What Does My Cholesterol Level Mean?

Depending on how you look at it, cholesterol can be an incredibly simple topic, or an incredibly confusing one. Contemporary medicine teaches that cholesterol is “bad” and should be low. That seems pretty simple, right? Get it tested, if it’s high, start a drug to lower it. 

Times have changed. Now, cholesterol is much more complex, and we all need to be armed with knowledge before we sit down with our doctors to evaluate our cholesterol levels.

Here is my guide to you and your doctor for evaluating your cholesterol.

1. Understand the difference between Total Cholesterol (TC) and high density lipoprotein (HDL) and low density lipoprotein (LDL)

If you doctor is referring to your total cholesterol (TC) and is making decision based on your TC— Run, don’t walk. Run away and find another doctor. TC is comprised of low density lipoprotein (LDL), so-called “bad cholesterol” even though it isn’t bad. High density lipoprotein (HDL), so-called “good cholesterol”, and remnant cholesterol (VLDL and IDL). Initial studies in the 1960s and 70s looked at TC and risk of cardiovascular disease (CVD) and found a weak association.  That was prior to when scientists learned how to measure LDL and HDL.

Studies then looked at the individual lipoproteins (i.e. LDL and HDL) and found the higher the LDL, in general, the higher the risk for CVD. And the higher the HDL< the lower the risk of CVD. So, while talking about TC was cutting edge in the 60s and 70s, it is woefully outdated today. That is why if your doctor is still evaluating and treating TC—Run!

2. Does Your Doctor Know Your TC to HDL and TG to HDL Ratios?

If your doctor does not know your ratios, this is another reason to run away and find another doctor (We are doing lots of running here, bonus exercise!) Studies in the early 2000s and more recently have shown that total cholesterol to HDL ratio (TC:HDL) and triglyceride to HDL ratio (TG:HDL) are BETTER predictors of cardiovascular risk than isolated LDL, TC or HDL.

By incorporating TG and HDL into the analysis, these ratios incorporate the impact of remnant cholesterol and track with insulin resistance, both strong predictors of CVD. These ratios are calculated from a standard lipid profile, so they do not require any special testing or special labs. They are widely available for everyone to see. So if your doctor is not using them to evaluate your lipids, it’s time to find a new one.

3. Understanding a Familial hypercholesterolemia (FH) diagnosis

Familial hypercholesterolemia (FH) is a diagnosis that requires (wait for it…) a family history! As the name suggests, it is an inherited condition passed from generation to generation. All too often, doctors will see an LDL level over 190 and make the diagnosis of FH. If your doctor makes that diagnosis that based on level alone without a family history, run!

There is a well-accepted scoring system, The Simon Broome Criteria, to help determine if someone has FH. This equation factors in age of diagnosis, absolute level of LDL, in addition to family history of early onset hyperlipidemia or early onset heart disease. It makes a big difference if you have FH or not. Don’t let your doctor label you as having FH without applying the full criteria. Just wait for the look on their face when you respond, “What was my Broome score? Did it confirm I have FH?” and hope you don’t hear crickets.

4. What is Advance Lipid Testing?

Advance lipid testing may be helpful. And it may not. Advanced lipid testing can tell us the size, density, and inflammatory characteristics of our lipoproteins. This can help further risk stratify the potential danger of our lipids. For instance, small, dense LDL tend to correlate more strongly with CVD, whereas so-called pattern A LDL (the larger, less dense version) does not correlate as well.

Here is the interesting part. Those with high TG and low HDL almost uniformly have small dense LDL and increased inflammation. Conversely, those with low TGs and high HDL have Pattern A, larger less dense LDL. Are you starting to see a pattern? Low TG and high HDL=good. High TG and low HDL=bad.

Sometimes, however, there can be variation in this equation. Therefore, I usually suggest people get advanced lipid testing one time to see if their results correlate. If they do, then you can just follow your ratios to predict your advanced results. Why not get them all the time? They are frequently not covered by insurance and can be expensive.

5. Interpret your lipids in context

Lipids don’t exist in a vacuum. They exist in your body, so it’s important to take into account what else is going on in your body. Insulin resistance and inflammation can directly affect your lipids and increase your risk in general. Hypertension, obesity, and family history of heart disease also play crucial roles in determining your risk.

