In my last post, I examined the efficacy and safety of statins, the cholesterol-lowering drugs that tens of millions of Americans are currently taking.
I decided to write that post after I’d visited my doctor and refused a statin prescription.
After reviewing my lipid panel, my doctor said I needed statins because my cholesterol was high, especially my LDL-C. He said that because of these numbers I was at an increased risk of cardiovascular disease (CVD).
He assured me, “Statins will lower your LDL-C and your risk of CVD.”
I subsequently refused his offer and gave him three reasons why.
First, I told him I believed that statins are often ineffective in lowering CVD risk. Second, they can cause potentially dangerous adverse reactions. Finally, I told him I didn’t believe I need them because I don’t have diabetes or CVD. Therefore, basing my CVD risk primarily on LDL-C levels was not in accordance with current scientific research.
Ooooh… I got such a look.
Doctors don’t like being told they’re wrong. My doctor decided not to argue the point with me. That was wise as I was much more informed on statin use than he was.
In this post, I’ll show you why my doctor was wrong to offer me statins. I’ll also present some strategies you can use to optimize your cholesterol levels.
Remember, statins are not the harmless drugs they’re made out to be. See my post here. They come with the potential for severe adverse reactions.
If you’re on statins or your doctor wants to put you on them, consider this information carefully. Then discuss it with your doctor. It’ll make you a better-informed patient.
Mainstream Medicine’s Criteria For Statin Therapy
Most mainstream physicians evaluate a patient’s need for statin therapy in accordance with the patient’s risk for cardiovascular disease (CVD) as indicated by his or her cholesterol numbers.
For example, the American College of Cardiology (ACC) and the American Heart Association (AHA) define a high-risk individual as one who has:
- A history of CVD or a history of diabetes
- Or an LDL level over 190 mg/dl
- Or an LDL level of 70 to 189 mg/dL, without clinical CVD or diabetes and an estimated 10-year CVD risk > 7.5% (you can find your 10-year CVD risk according to the ACC here).
If the nation’s doctors strictly observed these guidelines, then 80% of individuals over 65 years old and 44% of people between the ages of 40 to 64 in the United States would be on statins.
Currently, there are about 46 million people on statins. That number would jump to more than 70 million if the recommendations of the ACC and AHA were followed.
A Closer Look At The ACC/AHA Guidelines
That means that millions of asymptomatic individuals are considered to be at high risk for CVD simply because they have an LDL-C level above what the ACC/AHA considers normal.
Let’s take a look at the practical implications of these guidelines by examining my cholesterol levels.
My Lipid Panel
These were my cholesterol levels in October, 2017:
Triglycerides: 91 (normal range 30-200)
HDL cholesterol: 51 (normal range 40-60)
LDL-C cholesterol: 202 (normal range 0-130)
These results are all in mg/dl units.
As you can see, my TC and LDL are high. Those values were a signal to my doctor that I needed to be on statins.
Even though I have neither diabetes nor CVD, my LDL-C level is over 190 so I’m considered at high-risk for CVD. According to the ACA/AHA that makes me a good candidate for statin therapy.
However, consider this. If I reduce my LDL-C to 189 by natural means (diet), would I still be a candidate for statins? How about if I brought it down to 150?
Estimated 10-year CVD Risk
Since my LDL-C was over 70, my doctor would calculate my 10-year CVD risk. If it was > 7.5%, he would immediately recognize that I fulfilled category 3 of the ACC/AHA guidelines for statins.
By the way, my 10-year risk was over 7.5% even though the only risk factors I had were perhaps my age (60) and a high LDL-C and TC.
However, do you see the major problem with this risk calculation?
Two data points required in the calculation are your TC and LDL-C levels. This means that high TC and LDL-C are already presupposed to be risk factors.
But if they’re not, then the calculation for your 10-year risk determination is worthless.
So, the important question remains: is an LDL-C of greater than 190 mg/dl always an indicator of high risk for CVD?
Does my LDL-C number of 202 make me a good candidate for statin therapy? Yes or no?
I say no.
Let’s start debunking the “cholesterol-heart disease” myth.
Total Cholesterol Levels Aren’t a Good Indicator Of Heart Disease Risk
For years, we were warned that consuming foods high in cholesterol would eventually give us heart disease by gunking up our arteries. So we refrained from eating foods like eggs and red meat.
