Is the Keto Diet Heart Healthy? 7 Reasons Why This Cardiologist Agrees

I am a board certified, card-carrying cardiologist, and I want my clients to eat more fat, more meat, more cheese, more eggs, more avocado, more, more, more.

For decades medical establishments have convinced us to eat low fat, higher carb diets. How has that worked for our health? Here’s a hint, we have record numbers of obesity, diabetes and dementia. Yet, as a cardiologist, that’s the party line I am supposed to support.

But I can’t. It’s just wrong, and I can’t support that line of thinking, not for a second.

Instead, I am a Low Carb Cardiologist. Here are the top Seven reasons why

1. Reducing Insulin is Essential to Health and Weight Loss.
   Insulin is a hormone naturally secreted by the pancreas to help regulate blood sugar levels. Everything we eat (except possibly for 100% fat meals) causes insulin to rise. That is normal physiology. The problem occurs when our bodies become resistant to the effects of insulin, thus requiring our pancreas to make more and more and more insulin.The problem? Insulin promotes fat storage, increase inflammation and oxidation, and can even help fuel the growth of cancer cells. Therefore, the healthiest approach is one which reduced the level of insulin to the lowest possible levels. As it happens, a Low-carb High-fat or ketogenic lifestyle (LCHF/Keto lifestyle) dramatically improves your body’s sensitivity to insulin, reduces the amount of insulin secreted, and it allows your body to naturally use your fat stores for what they are designed for: Break them down into energy! Once we see that we need to fight chronic elevations of insulin, it becomes obvious why a low-fat diet is harmful, and why a low carb diet is the true path to health.
   
2. Eating Fat Improves Your Cholesterol!
   Wait, what? Eating fat can improve my cholesterol? Sounds crazy, right? That goes against everything we have heard from the medical establishment. Notice I said “cholesterol.” I didn’t say the “bad” low density lipoprotein (LDL), I didn’t say the “good” high density lipoprotein (HDL), or any one specific type of cholesterol. We have over emphasized the solitary variable of LDL for too long. Total cholesterol to HDL ratio, Triglyceride to HDL ratio, lipoprotein size and density, insulin sensitivity, and other metabolic measures are more powerful predictors of cardiovascular health than just LDL.Once again, we see that all these markers improve with a Low Carb High Fat (LCHF) lifestyle. The medical establishment needs to realize that we are more complicated than one lab value. The key is to look at the whole picture, and this picture dramatically improves with a LCHF lifestyle.If you want to learn more about lipids and cholesterol, I recommend checking out my new dedicated cholesterol course: The Truth About Lipids.
3. Higher HDL is Associated with a Lower Risk of Heart Disease.
   HDL is your friend, but drugs are not. Observational evidence has consistently shown that higher HDL is associated with a lower risk of cardiovascular disease. However, our healthcare establishment does not prioritize HDL for one simple reason- Drugs that raise HDL don’t make you healthier. Trial after trial has failed to show any benefit from drugs that significantly increase HDL.Instead, it’s the HDL-raising lifestyle that provides the benefit, not artificially increasing it with drugs. What’s the best lifestyle to naturally raise HDL? You guessed it. LCHF/Keto lifestyle. Add in some resistance training and you have your friendly HDL climbing the way it was meant to…Naturally.
4. LCHF Leaves You Feeling Great, Leading to Healthier Decisions
   What kind of health decisions do you make when you are fatigued, achy, and find it difficult to concentrate? That’s a rhetorical question, I already know the answer. When things look glum and we don’t feel well, it’s far too easy to sit on the couch or reach for the chips and cookies. Compare those decisions to those you make when you are well rested, energetic, and seeing the world more clearly. For most people, the better you feel, the better decisions you make.Guess what? The majority of people who change to a LCHF lifestyle feel better! It may take a few days or weeks, but in general, they feel more in control of their health, more energetic, and they are able to make better health decisions. I admit this is difficult to prove in a scientific trial. That is why we all should become our own n=1 scientific trial. How do you feel and how are your health decisions after going to a LCHF lifestyle? What matters most is what works for you, not what works for hundreds of people who are kinda-sorta like you.
5. Keto helps you with fasting.
   Eating better helps you not eat. People who eat a high carb diet eat a lot, don’t they? They are always grazing and snacking. Our bodies go through the roller coaster of blood sugar and insulin spikes, making it a challenge to go 24, 18, or even 6 hours without eating. This creates a constant, unwavering supply of insulin in our blood stream.Why is this harmful? For one, it promotes fat storage and keeps us from using our fat as fuel. Secondly, chronically elevated insulin can predispose to heart disease, strokes, cancer, dementia and other devastating health conditions. When people change to Keto, however, they realize they do not need to eat nearly as much or as frequently. Avoiding the carbs and increasing the fats keeps us full longer, and our bodies quickly adapt to longer periods without eating. The result? We can use our fat stores for what they were designed- a source of fuel! It also allows our body to maintain lower insulin levels, and also allows our cells to take care of their health chores, referred to as Autophagy.If you’re interested in Fasting and want to make sure you’re doing it correctly, download my free Full Guide to Fasting.
6. LCHF Promotes Health Through Increased Autophagy.
   Autopha-What? In medicine we like using fancy words to make us look smart. Autophagy is a big word to describe cellular housekeeping. When we have low enough intake of carbs and protein, or when we do intermittent fasts, our bodies can take care of their “to do” lists.  That list includes breaking down weak or damaged cells, recycling the good parts and discarding the rest, and slowing down the processes that can lead to abnormal cell growth (i.e. excess proteins in Alzheimer’s disease, abnormal cancer cells etc.).Admittedly, long term outcome studies evaluating fasting or LCHF and cancer or dementia risk have not been done. But, on the flip side, drug trials to prevent the same are showing no benefit despite hundreds of millions of dollars invested. If you asked me (which you sort of did since you are reading my article), I’d vote for autophagy as a preventative strategy any day. It makes good physiologic sense, and it is so easy to achieve.
7. With Keto You Will Enjoy Eating Again!
   That’s right. A way of eating that helps you lose weight, helps you feel better, improves your health and is actually enjoyable! No fake processed soy products, no cardboard tasting rice cakes. True, it also means no more candy, processed snack foods, doughnuts and danishes. But once you swear them off for a few weeks, and you are eating all the eggs, avocados, nuts, fish, steak, cheese etc. that you want, you won’t miss those old crutches any more. Let the enjoyment begin!