Therefore, if your doctor checks only your lipids and bases decision on those labs alone—Run! Instead, you should get a hsCRP, Hgb A1c, fasting glucose, insulin and HOMA-IR, BP measurement, family history assessment, and complete history. This is the context in which your lipids should be evaluated. Not alone in a vacuum.

6. Why test a risk factor that may be related to CVD risk when you can test the disease itself?

Good question, right? To truly know what your lipids mean to you, you also need to know if you have evidence of CVD. Coronary artery calcium scores and Carotid Intima Media Thickness (CIMT) are two easy, relatively inexpensive tests, that you can get to show you whether or not you have current evidence of CVD. The presence or absence of disease significantly impacts the risk of lipid levels.

So, What Does Your Cholesterol mean to You? It depends.

It depends on many factors, and only by evaluating ALL of those factors can you truly know what impact your lipids may be having on our health. Anything short of this evaluation is an inadequate and antiquated approach to lipids.

Now you are forewarned and forearmed, and you can walk into your doctor’s office ready to ask the important questions and help guide the workup so that you can know what your cholesterol means to you.

Thanks for reading, and as always, please let us know If you have any comments or questions.

Bret Scher MD FACC

Founder, Boundless Health

www.LowCarbCardiologist.com

Can we be certain that elevated LDL (Low-density lipoprotein) particles have no meaning and can be completely ignored?

Certainly not.

Can we be certain that all LDL particles are deadly and need to be treated to microscopically low levels?

Certainly not.

So, what do we do?

I have seen countless second opinion consults and enrolled numerous clients in my Boundless Health Program who have this exact question.  What’s the deal with LDL? Do we worry or don’t we?

Life is much easier when it is black and white, good and bad. I, however, believe in looking for the nuance and trying to understand things a little deeper.

But first, let’s back up a little.

What is LDL and LDL-P?

Cholesterol can be a complex topic that we frequently oversimplify, which I am about to do. In brief, LDL is known as the “bad” cholesterol, the cholesterol that is found in plaque buildup in our hearts. But the truth is that LDL is not inherently bad. In fact, LDL has a purpose in our bodies as part of our immune response and as a fuel and vitamin delivery mechanism to name a few.  If vascular injury and inflammation are present, then modified LDL may invade vessel walls and participate in a cascade of events leading to plaque buildup and an eventual heart attack.

LDL-C is a measure of the total amount of cholesterol in our LDL lipoproteins. LDL-P is the total number of the LDL lipoproteins. Studies show that LDL-P is a much better marker for CVD risk than LDL-C. As an analogy, the number of cars on the road matter more than the number of people in the cars.

What are the risks of LDL-P?

On the one hand, trials in the general population show that elevated LDL-P is a risk factor for cardiovascular disease (CVD).  This includes a combination of observational trials, genetic mutation trials (mendelian randomization), and drug treatment trials.

All things being equal, based on these trials alone, we should want our LDL-P to be low.

But does LDL alone cause heart attacks and death? Or are there other factors involved?

Of course there are other factors involved in CVD. Vascular injury and inflammation being the two most prominent factors.

Can lowering our LDL-P have risks greater than the potential benefits for certain populations?

Absolutely.  Since primary prevention statin trials show we have to treat over 200 people for five years to prevent one heart attack with no difference in mortality, it seems reasonable that certain populations will experience more potential risk than reward.

The Low Carb High Fat Reality

How many LDL or statin trials have specifically looked at individuals on a healthy, real foods, LCHF diet?

None. Not a single one.

How many LDL or statin studies have looked specifically at red headed, left handed boys born the second week of March? 

None, at least to the best of my knowledge.

This seems glib but bear with me.

Is there any reason to think a red headed, left handed boy born the second week of March would behave any differently than everyone else in these LDL studies? Not really. Especially if they are eating a standard American diet or a low -fat diet as was almost exclusively studied in every cholesterol or statin trial.

Here’s the more important question. Is there reason to believe individuals on a healthy, real foods, LCHF diet would behave any differently than everyone else in the decades of lipid and statin studies?

There absolutely is reason to believe they may behave differently. There is not clear proof, but there is plenty of reason to suspect it.

Think about the benefits of a LCHF lifestyle.

• Lowers inflammation
• Reverses insulin resistance
• Naturally raises HDL and lowers TG
• Converts majority of LDL particles to larger, more buoyant particles
• Lowers blood pressure
• Reduces visceral adiposity

Could these create an environment where an elevated LDL is less of a concern?

It sure could.