However, the “cholesterol-heart disease” theory, perpetrated by the AHA, was debunked years ago.
Today, it’s acknowledged that total cholesterol levels tell us nothing about our overall risk of heart disease risk. That’s why the ACC/AHA no longer use it in their guidelines.
The only caveat here would be if an individual had a condition called familial hypercholesterolemia.
Watch below as in about one minute Dr. Malcolm Kendrick destroys the cholesterol-heart disease hypothesis.
Low Cholesterol Could Be Unhealthy
Cholesterol is vital to our existence. It’s a necessary component of cell membranes, a precursor for many hormones, necessary for our body’s use of vitamin D, and important in neurologic and digestive functions.
Since we don’t know exactly how much cholesterol is needed for these processes, lowering cholesterol too drastically could cause unintended negative health consequences.
Dr. Diamond in the Expert Review report noted that,
“there is a well-established role of viruses in cancer development, and it is well-known that reduced levels of cholesterol are associated with a greater incidence of viral infection and cancer…”
Remember that statins lower total cholesterol levels. This could be a reason for the increased cancer risk associated with statins.
Taking it a step further, Zoe Harcombe has done an excellent job showing that lower cholesterol levels are in fact associated with a higher mortality rate.
Okay, so it appears that my total cholesterol of 252 is not necessarily a risk factor.
Now, let’s take a look at LDL-C.
What Is LDL?
You’ve probably heard LDL-C called the “bad cholesterol”. It’s termed that because at high levels it’s been associated with atherosclerosis and heart disease.
However, LDL-C is not cholesterol at all. It’s a low-density lipoprotein (LDL) that is responsible for carrying lipids, including cholesterol and triglycerides, around your body.
You’ve probably noticed by now I’ve abbreviated LDL as LDL-C.
This is because a standard lipid panel blood test doesn’t directly measure your LDL. Your LDL is calculated by using total cholesterol, HDL, and triglycerides.
Therefore, LDL-C is basically an estimate of your LDL level.
However, many researchers believe this estimated version of LDL is not the best way to assess CVD risk. They suggest a better way of evaluating risk is by considering the number and size of LDL particles.
LDL Particle Number
LDL-C is actually a measurement of the cholesterol mass within LDL-particles. Let me illustrate what this means.
You can think of LDL particles traveling in your bloodstream as cars with passengers traveling down a highway.
Cholesterol and triglycerides (as well as other fats) are passengers on the LDL molecule.
LDL-C is an estimate of the number of cholesterol passengers in the LDL particle.
At one time, researchers thought it was the cholesterol concentration in the LDL particle that was the driver in CVD.
Today, however, researchers believe that it’s the number of cars on the road, not the number of passengers that is the problem.
In other words, it’s the number of LDL particles in the blood that drives CVD not the amount of cholesterol in an individual particle (LDL-P).
Often an abnormally high LDL-C will reflect high LDL-P values. This is probably why a high LDL-C is associated with CVD risk. However, frequently the opposite is true.
In many individuals, LDL-C and LDL-P are discordant. That means their LDL-C and LDL-P levels are not in agreement.
In fact, one study showed that 30 – 40% of individuals with low or normal LDL-C may have elevated LDL-P.
That means that even while their LDL-C level indicates a low risk for CVD, their LDL-P value indicates that they actually have a high risk for CVD and of also developing metabolic syndrome.
Now, discordance can also work the other way. If a person has a high LDL-C and a low LDL-P, then that person is at a lower risk for CVD.
Unfortunately, since that person’s doctor is only concerned with LDL-C, the doctor would still want to put their patient on a statin.
An important recent study, which included 68,000 individuals, showed that high LDL levels were not associated with increased death in people over 60. In fact, the study showed that elderly people with high LDL-C live as long or longer than those with low LDL-C.
Therefore, LDL particle size is another factor to consider in CVD risk.
LDL particles exist in different sizes. There is a small dense particle and a larger buoyant particle.
Another study showed that small LDL-P appeared to penetrate the coronary artery walls 1.7 times more than large LDL particles.
Current research is also discovering that small LDL particles are not the sole driver of CVD.
