Is a Low Carb High Fat Diet Heart Healthy?

We hear the words Heart Healthy a lot, especially when it comes to our nutrition.

 

By now, you’re likely used to seeing cereals with the “heart healthy” moniker. Is it really heart healthy? We all too frequently refer to foods as “heart healthy”, or we say that our doctor gave our hearts a “healthy” checkup.  

 

It all sounds nice. But what does it mean? How do we define heart health?

 

How does LDL Cholesterol affect Heart Health?

 

Unfortunately, most of our current definitions center around LDL cholesterol concentration.  While LDL cholesterol plays a role in heart health, it by no means defines heart health in totality.

 

In fact, in many cases it is the least important factor.

 

Our healthcare system has simplified things too much, so as a result we focus on one bad guy, one demon to fight. In reality heart disease is caused, and made more likely to occur, by a constellation of contributing issues.

 

Elevated blood sugar, elevated insulin levels, inflammation, high blood pressure, poor nutrition, and yes, lipids all contribute to heart health.  It does us all an injustice to over simplify it to one single cause.

 

What food is heart healthy?

 

Our superficial definition of cardiac risk is how industrial seed oils containing polyunsaturated fatty acids (PUFAs) became known as “heart healthy.”

 

Studies show that they can lower LDL. But they can also increase inflammation and have no clinical benefit and even increase risk of dying. According to our simplified definitions, that doesn’t stop them from being defined as “heart healthy.”

 

 That’s right! Something that increases our risk of dying is still termed “heart healthy.”  How’s that for a backwards medical system?!

 

Same for blood sugar. If you have a diagnosis of Type 2 Diabetes (DM2) that is a risk for cardiovascular disease. If you don’t have the diagnosis, you are fine. That ignores the disease of insulin resistance that can predate diabetes for decades and increases the risk of heart disease and possibly even cancer and dementia.

 

Cereal can also be called “heart healthy” as they may minimally lower LDL. But is that a good thing if they contain grains that also worsen your insulin resistance and metabolic syndrome? I say definitely not.

 

Time has come to stop this basic, simplified evaluation and start looking at the whole picture.

 

How Low Carb High Fat Diets Improve Heart Health

 

Low carb high fat diets have been vilified as they can increase LDL. But the fact of the matter is that it does so only in a minority of people. The truth is that they can improve everything else!

 

These diets reduce blood pressure, reduce inflammation, improve HDL and triglycerides, and reverse diabetes and metabolic syndrome! Shouldn’t that be the definition of “heart healthy” we seek? Instead of focusing on one isolated marker, shouldn’t we define heart health by looking at the whole patient?

 

Only by opening our eyes and seeing the whole picture of heart healthy lifestyles can we truly make an impact on our cardiovascular risk and achieve the health we deserve.

 

Join me in demanding more. Demand better.

 

Thanks for reading,

Bret Scher, MD FACC

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

Is Aspirin Dangerous? New Evidence Sheds New Light

Is Aspirin Dangerous?

 

No medication is sacred. Doctors have long regarded Aspirin as an easy “no brainer” for potential benefit with minimal downside. Many of us don’t even notice when Aspirin is on a patient’s medication list. It hardly warrants our attention.

 

Now that needs to change.

 

Aspirin had a bad week earlier last month. Two studies yielded four separate publications, all casting serious doubt about the risk/benefit ratio for Aspirin in those at moderate risk for Cardiovascular Disease (CVD).

 

In brief, the ASPREE study investigated 19,000 US and Australian individuals older than 70 without a history of CVD. Half got 100mg of Aspirin and half got placebo. No other changes were made. After 4.7 years, they found the following:

 

Another study, The ASCEND trial, investigated 15,000 subjects with diabetes and likewise randomized them to 100mg of Aspirin or placebo. After 7.4 years they found a 1% reduction in vascular events in the aspirin group (8.5% vs 9.6%.) However, this was offset by a 1% increased risk of major bleeding (4.1% vs 3.2%).

 

Does Aspirin Increase Risk of Cancer?

 

The most shocking finding for me was that those taking Aspirin seemed to have a higher risk of cancer. This is in stark contrast to the studies showing that aspirin reduces the risk of cancer, especially colon, breast and prostate cancer.  One study does not necessarily disprove an accumulation of data, but it sure does suggest a problem, especially when the new study is a randomized trial and the prior studies are mostly observational trials. For me, that is enough to stop thinking of aspirin as protective for cancer until we have more solid randomized data.

 

Of note, while some of the data comes from randomized studies, most of it comes from observational trials (more on this later). Large meta-analysis of randomized trials demonstrated a very small 0.6% reduction in cancer deaths for those taking Aspirin. Should we view this as caution against very small outcome differences? (More on this later)

 

Is Aspirin Beneficial?

The big picture take home, however, is that in a primary prevention setting, Aspirin is not protective for death, cardiovascular disease events, or risk of dementia and disability. At least not without any benefit being off-set by an increased bleeding risk.

 

Again, the randomized trial finds contrary evidence to what prior observational trials suggested (although some randomized trials were also negative, such as this one and this one, although they were twisted to promote a beneficial finding despite the statistics not supporting that). This is such a powerful lesson on why we need randomized studies and cannot rely on observational trials or trials with miniscule differences to make definitive recommendations.

 

 

Importance of Randomized Studies Over Observational Trials

 

Does this sound familiar? I have been harping on this when it comes to low fat vs. low carb eating for years. The statistical counter argument is that, sometimes, it is just obvious. Smoking should not need a randomized trial to see if it causes lung cancer. Parachutes don’t need a randomized trial (this is my personal favorite anecdote, as it shows how absurd people can get).

 

And that is true. The observational trials in smoking had a hazard ratio of over 3. That means there was over a 300% increased risk of developing cancer if you smoked.

 

The differences we talk about with animal protein intake and risk of cancer or cardiovascular disease tends to be a 10-20% increase at most (with many trials refuting that completely). But the point is that small differences like this may be simply noise or chance when it comes to observational trials. Small differences, especially in observational trials, are not causative or conclusive results. They are suggestions that require further follow up studies before drawing conclusions.

 

Last, we also need to consider the outcomes. Are we measuring a marker that may be important in the long run? Or are we measuring what really matters to people, like living and dying, or life free of dementia and diasbility. Reducing one risk while increasing another is hardly a victory. That is why measuring the right outcome is so important.

 

That is when we need the randomized trial to answer the question. ASPREE and ASCEND have done that for Aspirin.

 

May Aspirin for primary prevention rest in peace.

 

And may science live on, with randomized controlled trials and meaningful outcomes leading the way.

 

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

 

Bret Scher, MD FACC

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