Dr. Scher’s one-on-one Consultation was extremely valuable in my search for advice about cardiovascular health on a low-carb diet. During our discussion, I learned that interpreting lab results using the standard reference ranges can be misleading for anyone on low-carb or keto. He helped me better understand my test results and develop effective strategies to improve my cardiovascular health through nutrition and exercise. Dr. Scher is a good listener and a pleasure to work with. He is an excellent preventive cardiologist with a deep understanding of lipidology and metabolism, and the issues and challenges specific to a low-carb lifestyle.

Gabriel B.

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 live in McAllen, Texas, where it’s difficult to find a doctor who’s knowledgeable on the benefits of a low-carb lifestyle. Because I battle a high A1C AND high cholesterol, I reached out to Dr. Scher for a consultation to monitor my blood work and develop a plan that will keep my heart healthy and my A1C in check. Before our video-consultation, he responded personally to every question I had via email. When I first reached out, I figured it would take at least a month or more to schedule our consultation, but to my surprise, it was planned just over a week from my initial email!

I like Dr. Scher’s commonsense approach to a healthy lifestyle. He came up with a very-easy-to-follow plan and agreed to review my bloodwork every 6-8 weeks to make sure I’m on the right track. Because of my family’s history, it’s comforting to know I have a cardiologist monitoring my health so that I can prevent a significant problem down the road.

Nicole Southwell

What do I mean by “misunderstood?” Look no further than the common misnomer of “good” or “bad” cholesterol.

Good and Bad Cholesterol

While it may be true that High-Density Lipoprotein (HDL) has potentially beneficial functions (reverse cholesterol transport), we have to remember there is no such thing as good and bad cholesterol. The cholesterol carried by HDL is the same as that carried by LDL. The only thing that makes it good or bad is if it ends up synthesizing our hormones or bile acids (good), or if it ends up in our vessel walls (bad).

If it’s true there is no such thing as good and bad cholesterol, why do we care about our HDL levels?

First, let’s start with the basics.

HDL is the smallest and most densely packed lipoprotein and has one or more ApoA protein on its surface. HDL can help lipids move around in circulation by accepting triglycerides or cholesterol from other particles, thus helping a VLDL turn into an LDL, or helping an LDL contain less cholesterol (turning a small dense LDL into a less densely packed LDL).

Like LDL, HDL transports cholesterol to the liver for recycling or excretion, or to the hormone producing cells like in the adrenals. Unlike LDL, HDL does not have the potential to get retained in the vascular wall and does not, therefore, contribute to plaque formation. In fact, functioning HDL can remove cholesterol from the vessel wall, thus putting it back into circulation and possibly removing it from the body.

Back to the question at hand.

Why should we care about HDL levels?

Early epidemiological trials showed that lower HDL levels were associated with a higher risk of cardiovascular disease and even death.  With such a strong association, the medical profession promoted elevated HDL levels as protective and low levels as something we need to avoid.

Since these were observational epidemiological studies, they do not prove that the low HDL caused the problems, only that HDL was associated with it. For instance, HDL is also known to be low in diabetes, metabolic syndrome and insulin resistance. It may, therefore, simply be a marker of underlying metabolic dysfunction that contributes to increased risk.  Yet, HDL’s function in reverse cholesterol transport, and its ability to remove cholesterol from vessel walls suggests a more direct impact on cardiovascular health.

It is also important to note that the Framingham data suggested that increased cardiovascular risk with elevated total cholesterol and LDL-C was lost in the presence of high HDL. In fact, very low levels of LDL combined with very low HDL levels had a much higher risk than markedly elevated LDL levels when combined with elevated HDL.

Thus, HDL proves to be a useful marker to help predict cardiovascular risk. For instance, one large meta-analysis showed that total cholesterol/HDL ratio was a much stronger predictor of cardiac mortality than total cholesterol alone.

In addition, the PURE study, an observational trial in over 135,000 subjects, showed that when considering lipid changes brought about by nutritional changes, ApoB/ApoA1 (essentially LDL-P/HDL-P ratio) is the best predictor of clinical outcomes.

Thus, HDL level is important in assessing cardiovascular risk.

Drugs Muddy the Picture

While HDL may be a good predictor of risk, raising it with drugs does not seem to confer added benefit.

For instance, cholesterol ester transferase protein inhibitors (CETP inhibitors) significantly reduced LDL by 20-30% and increased HDL 100-fold, yet showed either no clinical benefit or even worse, an increased risk of death.

This was a shock to many in the lipid world as the notion of “good” and “bad” cholesterol would clearly predict lowering LDL and raising HDL would confer dramatic health benefits. So much so, that multiple pharmaceutical companies invested hundreds of millions of dollars developing these drugs only to abandon them when the trials showed no benefit.

Part of the issue is that not all HDL lipoproteins function the same. There are subsets of people with genetically determined markedly elevated HDL levels who have an increased risk of CVD. They may have plenty of cholesterol circulating in HDL particles, but the HDL particles are dysfunctional and therefore  do not effectively remove cholesterol from vessel walls or LDL and do not effectively transport it to the liver. Conversely, there are those with a specific genetic mutation called ApoA1 Milano who have very low HDL-C and lower cardiovascular risk.

Simply measuring the HDL cholesterol content, therefore, may not accurately reflect its function. While we do not have easily available tests to measure HDL function, we can potentially use HDL particle assessment as well as the company it keeps (i.e. low triglycerides, larger less dense LDL particles) to better assess the potential benefits of HDL. Thus, if there is any concern about potentially dysfunctional HDL, I usually recommend advanced lipid testing to see the specific subtypes of HDL.

What can we conclude from all the HDL confusion?

Raising HDL with drugs does not reduce cardiovascular events, yet having a naturally low HDL is associated with increased risk.

The best answer, therefore, is to live a lifestyle that helps you have a “not low” HDL level. This means first and foremost avoiding the medical conditions associated with low HDL (i.e. insulin resistance, diabetes, and metabolic syndrome).

Textbooks predictably state the interventions to naturally raise HDL include exercise and moderate alcohol intake. Unfortunately, these have minimal effects. In fact, they pale in comparison to a low carb high fat lifestyle. In my 20+ years in the medical field, I have never seen an intervention as effective as LCHF in raising HDL, and the studies agree.

This brings us back to our question once again.

Why are HDL levels important?

HDL levels are important because it is a reflection of our underlying metabolic health and our lifestyle. A properly constructed LCHF lifestyle lowers triglycerides, raises HDL, and reduces the small dense LDL, among other benefits. Such a lifestyle likely reduces overall cardiovascular risk and will likely be shown to improve longevity and health span. While HDL may not be the main reason for this, we can’t ignore its role simply because it is more nuanced than “good” and “bad” cholesterol.

My advice, therefore, is to see the whole picture. Embrace the nuance. And make sure you get a thorough and proper evaluation of your cardiovascular risk.

If you are hungry for more, I created my Truth About Lipids program, a program focused on Cholesterol, to help break through the confusion and provide you with everything you need to thoroughly understand cholesterol and its impact on your health.

Learn more: Truth About Lipids Program

If you still have questions, you may want to consider a one-on-one health coaching consultation so you can get the individual attention you deserve  with a thorough assessment of your lifestyle and its impact on you as an individual.

Please comment below if you have any questions or comments that may help further the discussion.

Thanks for reading.

Bret Scher MD FACC

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