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

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

A new study published in the European Heart Journal says we should care about blood levels of a metabolite trimethylamine N-oxide (TMAO), but is that true?

NBC News: Study explains how red meat raises heart disease risk

For starters, this was a well run and controlled study. Researchers randomly assigned 133 subjects to one of three isocaloric diets with the only difference being the presence of red meat, white meat, or vegetarian protein. Similar to the study by Dr. Ludwig that we referenced earlier, a strength of this study was that the study team supplied all meals for the subjects. Therefore, there was no guessing about what the subjects ate or if they complied with the recommendations. That makes this a strong nutritional study.

Subjects stayed on each diet for four weeks and then had a washout period before transitioning to the next diet. The main take home is that eating red meat increases the blood level of TMAO, which declines after four weeks off the red meat diet. As described in the article:

a red meat diet raises systemic TMAO levels by three different mechanisms: (i) enhanced nutrient density of dietary TMA precursors; (ii) increased microbial TMA/TMAO production from carnitine, but not choline; and (iii) reduced renal TMAO excretion. Interestingly, discontinuation of dietary red meat reduced plasma TMAO within 4 weeks.

It is important to note in our era of frequent conflicts of interest, NBC news reported that the lead investigator for the study is “working on a drug that would lower TMAO levels.” While that in no way invalidates the findings, it does legitimately raise suspicion for their importance.

Interestingly, the study did not test eggs, another food reportedly linked to TMAO. They did, however, note that increased choline intake, the proposed “culprit” in eggs, had no impact on TMAO levels.

The study also did not investigate fish. Fish, traditionally promoted as “heart healthy,” has substantially higher concentrations of TMAO than meat or eggs. One thought, therefore, is that high TMAO levels are produced by gut bacteria rather than the food itself. Although this is an unproven hypothesis, it would also explain variability among subjects.

Now for the harder question. Does any of this data matter? For this study to be noteworthy, we have to accept the assumption that TMAO is a reliable and causative marker of heart disease.

The main NEJM study linking TMAO to an increased risk of cardiovascular disease is not as conclusive as many promote. First of all, only those at the upper quartile of TMAO level had a significant increase in cardiovascular disease risk. Lower elevations had no significant correlation.

Second, those with increased TMAO and cardiovascular disease risk also were more likely to have diabetes, hypertension and a prior heart attack; furthermore, they were older, and their inflammation markers, including myeloperoxidase, a measurement of LDL inflammation, were significantly higher. With so many confounding variables, it is impossible to say the TMAO had anything to do with the increased cardiovascular disease risk.

This study in JACC that saw a correlation with TMAO and complexity of coronary lesions, also found an increased incidence of diabetes, hypertension, older age in the high TMAO group.

Finally, this study found no association at all between TMAO levels and increased risk of cardiovascular disease.

Based on these mixed findings, the jury is still out, and we have plenty of reason to question the importance of elevated TMAO as an independent risk marker or causative factor of coronary disease.

Most importantly, however, since multiple studies continue to show no significant association between meat and egg consumption and increased heart attacks or mortality risk (references here, here, here, here and here) the weak surrogate markers don’t seem likely to matter much. Don’t get caught in the minutiae. Focus on a real-food diet that helps you feel better and improves the vast majority of your markers. And if you have elevated TMAO, the studies suggest you should also check your blood pressure, blood sugars, and inflammatory markers as they may also be elevated. In my opinion, until we have much more convincing data on TMAO, you are far better off targeting those more basic parameters than a blood test of questionable value.

Thanks for reading,
Bret Scher, MD FACC

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

We had an incredible turnout for our Webinar, aimed to help you transform your health in 2019. As a result, we decided to create a blog post that includes the full webinar recording, as well as an overview of the learnings for those that were unable to attend.

Webinar Recording

https://www.youtube.com/watch?v=pIyi11wMq5U&ab_channel=LowCarbCardiologist

Webinar Overview

Cardiovascular Disease Is the #1 Killer for Men and Women

• 1/3 of all Americans die from Cardiovascular disease
• Around 92 million Americans are living with CVD
• Every 34 seconds someone suffers a heart attack
• Annual health expenditure and lost productivity from CVD ~$330 billion

It’s been estimated that 50-80% of these are preventable! Unfortunately, our healthcare system and associated lifestyle guidelines have failed to prevent disease. We could say at best they have failed to prevent heart disease, obesity and diabetes. At worst they have been implicit in its prevalence. While this graph doesn’t show causation, it certainly shows the association of instituting national nutritional guidelines and the rise in diabetes.