To be clear, I openly acknowledge that we do not have definitive proof that we should have no concern with LDL in this situation. In my opinion, this is a specific scenario that the existing trials simply do not address one way or the other.

So, it seems we have two choices.

1. Since we don’t have any proof we can ignore LDL in this setting, we plug the numbers into the 10-year ASCVD calculator and start a statin if the risk is above 7.5%, or we ask the individual to change their lifestyle in hopes the LDL will come down.
2. If the individual is enjoying multiple health benefits from their lifestyle, and they are rightly concerned about the potential risks of statin therapy, then we can follow them for any sign of vascular injury or plaque formation, or any worsening of their inflammatory markers or insulin sensitivity. In the absence of any potentially deleterious changes, we can reason that the risk is low, and the benefits of living the healthy lifestyle may outweigh the risks.

The “problem” is that the second option requires a detailed discussion of the risks and benefits. It requires close monitoring and follow up. It requires us to think outside general guidelines and consider everyone as an individual with their own unique circumstance. These are qualities that our current healthcare system sorely lacks.  Yet that is the exact care that each individual deserves.

What do we do in the meantime?

I hope someday soon we will have definitive long-term evidence that a high number of large buoyant LDL particles along with elevated HDL, low TG and low inflammatory markers is perfectly safe.

Until that day, we will have to continue to talk to our patients. To see them as individuals. To weigh the lifestyle benefits with the possible risks. That includes seeing the risks in real numbers- not quoting a 30% benefit with statin therapy. Instead, having a real discussion that statins may reduce your risk a heart attack by 0.6% with an increased risk of muscle aches, an increased risk of diabetes, and a potential increased risk for cognitive and neurological dysfunction.

And we will have to understand that the answer won’t be the same for each person. And we can be OK with that.

So, do you have to worry about your LDL? I don’t know. But I welcome the opportunity to explore the question and reach the best answer for you.

Do you have questions about what your lipids may mean for you? What they mean when taken in the context of your lifestyle and overall health picture? If so, you may want to learn more about my Health Coaching Consult.

Thanks for reading,

Bret Scher, MD FACC

Can you find a more polarizing topic than statins? One article says they are miracle drugs that should be given to everyone. Then you turn the page, and you read how they are poison and you should stay away from them no matter what.  How can one drug cause such differing views? And which should you believe?

The statin debate has intensified ever since the 2013 ACC/AHA cholesterol treatment guidelines increased the number of people without heart disease who “should” take a statin to 43 million Americans. That is for primary prevention, meaning the individual has never had a diagnosis of cardiovascular disease, never had a heart attack, and never had any type of a heart problem.

As you can imagine, this has been a windfall for the drug companies. But are we healthier and better off as a result? That is unknown.

The problem is understanding the bias of whoever is writing the story.

Subtleties of Science

But wait, you say. Won’t the science tell us if statins are good or not? Isn’t it an objective fact if they are good for us?

Not so fast. Beauty is in the eye of the beholder, and so is the application of science.

Are you getting advice from someone who believes prescribing more medicine is better? Or someone who believes a more natural lifestyle is better? 

Are you reading a report sponsored by the pharmaceutical company that paid for the research?

Or are you getting advice from a scientist who is more focused on statistical benefits, or someone who is more concerned with the potential benefit for the one individual they are taking care of at the moment?

It is a confusing sea of conflicting information, and you have to find which approach resonates more with your beliefs and your life.

The Three Keys

Regardless of who you are and your beliefs, I promised you the three most important things you need to know about statins. Here they are:

1. All statin studies are worthless! That’s right. All statin studies that have been done to date are worthless and don’t apply to anyone who follows healthy lifestyle principles.
2. Statins will not prolong your life. Not at all. Not for a single day.
3. Statins DO reduce your heart attack risk, by about 0.7% over 5 years.

All of a sudden, statins don’t seem so powerful, do they? Let’s go deeper into these points to learn why.

1-All Statin Trials Are Worthless

When designing a trial, you have to decide what your control group is going to be. You have to show that the drug is better than something. The key is defining what that something is.

Therein lies the problem. In order to show beneficial effects, primary prevention statin trials need thousands of subjects, studied over years. That is very expensive to do. The vast majority of trials, therefore, rely on drug company funding.

Do you think they are going to fund a trial that makes it easier or harder to show a benefit? Of course, that was a rhetorical question.

Pharma companies don’t have an interest in your health and wellbeing. Their priority is to their stock holders and their bottom line. They are going to sponsor trials that are most likely going to benefit them.

