Management of blood cholesterol just got personal

Don’t look now, but the updated clinical practice cholesterol guidelines from the American College of Cardiology, the American Heart Association and others are getting personal. Although the guidelines still contain their familiar approach — that I consider too aggressive with drug therapy — the latest 2018 version of the guidelines now includes an impressive update to emphasize lifestyle intervention, plus a more individualized approach for risk assessment.

MedPage Today: AHA: Revised Lipid Guide Boosts PCSK9s, Coronary Calcium Scans

Could this be the start of a progressive trend away from shotgun statin prescriptions? I sure hope so.

Prior guidelines emphasized the 10-year ASCVD risk calculator as the main determining factor for statin therapy. In the 2018 update, the guidelines acknowledge that the calculator frequently overestimates the risk in those individuals who are more involved with prevention and screening. (In other words, those patients more interested in and proactive about their health; I find many in the low-carb world fall into this category.)

The ensuing discussion with a healthcare provider should then focus on:

[T]he burden and severity of CVD risk factors, control of those other risk factors, the presence of risk-enhancing conditions, adherence to healthy lifestyle recommendations, the potential for ASCVD risk-reduction benefits from statins and antihypertensive drug therapy, and the potential for adverse effects and drug–drug interactions, as well as patient preferences regarding the use of medications for primary prevention… and the countervailing issues of the desire to avoid “medicalization” of preventable conditions and the burden or disutility of taking daily (or more frequent) medications.

I appreciate the attention the new guidelines bring to the depth of the discussion that should ensue between doctor and patient. Considering the treatment burden is equally as important as the burden of disease, and possibly even more important in patients who have not been diagnosed with heart disease, these individualized discussions about trade-offs are critical to personalized care.

Also worthy of mention is the increased use of coronary artery calcium scores (CAC) to help individualize risk stratification. The updated guidelines specify CAC may be useful for those age 40-75 with an intermediate 10-year calculated risk of 7.5%-20%, who after discussion with their physician are unsure about statin therapy. They specify that a CAC of zero would suggest a much lower risk than that calculated by the ASCVD risk formula, and thus take statins off the table as a beneficial treatment option.

This is huge. I cheered when I read this! I have been critical of prior guidelines that focused on ways to find more people to place on statins. The mention of finding individuals unlikely to benefit from statins is a giant step in the right direction.

The guidelines go even further: they mention that a CAC either over 100 or greater than the 75th percentile for age increases the CVD risk and the likely benefit of a statin. A CAC between 1-99 and less than the 75th percentile does not affect the risk calculation much and it may be worth following the CAC in five years in the absence of drug therapy. I would still argue that a CAC >100 does not automatically equal a statin prescription and we need to interpret it in context, but I greatly appreciate this attempt at a more personalized approach.

The guidelines also go beyond the limited risk factors included in the ASCVD calculator by introducing “risk modifying factors” such as:

  • Premature family history of CVD
  • Metabolic syndrome
  • Chronic kidney disease
  • Chronic inflammatory conditions such as rheumatoid arthritis and psoriasis
  • Elevated CRP > 2.0 mg/L
  • Elevated Lp(a) > 50 mg/dL or 125 nmol/L
  • Elevated triglycerides > 175 mg/dL

Although they use these criteria to define an increased risk, the opposite would likely hold true. An absence of those criteria could define a lower risk situation.

Some changes deserve mention from a controversy standpoint as well. For instance, the new guidelines recommend checking lipid levels as early as two years old in some circumstances. Two!

They also recommend statin therapy for just about everyone with diabetes with no mention of attempting to reverse diabetes before starting a statin, a drug that has been shown to worsen diabetes and insulin resistance. In addition, the new guidelines do not mention the likely discordance between LDL-C and LDL-P in those with diabetes.

Last, the new guidelines define an LDL-C > 190 mg/dL as an absolute indication for statin therapy with a treatment goal of 190 mg/dL is in familial hypercholesterolemia populations (and even then has heterogenous outcomes). There is a clear lack of data supporting that same recommendation for metabolically healthy individuals with no other cardiac risk factors and no other characteristics of familial hypercholesterolemia. This is a clear example of when a guideline turns from “evidence based” to “opinion based.”

In summary, the guideline committee deserves recognition for its emphasis on an individualized care approach, its use of CAC, and its broader description of discussing potential drawbacks of drug treatment. It still combines opinion with evidence and believes all elevated LDL is concerning, but I for one hope it will continue its progression away from generalizations and someday soon see that individual risk variations exist, even at elevated LDL-C levels.

Thanks for reading,
Bret Scher MD FACC

Originally Posted on the Diet Doctor Blog 

Low Carb LDL- A Call for Reason

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

Dave Feldman Challenges Everything We Think We Know About LDL Cholesterol.

Dave Feldman brought down the house yet again with a rousing presentation at Keto Con 2018. In his presentation, he postulated that a subset of LCHF individuals, which he terms Lean Mass Hyper Responders (LMHRs), are unknowingly changing the world of cholesterol.

 

Traditionally we are taught that any elevation of LDL cholesterol leads to heart disease. Not so fast, says Dave. In this episode, we discuss why this does not apply to LMHRs and what that means for LCHF individuals and what it means for the medical world as a whole. We also discuss how recent PCSK9i drug trials prove his point, even though contemporary medicine promotes them with an opposite conclusion. Sound confusing? Well, it isn't once you hear Dave explain his case.  

 

Once again, Dave brings his passion, his engineering mindset, and his intellectual honesty to the table for a rousing interview that is sure to cause a stir among old-school doctors and lipidologists. You don't want to miss this one!

 

What Does My Cholesterol Level Mean?

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

 

Reverse Engineering Cholesterol Misconceptions

Siobhan Huggins

This week's guest, Siobhan Huggins, is a stellar citizen scientist who has a passion for dissecting complex topics, and understanding how misbeliefs lead us astray. She has a remarkable gift of analyzing complex topics and reframing them from a systems and engineering point of view. Plus, her own personal journey through the low-carb keto lifestyle prompted her deeper dive into lipids, inflammation, insulin resistance and more. She understands that cholesterol is not inherently evil. Rather, it actually serves a purpose to help us. It's our lifestyle that alters it into something potentially harmful.

 

Most exciting of all, she has recently joined forces full-time with Dave Feldman at CholesterolCode.com, so we will be hearing much more exciting research and perspective shifts from Siobhan in the near future.

 

Key Takeaways:

 

[6:03] A keto diet has given Chivon improved health and changed her personality.

[8:58] Research and reading has qualified Chivon to write for Cloresteralcode.com

[12:07] Understanding inflammation and the chronic oxidation of LDL.

[17:07] Scavenger receptors and small, dense LDL.

[28:42] The human body wasn't designed to take on a constant barrage of insulin damage.

[35:32] What causes vascular calcification?

[43:32] The differentiator in familial hypercholesterolemia is the level of insulin resistance.

[47:13] Lipoprotein(a): What is it used for?

 

Mentioned in This Episode:

Low Carb Cardiologist Website

Dr. Scher on Twitter

Dr. Scher on Facebook

Cholesterol Code

 

This Episode is Sponsored by LowCarbCardiologist.com and Your Best Health Ever! The Cardiologist's Surprisingly Simple Guide to What Really Works,
by Bret Scher, M.D., FACC

 

Bret Scher, MD FACC

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