Inflammation Is Another Driver Of CVD
There is good evidence that there’s an inflammatory process behind the development of CVD, and that this inflammation exists prior to the formation of the atherosclerotic plaque.
It seems that LDL particles must be oxidized before they adhere to the coronary arteries. For a good discussion on this, see here.
Insulin resistance, type 2 diabetes, and metabolic syndrome produce highly inflammatory states within the human body which could be a participating factor in CVD.
So, as we’ve seen, simply looking at LDL in isolation will not give you a good picture of how cholesterol is affecting your body.
If you want a true picture of your CVD risk in terms of LDL, you have to find out what your particle number and size is. There are lab tests that detect these levels.
A Good Way to Assess Your Heart Disease Risk In Terms Of Cholesterol
While total cholesterol and LDL-C levels in isolation tell us very little about heart disease risk, there is a better way to predict risk.
Triglycerides (TG) are a type of fat found in your blood. High-density lipoprotein (HDL) is considered your “good cholesterol”.
This study found that a TG/HDL ratio above 4 is an extremely powerful predictor of developing CVD.
Interestingly, the predictive value of TG/HDL ratio was the same for men and women.
What’s The Ideal TG/HDL Ratio?
A TG/HDL ratio below 2.0 is considered ideal. A ratio above 4 is considered too high, and a ratio above 6 is considered extremely high. Note that these values are U.S. measurements. In other parts of the world, a different measuring system is used.
Remember that high TG/HDL numbers are usually found in people with type 2 diabetes and metabolic syndrome.
My TG was 91 and my HDL was 51. So my TG/HDL ratio is 1.78. According to this indicator, I’m at low risk for CVD even though my total cholesterol and LDL were elevated.
The Total Cholesterol/HDL Ratio
Another ratio to determine heart disease risk is the TC/HDL ratio. It’s an older means of assessing risk, but some doctors still use it.
A ratio of 5 signifies average risk for heart disease; 3.4, about half the average risk; and 9.6, about double the average risk. Women tend to have higher HDL levels, so for them, a ratio of 4.4 signifies average risk; 3.3 is about half the average; and 7, about double.
However, the Mayo Clinic suggests that this ratio should be closer to 3.5.
If the Mayo Clinic is correct, then my TC/HDL ratio (4.9) is a little high. This has prompted me to try and raise my HDL (good cholesterol) level.
In order to do this, I’ll try to keep my carb intake below 30 grams/day and add in more intermittent fasting.
NB: I was not on a ketogenic diet at the time I wrote this post
How To Optimize Your Triglyceride/HDL Cholesterol Ratio
It’s possible to optimize your TG/HDL without taking statins. I mentioned before that insulin resistance, type 2 diabetes, and metabolic syndrome (including obesity) all contribute to lipid and cholesterol abnormalities.
Correcting these risk factors is essential to regaining a good TG/HDL ratio.
The following is the strategy I’m using to optimize my TG/HDL ratio.
- Lose weight. Even modest weight loss can lower triglyceride levels. I’ve lost about 25 pounds and shed a good deal of excess body fat.
- Avoid the intake of sugar and fructose (especially high fructose corn syrup).
- Avoid a low-fat, high-carbohydrate diet. Mainstream medicine tells us that diets high in fat, especially saturated fats increase the risk of heart disease. This is simply not true. See here and here. See my post on saturated fats here.
- Follow a low-carbohydrate, healthy-fat diet (LCHF). I’ve been on a very low carbohydrate diet (<50 grams, often <30 grams/day) for about 10 months. Recent studies show that an LCHF diet is beneficial for improving TG/HDL ratios as well as other biomarkers. See here and here. See my post on why LCHF diets work for weight loss.
- Consuming Omega-3 fatty acids like those found in fish oil. They have long been recognized for their ability to lower triglycerides. See here and here. I get my fish oil by eating salmon and sardines at least once a week.
- Exercise often. See here and here.
That’s a wrap for this week. What’s your take on statins? We’d love to hear from you.
(At the time I wrote this post I was not on a ketogenic diet. I went keto in October 2017 and have been on a ketogenic diet ever since. I lost another ten pounds. My weight has stabilized at 160 pounds and my waist is now 32″. My weight lifting totals have suffered minimally. I’ll have new blood results done in the near future to check my lipid levels.)
Disclaimer: The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician.
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