LifeCare Chiropractic

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cholesterol

HDL raising effect of orange juice in hypercholesterolemia – (11-27-00)

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HDL raising effect of orange juice in hypercholesterolemia

There are several ways to lower cholesterol levels safely, and increasing intake of fruits and veggies is such a wonderful way. In addition to helping with cholesterol, it will also lower your risk of many other diseases. Adding exercise will also increase HDL levels, as well as the addition of soy to your diet. Want a great cholesterol fighter? How about a smoothie made at home? Frozen yogurt, toss in some probiotics, filitered water, ice and several servings of fruit. Drink it on your way to work!!

AJCN — Abstracts: Kurowska et al. 72 (5): 1095

Read entire article here

Use of Nicotinic Acid, Bile Acid-Binding Resins, and Fibrates – (10-26-00)

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Use of Nicotinic Acid, Bile Acid-Binding Resins, and Fibrates

Although this article focuses on nicotinic acid, niacin has successfully been used to treat high cholesterol levels safely. This is a very good review covering the different types of niacin available. And, interestingly, the author notes that nicotinic acid has the longest history of use; and yet most doctors and patients are unaware of its benefits.

Clin Rev Spring:52-57, 2000 Nicotinic acid and nicotinamide together represent the essential vitamin niacin in the diet. Of these two, only nicotinic acid is active as a lipid-modifying drug. Thus, while nicotinamide is often marketed as a superior lipid-lowering version of niacin with none of the unpleasant side effects of nicotinic acid, such as flushing and itching, in truth this compound is totally ineffective as a lipid-lowering drug. The recommended dietary allowance of niacin is less than 20 mg/day. Pharmacologically effective doses of nicotinic acid begin at 1,000 to 2,000 mg/day and range up to an effective maximum of 6,000 mg/day. In 1955, this dose range of nicotinic acid was shown to lower total serum cholesterol, and in 1961 it was shown to lower triglyceride and low-density lipoprotein (LDL) cholesterol levels and raise high-density lipoprotein (HDL) levels in hyperlipidemic patients. Thus, of the drugs currently available for treating hyperlipidemia, nicotinic acid has been used the longest. Over the past 40 years, nicotinic acid has been used in numerous clinical trials and has been proven to reduce lipids and prevent and/or reverse coronary artery disease. In 1988 the National Cholesterol Education Program’s (NCEP) Adult Treatment Panel recommended nicotinic acid as a drug of first choice.

Think You Know the “Cholesterol Story?” Think Again…

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Ever since Nikolai Anitschkow fed rabbits a high cholesterol diet in 1913, medicine has been obsessed with this molecule and its relationship with heart disease.

First, a primer on what cholesterol does do in the body, since most seem to glaze over the fact that it’s actually there for a reason. Here are a few functions of the cholesterol molecule:

  1. It is an essential component of every cell membrane in your body.
  2. It is an essential component of the myelin sheath that helps nerves transmit impulses.
  3. It is the building block for our steroid hormones like cortisol, aldosterone, testosterone, progesterone and estrogen.
  4. In addition, the same pathway that makes cholesterol makes CoQ10, a critical molecule used by every cell in the body to make energy.

Other than this, cholesterol is an evil molecule that needs to be squashed out of our diets and lowered to almost zilch with high levels of statins drugs put into our water supply alongside hydrofluorosalicylic acid.

Maybe this dysfunctional view was created alongside the statins. It would not be the first time that mainstream medicine found something to treat with a drug they wanted to promote. But it seems like, much like hormone replacement therapy and the cigarette-smoking-is-good-for-you idea, the cholesterol hypothesis may be dying.

And good riddance to it when it happens. But it’s not quite time to write the obituary.

Never, ever, ever, EVER forget that cholesterol is the symptom, not the cure. Lowering it artificially with drugs will not produce the same outcome as lowering it with medications. It’s the equivalent of putting ice on the thermostat inside of a burning house. Sure—the temp is going to LOOK good, but you’ve really done nothing to change the outcome.

So what does my ranting have to do with this article? Researchers are beginning to tease apart just how worthless it is to look at just a single marker in the bloodstream and try to determine what your risk of disease is going to be.

Initially, the equation was simple total cholesterol > 200 = heart disease = statins.

Then, we matured, realized total cholesterol was relatively worthless and instead, focused on LDL (the “bad” cholesterol). Then, equation became LDL cholesterol > 130 = heart disease = statins.

Now, we may be maturing again. In this particular study, researchers looked at the “discordance” between estimating heart disease risk using purely LDL numbers versus using them along with other lipid markers. Here are the other lipid lab values that were checked:

  • Non–high-density lipoprotein cholesterol (NHDL-C)—calculated by subtracting HDL-C from total cholesterol (TC). It combines LDL-C, very low density lipoprotein cholesterol (VLDL-C), intermediate density lipoprotein (IDL-C) and lipoprotein (a) (LP(a)). Lower is better.
  • Apolipoprotein B (apoB)—a component of LDL proteins, lower is better.
  • LDL particle number (LDL-P)—a more accurate measure of LDL cholesterol.