How does this make the trials worthless? They compare statins to “usual care.” That means a brief, and ineffective attempt to educate people about healthy nutrition and physical activity.

In addition, the specific nutritional guidance that was used has always been a low-fat diet. As we now know, what does a low-fat diet usually include? Lots of sugars and simple carbohydrates. What does that diet do? Increase your risk of obesity, diabetes, inflammation, and eventually heart disease.

That’s setting the bar pretty low to show a benefit from statins. And that is exactly what the drug companies want.

What we need is a control group that is involved in a comprehensive lifestyle intervention program. A program that helps participants get regular physical activity. Helps them eat vegetable based, real food, low in added sugars and simple carbs, and high in natural healthy fats.

Since that is the way we should all be living, THAT is what the control group should be. I guarantee you, the results would be far different compared to the standard control groups used to date.

That is the trial the drug companies never want to see and will never fund. And that is why all statin trials to date are worthless.

If you can focus on proper lifestyle interventions, using healthy foods, physical activity and stress management as medicine, then we have no idea what effect, if any, statins would have. But I assure you it will be minimal if any benefit.

2-Statins Will Not Prolong Your life

You read that right. For people who have never had heart disease before, the multi-billion dollar drug won’t help you live longer. The overwhelming majority of primary prevention trials involving statins show no difference in overall mortality between those who took the drug and those who did not.

That surprises a lot of people. Statins are promoted as if they are wonder drugs that save lives left and right. That’s good marketing and good PR. Reality is far different.

If they don’t help you live longer, they must increase the quality of your life, right? Nope. In fact, 30-40% of people on statins will experience muscle aches and weakness causing them to exercise less and decreasing the overall quality of their lives.

So, if they don’t help us live longer, and they don’t increase the quality of our lives, why do we take them????

3-Statins DO Reduce Your Heart Attack Risk

If the news was all bad there wouldn’t be any debate about their use. But the truth is that statins do reduce the risk of heart attacks, and that is why in some cases it may be beneficial for you to take one.

But the big question is: How much do statins reduce your heart attack risk? The answer is not as much as you would think. Considering the recommendations keep getting more and more aggressive for statin therapy, you would think statins would be immensely powerful at reducing heart disease risk.

In reality, they reduce the risk of a heart attack by 0.7-1.5% over 5 years. That means you need to treat 66-140 people for 5 years to prevent one heart attack.  (as an aside, for people with pre-existing heart disease, so called secondary prevention, you need to treat approximately 40 people for 5 years to prevent 1 heart attack and 85 people to prevent 1 death)

When presented like that, it should certainly temper the enthusiasm for statin therapy. Again, it may still be the right choice for some people, but given the potential risks and side effects, I would hope for a much greater benefit.

Better Than Statins

A common response is that statins are “the best we have to offer” to reduce one’s risk of cardiovascular disease.  If you are talking about a drug manufactured in a laboratory, then that would be correct. But what else are options?

It turns out following a Mediterranean eating pattern with vegetables, fruit, fish, legumes, and lots of nuts, olive oil and avocados reduces the risk of cardiovascular events as well. For something as simple as nutritional choices the benefit must be much less than a statin, right?

That is what the drug companies would want you to believe. In reality, you need to “treat” 61 people with the Mediterranean diet for 5 years to reduce 1 cardiovascular event (a “combined endpoint” of stroke, heart attack or death).

To be fair, you cannot compare one trial to another as they have very different populations studied, and the outcome measures are different. So, it is not scientifically fair to say, “The Mediterranean diet has been proven to be more beneficial that statins.”  That would require a head-to-head trial. Unfortunately, that trial is unlikely to ever happen.

But it makes for an obvious answer when asked “If statins aren’t all that helpful, what else can I do to reduce my risk of cardiovascular disease?

• Follow a real food, vegetable-based, Mediterranean style diet, low in sugar and high in healthy fats.
• Maintain a physically active lifestyle.
• Exercise with some form of moderate cardio exercise, resistance training and higher intensity interval exercises.
• Practice stress reduction techniques.
• Don’t smoke.
• Manage your other risk factors such as diabetes and high blood pressure.

If you can follow these healthy lifestyle principles, you will be doing far more for your health than any pill you could take. And the best part? The only side effects are having more energy, feeling more empowered, and reducing your risk for chronic diseases.  Sounds like a good trade off to me!