Drugs Don’t Fix the Problem

• 60% of Americans take at least 1 prescription drug
• 15% take more than 5 drugs
• Despite this, our overall health and life expectancy continue to decline

HEALTH IS NOT THE ABSENCE OF DISEASE!

In this webinar, we will discuss how to be your own best advocate, why low carb, high fat nutrition should be an option for everyone, and how lifestyle really is the best medicine.

3 Interventions to Improve your Healthcare Experience and Be Your Best Advocate

1. Make sure your doc is working with accurate information! Lipids and blood pressure are two prime examples of when doctors make decisions based on limited and faulty information.
2. Get your questions answered by writing them down ahead of time so you don’t forget anything and tell your doctor at the beginning of the appointment that you have some questions you’d like to ask at the end.
3. Make sure you understand the purpose and benefit of each and every medication. Not some vague answer like “It will improve your cholesterol,” or “It will lower your blood pressure.” Rather, “what impact will it have on my longevity and quality of life?” Will I live longer? Will I feel better? What are the chances the drug will actually benefit me? These are the questions we need answered.

Why Low Carb, High Fat Nutrition Should be an Option for Everyone!

LCHF vs Low Fat Diets

LCHF Benefits

• Decreased hunger, increased energy, mental clarity
• Treats metabolic syndrome/insulin resistance
• Better weight loss
• Improves overall cardiovascular risk for most people

LCHF may not be the best for everyone, but it certainly should be an option for everyone. If you want tips that do work for everyone, follow these bonus tips for weight loss and overall health!

• Don’t drink your calories – even “natural” drinks are full of unnecessary calories. Think about it this way, you would drink a glass of orange juice, but would you really sit down eat the 5 or so oranges it takes to make it? If not, why drink that same amount?
• Get rid of “Food Delivery Systems” – Think about the big sandwiches or burritos we see everywhere in our culture. What is the food? The stuff in the middle! The meat, the cheese, the veggies. What is the unnecessary food delivery system? The bread, the tortilla, the outer layer that has a fraction of the nutrients and a multitude of the carbs!

Lifestyle Really is the Best Medicine!

Science says lifestyle, not drugs, reverse disease:

• NEJM study reported findings on patients at highest genetic risk for heart attack, over 90% more likely to suffer heart attack. Those with healthy lifestyles had a 50% reduced risk with no drugs and no surgeries!
• JACC study found 85% of all heart attacks could be prevented with greater attention to lifestyle.
• A 2018 British Journal of Sports Medicine study found that increasing walking pace to “brisk” for those over 50 reduced all-cause mortality and cardiovascular mortality by 20-24%.

Why is it so hard?

We have all been told that in order to be healthy, we need to eat less, move more, and reduce fat in our diets. But if that is the case, why is it that only 12% of Americans are metabolically healthy, and only 3% of Americans follow a healthy lifestyle?

Because the simple Eat Less, Move More, Reduce Fat approach DOESN’T WORK!!!

I want to assure you that it’s not your fault, you’ve been given the wrong information.

“I was always told I simply didn’t have enough willpower to stick to a diet. I couldn’t understand why I was always hungry and craving foods. I figured it was all genetics. But working with Dr. Scher showed me there is a better lifestyle that I can stick with and still feel great and enjoy my life! Thanks Dr. Scher!”

• E

Keys to Making Lifestyle Change Stick

• Beware of one-size-fits-all nutrition and lifestyle claims
• Individually tailored and flexible nutrition is the key.
• When you eat is just as important as what you eat
• Move your body more
• Get Serious about your sleep
• Don’t be afraid to test and adjust

A Word of Caution

Don’t try to Change Everything at one time.

Choose YOUR most important first step (nutrition, stress, fitness, etc.) and work on that until a new habit is created!

And remember, you don’t have to do it alone! Working with an expert who can help you on your health journey will increase your likelihood for long term success.

As you can see, this was a quick tour to highlight the main points in the webinar. To get the full benefit, I recommend watching the full recording to get all of the context and be able to see the Q&A session at the end.

If you want to get the full experience, here is that recording again:

https://www.youtube.com/watch?v=pIyi11wMq5U&ab_channel=LowCarbCardiologist

If you’d like to see the date and content of our next webinar, or be notified when our next webinar will be, please visit our Webinar Page.

I hope you enjoyed this recording, and that we will see you at the next live webinar!

Thanks for reading,

Bret Scher MD FACC