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Lighten the load

The other day I was flipping through a magazine that had nothing at all to do with healthcare, when I came across a line that read something like this: “As everyone knows, we should cut down on the cholesterol in our diets to protect us from heart attacks.”

You would think, with all the information we’ve seen about cholesterol in the media over the past few years, that some of the basics would have sunk in by now. Like, for instance: consumption of cholesterol doesn’t increase our cholesterol levels.

Obviously we still have a long way to go before the basics of cholesterol are widely understood. Today we’ll move a little further in the right direction with two recent e-mails I received from HSI members posing questions that will help us sort through some of the most typical cholesterol misconceptions. (Some of this will be familiar to long-time members and e-Alert readers, but bear with me – I’ve got some new information too.)

 

 

The good and the bad 

An HSI member named Ivan writes to say that he’s confused about what he feels are mixed signals about cholesterol. Ivan writes:

“As someone who has been concerned about their risk of heart disease for several years, I am intrigued by what you have posted. Things like: cholesterol is not a good indicator of risk, homosystene level is better. If cholesterol is not a good indicator then why do you advertise supplements that control it? I find this very conflicting info.”

This is a good question, especially in light of all the dangers of statin drugs (like Lipitor and Zocor) that lower cholesterol.

Ivan is right – cholesterol is not a particularly good indicator of risk to your heart. Much better indicators are your levels of triglycerides, homocysteine, and C-reactive protein. This is why it simply doesn’t make sense to take a statin drug that has plenty of known side effects, such as memory loss, muscle inflammation, kidney failure, irritability, etc.

Nevertheless, it’s not a good idea to ignore cholesterol either. Generally speaking, keeping your LDL cholesterol low and your HDL cholesterol high IS good for your heart health – but not to the point that you should create other health problems by risking the side effects of a pharmaceutical.

So if you don’t take statins, how can you get that “good” HDL cholesterol up, and the “bad” LDL cholesterol down? Exercise, maintain a proper body weight, stop smoking, limit alcohol consumption, increase your intake of omega-3 fatty acids, cut out the junk foods in favor of the soluble fiber in fruits and vegetables, and take supplements that are known to protect the heart. Making all of that happen is easier said than done, I know, but if you’re committed to supporting the health of your heart, these regimens should also bring triglyceride, homocysteine and C-reactive protein levels into line as well.

The free radical hunt

In addition to the lifestyle choices mentioned above, getting a good intake of antioxidants is also good for the heart. But a member named Bill has heard something to the contrary:

“I have low HDL. A recent medical study says that a high use of antioxidants can increase risk of heart events because HDL is lowered by them and studies show an increase in arterial plaque. This is devastating. I have been a religious user of antioxidants over the years. What is one supposed to thinkand do?” Bill, whatever you do, DO NOT get rid of the antioxidants! There is a large body of evidence that antioxidants assist in the prevention of heart disease by helping to keep arteries clear.

I haven’t found any studies concluding that antioxidants lower HDL cholesterol, and Bill didn’t include any further details (such as a journal citation) in his e-mail. So I have to think that Bill is probably referring to a 2001 study in which a combination of four antioxidants – vitamin E, vitamin C, beta-carotene, and selenium – were believed to inhibit the effectiveness of statin drugs in lowering HDL.

In an e-Alert I sent you in the summer of 2001 (“Antioxidants Heart Healthy, Despite Mainstream Slant” 8/18/01), HSI Panelist Randall Wilkinson, M.D., had this to say about the antioxidant/statin research:

“The biggest problem with the study isn’t the conclusion,” he said. “After all, it may well be that some antioxidants lessen the strength of statins. The real problem is the assumption the researchers make that statin drugs are simply the best thing to take for heart disease. While that may be assumed by the mainstream medical community, it simply isn’t true.

“Take vitamin E, for example. Double-blind, placebo-controlled human studies have shown that the tocotrienol form of vitamin E lowers cholesterol, improves LDL:HDL levels, and provides general heart protection. And unlike statin drugs, you’re not at the mercy of potentially dangerous side-effects when you take them.”

In other words, Bill, I sincerely doubt that there’s a valid study out there that shows antioxidants might have a negative effect on HDL levels, although they may have been shown to “interfere” with expensive prescription drugs doing their thing.

Liver cargo 

I’m going to finish up today’s cholesterol e-Alert with a comment (edited slightly for length) posted on the HSI Forum last month by a member named Gerry, a frequent contributor to the Forum. I’ve been reading Gerry’s postings for about a year now and I always find them interesting and insightful.

Gerry starts off by wondering why HDL (high density lipoprotein) and LDL (low density lipoprotein) are considered different substances. He says, “LDL is nothing but HDL with fat and/or cholesterol attached. This fat/cholesterol was made in the liver (mainly because of increase in blood glucose, and thus, insulin levels). The liver must not keep this fat in its tissue and must send it off to other parts of the body. To do this, it attaches the fat/cholesterol to a carrier: HDL. The process converts HDL to LDL and even V(ery)LDL.

“The LDL/VLDL then leaves the liver with its cargo and deposits its load in other parts of the body (harmlessly in fat cells, or harmfully in blood vessel walls and similar structures). Once LDL/VLDL drops its cargo of fat/cholesterol, it is now HDL again. Thus, HDL and LDL are the same molecule, except that LDL has an additional cargo. You might say that the body has a constant supply of HDL. If more of it is ‘loaded’ then you have ‘more’ LDL and ‘less’ HDL. If less carries a load, then you have ‘more’ HDL and ‘less’ LDL.

“So if you want to ‘raise’ your HDL, you’ll have to ‘lower’ your LDL. And as the mechanisms shown above reveal, you can only do this naturally by controlling fat/cholesterol formation in the liver, mainly by controlling blood glucose levels and insulin secretion. This is even proven by the fact that cholesterol lowering drugs act on the liver enzymes.

“In addition, lipoprotein, as the name implies, is made up of protein. So raising overall supply of HDL – whether loaded or not – will require additional protein. This is all clearly shown in any biochemistry or physiology textbook.”

As soon as I read that last comment I recalled yesterday’s e-Alert (“Jumpin’ Pax Flash” 6/9/03) in which a year-long controlled study found that the Atkins high protein diet significantly increases HDL cholesterol.

So in spite of not being the most important marker for heart disease, your cholesterol levels should be monitored and – more importantly – can be maintained in most cases without the use of statin drugs.

 

To Your Good Health,

Jenny Thompson
Health Sciences Institute

Sources:
“Antioxidant Supplements Lessen HDL Response To Cholesterol Drugs” American Heart Association, Journal Report, 8/10/01, americanheart.org

 

 

 

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