I could go on, but since it seems people like “7 Reason” articles, I will leave it at that. 

Now you know the secret: Look at the whole picture. Look for a lifestyle, (not a diet) that helps you feel better, increases your enjoyment, and still benefits your overall health.

Is LCHF/Keto the right lifestyle for you? It just may be. To learn more about Low Carb and Keto, download this free E-Book:

Thanks for reading,
Bret Scher, MD FACC
Founder, Boundless Health
www.LowCarbCardiologist.com

ADDENDUM!!

Since I have published this article, there has been a windfall of media buzz around low carb diets increasing our risk of heart disease or diabetes. Let’s look at where that information came from.

1- A study force feeding mice excessive amounts of industrial omega 6 oils. You can guess what I have to say about that. The article was incredibly helpful, and I immediately stopped force feeding my pet mice industrial seed oils. Thanks goodness for that article. As for how it applies to humans eating real food that contain fat, there is zero correlation.

2- Epidemiological study suggesting those who ate low carb (40% calories from carbs, which by the way is NOT low carb) as measured by two food journals over 25 years had a higher risk of dying. Oh and by the way, at baseline they were heavier, more sedentary, smoked more, and ate fewer veggies. Yet somehow they concluded it must be the low carb diet that “caused” the harm. Once again, it may not be bad science, but it sure was awful interpretation of the science.

In light of those two studies and the hoopla surrounding them, has anything happened to change my mind about a LCHF/keto diet being beneficial for our overall health and our heart health?

Absolutely not.

We still need to individualize our care and our lifestyle for who we are and how our bodies respond. That is always the case regardless of our nutrition, our medications, our exercise etc. As long as we do that, then this cardiologist still believes that LCHF IS HEART HEALTHY!

If you liked this post, you’ll love my free E-Book on Low Carb/Keto Starter tips to help you get started on your LCHF path!

Thanks for reading.

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 

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

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

Do we have to avoid meat if we have high homocysteine levels? Not really.

What our body does with homocysteine is more important than our food intake. I thought this was easier to explain in video form, so you can see my 4 minute explanation here:

https://www.youtube.com/watch?v=PYx4qvYy6_4&ab_channel=LowCarbCardiologist

The bottom line is we need to know our methylation status, make sure we have adequate levels of folate, B12 and B6, and make sure we have adequate choline (found in egg yolks).  If all those are perfect, and we still have elevated homocysteine, then we may want to experiment with a diet low in methionine to see if it makes a difference.

As always, however, we have to evaluate our overall health picture and not get too hung up on one blood marker. The more important questions to ask are how does homocysteine affect my overall health, and how will altering my supplements or diet change the big picture?

Hopefully this helps! Let me know if you have any comments or questions.

Thanks for reading (and watching!)

Bret Scher MD FACC