They then looked for the number of participants that fit into one of two groups:

  1. Those with LDL of 121 mg/dL or higher but lower than average of the other markers.
  2. Those with LDL lower than 121 mg/dl but higher than average on the other markers.

This mismatch was found in 11.6% for NHDL-C, 18.9% for apoB and 24.3% for LDL-P.

Women who had the lower than average LDL-C numbers but above average numbers on the other markers, the risk of a heart attack was underestimated (NHDL-C 292%, apoB 248%, or LDL-P 232%).

On the flip side, in women with above average LDL-C levels but lower than average numbers on the other markers, the risk of a heart attack were overestimated (NHDL-C 60%, apoB 66%, or LDL-P 58%).

Overall heart disease risk remained underestimated or overestimated by anywhere from 20% to 50% for women with discordant levels. That’s a pretty wide range.

For a system of medicine that prides itself on its perceived accuracy and drug companies that spend billions of dollars to determine if we should use Drug X when the blood value is at 14 units instead of 15 units this is almost laughable.

I do have to conclude and proudly proclaim that lifestyle changes, as opposed to drugs, are going to have a positive effect regardless of what your risk of a heart attack is. Drugs to lower cholesterol, on the other hand, still remain pretty much a crap shoot.

Could Statins Actually Help Prevent Heart Disease?

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Ok, so maybe I’ve been too hard on statins.  Just because they suck at preventing a first heart attack is no reason to throw the baby out with the bath water.

The list of side effects continues to grow, with diabetes being the most concerning (unless of course, it is you personally who happens to die from a fatal rhabdomyolosis, in which case you’re probably less worried about diabetes….), because for every 11 heart attacks avoided 8 new cases of diabetes will be created.

I have argued less against the use of statins in secondary prevention (those who have already had a heart attack and are now trying to prevent a second heart attack) because the data is a little stronger.  In general, though, statins will do very little to protect against a first heart attack.  The only real benefit is seen in those who have a greater risk.  In other words, the otherwise healthy, lean body weight, low blood pressure 45-year-old male with an isolated, elevated cholesterol will have ZERO benefit from taking a statin.  This doesn’t stop him from getting prescribed a statin by some overzealous primary care doctor who just got back from a conference sponsored by Pfizer, however.

As I have mentioned before, only 1 out of every 100 people will see a benefit from taking a statin.  My point has always been that lifestyle changes will blow the effectiveness of statins out of the water every single time with lower cost and no side effects.

But what if we could identify a (very) small subset of patients who have not had a heart attack and yet would most likely be that ONE person out of 100 that benefits from taking a statin?  Turns out we may be closer to this answer with this particular study.

I have, for a long time, been a vocal advocate for the “heart test,” or calcium artery scoring (CAC) using an ultra fast CT scan.  Overall, the studies and subsequent data on the use of the EBCT (electron-beam CT) continues to improve and radiation doses have continued to drop to the point where the radiation exposure can be less than a dental X-ray (as opposed to standard CT scans, which we hand out like candy in the ER, which have a much higher radiation dose and have been linked to some 29,000 cancers per YEAR).

In the study, researchers looked at the benefits of statins through the lens of those having high calcium scores, indicating a higher likelihood of having a blockage in the coronary arteries.  Specifically, they looked at the relationship between the CAC, statin use and outcomes (heart attack, chest pain leading to stents being put in, resuscitated cardiac arrest, stroke, cardiovascular death).  Here’s the specifics:

  • Researchers looked for those with Ultra fast CT scores over 100 (21% of participants with CAC 100 or higher).
  • They then looked at those with abnormal cholesterol levels:  LDL > 130 mg/dL, HDL < 40 mg/dL for men (50 mg/dL for women) and triglycerides > 150 mg/dL.

With these two factors in mind, here’s how the study data played out:

  • More than half of events (55%) occurred in the 21% of participants with CAC ≥100 (the CT scan group bore the brunt of the heart events).
  • Conversely, 65% of events occurred in participants with 0 or 1 lipid abnormality (in other words, heart events are happening to those with normal cholesterol)
  • In those with CAC ≥100, event rates were as high as 29.5 per 1000 person-years, regardless of lipid / cholesterol numbers.
  • On the other hand, when the CAC was a big fat zero, cardiac event rates were 5 times lower at 5.9 per 1000 person-years regardless of lipid / cholesterol numbers.

