sodium/salt intake, people have thought this meant reducing iodine, too.

I believe that people have drawn an equation in their minds:

Sodium = iodine

Of course, they are two entirely unrelated things.

Recall that the only reason iodine is added to many (not all) salt products is because it was a public health solution to solve the substantial nationwide iodine deficiency prevalent during the 20th century. But it was a solution conceived in 1924, when the FDA thought this was the best way to get iodine into Americans. And it worked.

Unfortunately, sodium does indeed present adverse effects in some people. As a result, "get your iodine from salt" has evolved into "reduce your sodium intake." Everyone forgot about the iodine: They forgot about the large disfiguring goiters, the poor school performance in iodine-deficient schoolchildren, the mentally-impaired offspring of iodine-deficient mothers.

So don't confuse sodium with iodine. You may need less of the former, but more of the latter.

For more on this, see "Help keep your family goiter free."

"I told my cardiologst that I stumbled on a program called 'Track Your Plaque' that claims to be able to help reduce your coronary calcium score.

"My cardiologist said, 'That's impossible. You cannot reduce coronary plaque. I've never seen anyone reduce a heart scan score."

Who's right here?

The commenter is right; the cardiologist is wrong.

I would predict that the cardiologist is among the conventionally-thinking, "statins drugs are the only solution" group who follows his patients over the years to determine when a procedure is finally "needed." In fact, I know many of these cardiologists personally. The primary care physicians are completely in the dark, usually expressing an attitude of helplessness and submitting to the "wisdom" of their cardiology consultants.

Quantify and work to reduce the atherosclerotic plaque? No way! That's work, requires thinking, some sophisticated testing (like lipoprotein testing), even some new ideas like vitamin D. "They didn't teach that to me in medical school (back in 1980)!"

Welcome to the new age.

Atherosclerotic plaque is 1) measurable, 2) trackable, and 3) can be reduced.

We do it all the time. (Amy still holds our record: 63% reduction in plaque/heart scan score.)

Though I pooh-pooh the value of statin drug studies, there's even data from the conventional statin world documenting coronary plaque reversal. The ASTEROID Trial of rosuvastatin (Crestor), 40 mg per day for one year, demonstrated 7% reduction of atherosclerotic plaque using intracoronary ultrasound.

I have NEVER seen a heart attack or appearance of heart symptoms (angina, unstable angina) in a person who has reversed coronary plaque (unless, of course, they pitched the whole effort and returned to bad habits--that has happened). Stick to the program and coronary risk, for all practical purposes, been eliminated.

A heart scan score is not a death sentence. It is simply a tool to empower your prevention program, a measuring stick to gauge plaque progression, stabilization, or regression. Don't accept anything less.

There's a specific combination of lipids/lipoproteins that confers especially high risk for heart disease. That combination is:

Low HDL--generally less than 50 mg/dl

Small LDL--especially if 50% or more of total LDL

Lipoprotein(a)--an aggressive risk factor by itself

This combination is a virtual guarantee for heart disease, often at a young age. It's not clear whether each risk factor exerts its own brand of undesirable effect, or whether the combined presence of each cause some adverse interaction.

For instance, lipoprotein(a), or Lp(a), by itself is the most aggressive risk factor known (that nobody's heard about--there's no blockbuster revenue-generating drug for it). Each Lp(a) molecule is a combination of an LDL cholesterol molecule with a specific genetically-determined protein, apoprotein(a). If the LDL component of Lp(a) is small, then the combination of Lp(a) with small LDL is somehow much worse, kind of like the two neighborhood kids who are naughty on their own, but really bad when they're together.

Interestingly, the evil trio responds as a whole to many of the same corrective treatments:

Niacin--increases HDL, reduces small LDL, and reduces Lp(a)

Elimination of wheat, cornstarch, and sugars--Best for reducing small LDL; less potent for Lp(a) reduction.

High-fat intake--Like niacin, effective for all three.

High-dose fish oil--Higher doses of EPA + DHA north of 3000 mg per day also can positively affect all three, especially Lp(a).

If you have this combination, it ought to be taken very seriously. Don't let anybody tell you that it is uncorrectable--just because there may be no big revenue-generating drug to treat it on TV does not mean that there aren't effective treatments for it. In fact, some of our biggest successes in reducing heart scan scores have had this precise combination.

"You can't reduce coronary plaque"

Lethal lipids