Reducing your cholesterol with drugs?

(Versión en español: pinchar aquí)

The graph below belongs to a 1998 article. It is a plot of how many people had a specific total cholesterol level. We can see separate data for people which developed coronary artery disease (CAD) at some point in the 26 follow-up years of the study, and people that didn’t (No CAD).

Forgetting about my doubts on the figure (which I detail at the end of this blog entry), the figure tells us that

For a specific total cholesterol level, if it belongs to the range between 150 and 300 mg/dL, we can’t say if that person has an elevated cardiovascular risk. In that range of values we find people with and without disease.

The total cholesterol doesn’t tell us a thing about cardiovascular risk of a person. The mean cholesterol value of people with CAD is only sightly bigger  (around 25mg/dL, if I am not wrong) than the mean value of people without  CAD. The exception is total cholesterol above 275-300 mg/dL, because 90% of those with a cholesterol above 300mg/dL developed CAD during the 26 follow-up years. But for smaller values:

  • almost half the people without CAD had a cholesterol above 200 mg/dL, and
  • 35% of people with CAD had a cholesterol in the “normal” range (between 150 and 200 mg/dL).

Let’s say your total cholesterol is 225 mg/dL, the most frequent value in people with CAD. For this specific value, according to the article’s author,  40% of people had CAD, and 60% of them hadn’t CAD. Prescribing a drug for people on that situation would result in 6 out of 10 people being medicated for no reason, with drugs, the so called statins, that have lots of negative side effects on the health for a big percentage of the users. The author of the article asked:

How do we determine which 40 of 100 people we see are at risk so that we do not treat people who do not need treatment?

And his answer was that more parameters needed to be considered (with special attention to the HDL).

But the question may be not how do we know who needs treatment, but, is it sensible to use a treatment to reduce cholesterol levels? If having a high cholesterol level were that bad, how do we explain that so much people with “normal” cholesterol levels has CAD? If the risk comes from having a hoigh cholesterol level, CAD is not supposed to happen with “normal” cholesterol levels. And we can’t redefine “normal”, because normal levels are stablished according to the cholesterol levels of people without CAD, and “normal” for healthy people is any value between 150mg/dL and 275 mg/dL.

Is cholesterol guilty of any charge?

Let’s assume the following hypothesis is true: for unknown reasons (diet, smoking, alcohol, etc.) our body suffers from “inflammation” (see) and that condition usually has the following consequences:

  • Our total cholesterol is raised, due in part to a raise of the HDL but mostly because LDL level raises. That would explain why people with CAD have cholesterol levels that are slightly greater than those of healthy people (using mean values). But the increase is usually so small that we can’t say if we have inflammation from the cholesterol level.
  • There is a bigger LDL (the “bad” cholesterol and that oxidized LDL , small and dense particles, is the one with a high atherogenic risk (see).
  • Our arteries get narrowed (decreased section), and the risk of occlusion increases.

Under those assumptions people suffering from inflammation would have a higher cholesterol level, but reducing that levels would be treating a symptom not the underlying cause, inflammation, and the risk woultn’tdecrease. On the contrary, statins create a bunch of health problems. And don’t forget that studies where cholesterol was decreased with seed oils, mortality increased (see), a consequence of the pro-inflammatory effect of those fats? In other cases, decreasing cholesterol levels with drugs didn’t change the cardiovascular risk(see).

Decreasing your cholesterol with drugs may be as sensible as cutting off your head to decrease your risk of suffering from Alzheimer’s disease. It is true that we need a head to suffer from that disease, but that doesn’t imply that it is the culprit of having the disease.

But statins do decrease the cholesterol levels and reduce a little your cardiovascular risk, don’t they?

In a few cases, but it is also said that that improvement may be created by a side effect of those drugs: they are anti-inflammatory (see or see), but not because of the reduction of the cholesterol levels.

As a conclusion, if inflammation were the real culprit, we shouldn’t be worried about having 250 mg/dL of cholesterol, but about having inflammation. And instead of using drugs as dangerous as statins to change a symptom, we should be seeking other ways to decrease inflammation. Is there an “anti-inflammatory diet“?  How can we avoid having a B-pattern of LDL, with lots of small and dense particles, the ones that are dangerous if oxidized?

A few thoughts:

  • A low-carb diet reduces inflammation in overweight people with atherogenic dyslipidemia (see).
  • A small reduction in the carb intake, even not reaching low-carb levels, is enough to reduce inflammation in diabetics (see), the opposite effect of a low-fat diet (labeled LFD in the table).


If you want to reduce the cardiovascular risk in diabetic patients: less carbs, not less fat…

  • A low-carb diets reduce triglycerides and raise HDL, both markers of a reduced cardiovascular risk, and it also improves inlammation markers (see)

  • A low-carb diet improves the LDL pattern, decreasing the amount of small and dense particles, the atherogenic ones (ver, ver).
  • Eating eggs (see) also changes your LDL to a less atherogenic pattern.

As a conclusion, may be inflammation, presumable culprit of cardiovascular diseases, raises a little our cholesterol levels, but the increase is small and just having a look at our cholesterol level we can’t say if we have inflammation and consequently a high CVD risk or not. Cholesterol levels above 275-300 mg/dL are scary.

We should reflect on the purpose of decreasing our cholesterol levels with drugs, because cholesterol is a substance needed by our body, and it is probably not the culprit of the cardiovascular disease, just an involved component. May be just as involved as our arteries, our heart or being alive in the progression of that disease.

Reading further:


There are a few things I don’t understand from the figure shown at the beginning of the article:

  • Distributions are not normalized (both curves have different area) and as the area under the curves is similar in both cases that means half the people in the survey had CAD. That is possible, but such a big percentage surprises me.
  • In the article it is said that for the people with a cholesterol in the range between 150 and 200 mg/dL, 20 out of 100 had CAD. But the area under the “No CAD” curve in that range is not four times bigger  (80%) than the are under the  “CAD” curve (20%).
  • For 225 mg/dL the “No CAD” point should be a 50% bigger than the “CAD” point, because in the article it is said that for that value 40 out of 100 had  CAD (40% versus 60%). It is not so.
  • The area under the “CAD” curve for values above 300 mg/dL should be 9 times bigger than the area for the “No CAD” curve in that area, because in the article it is said that 90 out of 100 had CAD in that range of values, but for that zone the “CAD” curve as an area equal to zero.

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