To summarize, those with higher CAC scores were at a much greater risk of a cardiac event, regardless of where his or her lipid numbers were at.  Medicine has been locked into using the blinders of cholesterol (sounds like some D & D special armor…) despite the fact that it just wasn’t making sense when we looked at current research.  While there has been some move away from cholesterol, it hasn’t been with a logical head.  The most recent guidelines on statin use have indeed thrown cholesterol levels out the window, but instead of replacing them with something smarter like the CAC, the blanket recommendation was just to give everyone a statin.

The smarter approach, based on this study, would be to use treatment for those at the highest risk based on CAC scores, NOT on cholesterol levels.  Let me point out though, that nothing in this study actually looked at whether or not statins could lower cardiac events in those with higher CAC scores, although this is an excellent question to ask.

Maybe, just maybe, one of these decades medicine will actually catch up to the research.

Plasma oxidized LDL: a predictor for acute myocardial infarction? – (03-31-03)

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Plasma oxidized LDL: a predictor for acute myocardial infarction?

Remember that LDL cholesterol itself does not do damage to the body until it gets damaged itself through oxidation (sometimes termed oxysterols). Here we see the development of yet another tool to assess heart disease risk. Keep in mind that, even with high cholesterol, high intakes of antioxidants can serve to protect the LDL particle from being damaged.

Synergy Abstract

Click here for more information.

Thirty-Eight Studies Find Soy Products Lower Cholesterol – (07-31-00)

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Thirty-Eight Studies Find Soy Products Lower Cholesterol

It seems that soy’s effect on cholesterol may actually be better researched than many of the pharmaceutical drugs on the market. As a side note, it is important to mention that soy is not ALL good. It does have a tendency to interact with other essential nutrients. It is important to not fall prey to every soy product on the market.

Increasing evidence supports the use of soy products to lower blood cholesterol, a heart-health publication edited by cardiologists reports. Heart and Health Reports cited a summary of 38 recent studies of the effect of soy on cholesterol: “This summary found that an average intake of 46 grams of soy protein per day reduced total cholesterol by an average of 9 percent, [low-density lipoprotein (LDL)] cholesterol by l3 percent, and triglycerides by 11 percent,” the publication said. Patients who had the highest cholesterol to start with had the greatest cholesterol-lowering benefit from soy, with some studies showing that soy raised high-density lipoprotein cholesterol.

Cholesterol Lowering Drugs and HDL—Do They Work?

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It’s pretty well established that, despite drug companies mounting a massive push and “educational” effort for years, total cholesterol by itself has little to do with heart disease rates.

However, I still have to educate people in the community and my practice on this little tidbit.  The focus away from total cholesterol was made quietly, most likely as an effort to save face by those who had been pushing cholesterol levels as THE answer to heart disease.

The research on HDL (the “good” cholesterol), LDL (the “bad” cholesterol), VLDL (the “worst of the worst”) and triglycerides, however, is stronger.

In my opinion, the HDL:triglyceride ratio is the most valuable, but overall it’s the entire picture painted by all the lipids that give us the best picture.  This viewpoint, however, is not what drug research and use is about.  Since drugs can usually only affect one blood value at a time (i.e. statins will lower LDL but won’t have a big impact on triglycerides), researchers have to push hard to find a relationship between a value and a disease (such as total cholesterol and heart disease) and then find a drug that affects that value.

Miraculously, despite all my Rantings on cholesterol lowering drugs as well as an eBook on cholesterol lowering drugs, I still have patients come in who think that the drugs they’re on will actually protect them from heart disease and stroke.  Needless to say, I’m not a fan of cholesterol lowering medication and will not hesitate to point out the research related to cholesterol.

Which leads me into this particular study.  In it, researchers looked at two types of lipids, HDL cholesterol and apoA-1.  Most know that HDL is generally considered the “good” cholesterol and lifestyles that promote higher levels will be strongly protective against heart disease and stroke.  ApoA-1, however, is less well-known.  Apolipoprotein A-1 is one of the major proteins that makes up the HDL molecule and helps to shuttle cholesterol around the bloodstream.  Having higher levels is more protective to the heart.

This study looked at the effect that HDL and ApoA-1 levels had on heart disease.  Then, they looked at what effect statins had on these relationships.  Here’s the specifics:

  1. HDL lowered the risk of a major cardiovascular event by 17%,
  2. ApoA-I level lowered risk 21%.
  3. In those patients taking statins whose LDL cholesterol levels were lowered to at least 50 mg/dL, an increase of HDL-C did not lower heart disease risk.
  4. However, in the statin responders, a rise in apoA-I did lower the risk of heart disease by 7%.

So what does this mean?  Higher levels of HDL and ApoA-1 are good for your heart.  But when those levels are artificially raised by a cholesterol lowering drug, it either didn’t help at all or the benefit was far less than higher levels occurring naturally.

When we find, from observational studies, that some lab value protects against some disease, it is LIFESTYLE that gives the benefit.  Cheating by using drugs to lower the value, if it works and doesn’t kill you from the side effects, will never produce the same benefit.