What if cholesterol isn't cholesterol?

Subject: What if cholesterol isn't cholesterol? Fri Jun 13, 2008 1:59 am

What if cholesterol isn't cholesterol?

by William Davis

What if the high cholesterol you and your doctor have been fussing over actually proved to not be high cholesterol?

What else could it be?

Lipoprotein(a), or Lp(a), is a kind of stealth cholesterol, often getting lumped together as LDL or total cholesterol in conventional cholesterol panelsâ”€but is an entirely different thing altogether. Lp(a) gets misleadingly lumped into LDL and total cholesterol because each Lp(a) molecule contains one LDL particle. But attached to the LDL is another protein that dramatically changes the behavior of the combined particle, making Lp(a) among the most potent causes of heart disease known, on a par with smoking and diabetes. Yet I'll bet you've never heard of it.

On its own, Lp(a) can increase risk for heart disease two-, three-, or four-fold over people without this factor. When combined with other heart disease triggers, like increased LDL cholesterol, oxidized LDL, small LDL, C-reactive protein, or homocysteine, and risk is multiplied even more. The combination of small LDL and Lp(a) is an especially disease-provoking duo.

Lp(a) rarely gets diagnosed in day-to-day practice. But it's sometimes easy to recognize people with Lp(a). They've often been through the ringer: doctors have thrown their hands up in frustration because of poor response to "standard" treatment (aka statin drugs); the patient doesn't understand why they might be thin and active yet have the high blood pressure of someone 70 lbs heavier; they have heart disease despite wonderful cholesterol values. One blood test and the answer becomes clear: They have Lp(a). It can account for all these phenomena.

They why don't more physicians order this simple test? Why don't we hear more about this prevalent (1 in 6 people with coronary disease have it) genetic pattern that amplifies risk for heart disease?

There are a number of reasons. But I believe the most powerful reason is simply that there is no big revenue-generating drug to treat it. Statins reduce LDL cholesterol to the tune of $27 billion dollars a year (2007 revenue). There's no such blockbuster for Lp(a). While niacin is the best treatment agent we've got for reducing Lp(a), prescription niacin (Niaspan®) has not been approved for this indication.

Another reason for Lp(a)'s unpopularity: Though there are mounds of data that document–without question–that Lp(a) is an important risk for coronary disease and other forms of atherosclerotic disease, we lack treatment trials. For instance, niacin vs. placebo for 5 years, then count the number of heart attacks and deaths. We have numerous, repetitive, overlapping, redundant trials with statins adhering to this design. We have none for niacin and the treatment of Lp(a).

Niacin is also a pain in the neck for your doctor. He/she rapidly tires of the calls about the crazy and disconcerting flushing with niacin. Most are unaware that proper hydration reduces or eliminates the flush for the majority of people. It takes a lot of time and energy to educate people. Should someone concoct a successful pharmaceutical treatment for Lp(a), it will make headlines in health magazines and the newspaper will blare about the importance of Lp(a). Yet it has been there all along, frustrating people and their physicians.

Red flags for Lp(a)

How do you know you have Lp(a)?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

(I've personally seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story, simply by recognizing telltale signs.)

Some of the red flags for Lp(a) include:

–High blood pressure in a slender person. Excess weight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve as a tip-off Lp(a) is present.

–High LDL cholesterol poorly responsive to statin drugs. For instance, an LDL cholesterol of 190 mg/dl will be treated with Lipitor® 40 mg, but drops to only 165 mg/dl, a very poor response. This can point towards Lp(a).

–Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

–Coronary disease (or a measure of coronary disease like a high heart scan score) in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts, figures ordinarily not associated with high likelihood of heart disease–yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possibility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking. Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcefulness and some ingenuity may be required on the part of your doctor. However, knowing that you have it shows you where to concentrate your efforts.

Can Lp(a) be controlled?

Though the national experience with Lp(a) is still growing and clear-cut treatment data like that enjoyed by cholesterol drugs is lacking, in my view the association between Lp(a) and heart disease is so persuasive that treatment should at least be seriously considered. But be warned: Given the current state of knowledge on Lp(a), not everybody is able to completely tame this beast; most need to be content with controlling it, often partially.

If you and your healthcare provider decide that 1) you have Lp(a), and 2) it warrants a treatment program, then strategies to consider include:

–Niacin– Although not FDA-approved for this purpose, prescription Niaspan® or over-the-counter Sloniacin® are our preferred preparations. While niacin doses of 750-1500 mg per day are effective for other patterns such as raising HDL cholesterol, Lp(a) often shows a reduction at higher doses. You will need to work with your healthcare provider when taking any dose >500 mg niacin per day, since there is a small risk of toxic liver effects, as well as some other uncommon effects. Generous hydration is key to tolerating the hot flush characteristic of niacin.

–DHEA– A fascinating adrenal gland hormone that falls as we age, much as most other sexual hormones like testosterone and estrogen. However, DHEA can be useful for reducing Lp(a) up to 18%, though it may be more effective for females.

–Flaxseed– Ground flaxseed is a wonderful grain that lacks the blood sugar-raising effect of wheat products and can also reduce Lp(a), though variably. Two to three tablespoons per day as a hot cereal or added to foods like yogurt has worked well for us.

–Raw almonds– Not only do raw almonds reduce LDL and blood sugar, they also reduce Lp(a) modestly.

–Healthy oils– Contrary to the common teaching on reducing fats to reduce cholesterol, most fractions of fats reduce Lp(a). Polyunsaturated, monounsaturated, and even saturated fats reduce Lp(a) (saturated fats curiously being the most effective). Hydrogenated ("trans") fats raise Lp(a), providing yet another reason to avoid this unhealthy synthetic fat.

After these basic efforts, there are a list of uncommon strategies that yield variable effects, such as very high-dose fish oil, acetylcysteine, l-carnitine, and others.

Note: Because of the substantial gap in knowledge on how to best treat Lp(a), as well as the funding struggles that researchers encounter when trying to develop Lp(a) research programs, we have taken the initial steps to forming the Lipoprotein(a) Research Foundation. Details will unfold over the next several months.

About the author: Dr. William Davis is founder of the Track Your Plaque program, a heart disease prevention program that shows how to identify and control risk for coronary disease. He can be contacted through www.TrackYourPlaque.com, or his blog at http://heartscanblog.blogspot.com.