Thanks for reading.

Bret Scher, MD FACC

Cardiologist, author, founder of Boundless Health

www.DrBretScher.com

There’s a common assumption in the medical and nutrition world that a low carb, high fat diet, like a ketogenic diet, will automatically increase one’s risk for heart disease. However, it’s crucial for us to realize that this assumption is inaccurate and not supported by data.

In fact, it’s been well documented that low carb diets can help someone reverse type 2 diabetes and improve metabolic health, changes that dramatically lower one’s cardiac risk. Research and clinical experience supports that a properly formulated low-carb diet can help someone improve, rather than worsen, their heart health.

But many may wonder, how can this be true when I’ve heard that eating fat is bad for us and bad for our hearts?

A big problem comes from assuming that our bodies react the same way to a diet high in carbs + fat as we do to a diet LOW in carbs and high in fat. The truth is that our bodies react dramatically differently to those two versions of a high-fat diet.

How It Works

You see, when we eat lots of carbs, our body uses the carbs as fuel first. Therefore, we won’t burn the fat for energy, and we end up storing it as adipose or fat stores. But when we eat a very low carb diet, our bodies prefer to burn the fat for energy, and therefore there is much less left over to store as body fat. This is dramatically different from a high carb diet!

Studies also demonstrate that people eating a low carb, high fat diet naturally reduce their calories, thus eating less and losing weight seemingly without trying. But those eating high fat and high carb diets tend to eat more calories and gain weight.

So you can see how we can’t just refer to a “high fat diet” as if it is one thing. It makes a big difference if it is also a high carb or low carb diet.

The Main Contributors

Let’s review the main contributors to heart disease, and see how a low carb, high fat diet impacts them.

1- Blood pressure
One study demonstrated a ketogenic diet lowers blood pressure better than the DASH diet, the diet previously felt to be the best for blood pressure management. And others have shown safe and effective blood pressure lowering when starting a low carb, high fat diet that is similar to a low-fat diet.

2- Type 2 Diabetes
Numerous studies demonstrate the efficacy of low carb diets for treating and even reversing type 2 diabetes. Since diabetes is a major contributor to heart disease, reversing it will significantly improve one’s heart health.

3- Inflammation
Ketogenic diets have been shown to reduce many markers of inflammation, including the commonly used CRP.

4- Triglycerides and HDL cholesterol
Having low triglycerides and normal to mildly elevated HDL cholesterol levels are predictive markers of better heart health, likely because they occur with good metabolic health. Numerous studies demonstrate that ketogenic diets reliably help lower triglycerides and raise HDL, thus improving overall cardiac risk.

5- LDL cholesterol
Many assume that high fat diets raise LDL cholesterol. But again, that is not the case. Multiple studies demonstrate no net change in LDL on a ketogenic diet compared to a low fat diet. In fact, one analysis of multiple studies found a net reduction in LDL particles for those following a ketogenic diet.

Important to Note

However, there is a subset of individuals who can see a dramatic rise in their LDL cholesterol when following a ketogenic diet. These so-called Lean Mass Hyper Responders, have unique physiology that predisposes them to an increase in LDL. But it’s important to realize that these individuals are the minority, not the majority. And there’s even emerging evidence suggesting that elevated LDL may not place these individuals at a higher risk, although with much still to learn.

In Summary

The data does not support the assumption that low carb, high fat diets increase heart disease risk. In fact, many studies demonstrate overall improvement in most, if not all, cardiac risk factors. We need to stop assuming all high fat diets are the same, and realize the unique heart health-improving impact of low carb/high fat diets.

If you would like to learn more about the misperception and misunderstanding about ketosis and heart disease risk, please see the video links listed here:

Does Keto Cause Heart Disease?

Debunking a study claiming low carb diets cause heart disease

Analysis of a study demonstrating lowering of cardiac risk with low
carb diets

Thanks for reading,

Bret Scher MD FACC

I recently had a one-on-one Health Coaching Consultation with Dr. Bret Scher. I cannot adequately express the gratitude and respect I have for Dr. Scher. He took the time to consider all facets of my health and really listened to me and my concerns. He was not quick to insist I be on prescription medications, but rather he explored various avenues of suggested treatment/preventative measures I might consider taking…guiding, as opposed to dictating a plan of of action. The consultation was well worth my time and money! Loved his approach so much that my husband and I have decided to work with him long distance.

Jami Miltenberger
MS Counseling Psychology