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.

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

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

Despite what the sugary beverage and processed snack food companies want us to believe, all calories are not created equal.

A new study from Harvard shows that individuals following a low-carbohydrate (20% of total calories) diet burn between 209 and 278 more calories per day than those on a high-carbohydrate (60% of total calories) diet. So the type of calories we eat really does matter.

The New York Times: How a low-carb diet might help you maintain a healthy weight

This isn’t the first study to investigate this topic, but it is likely the best.

The current study was a meticulously controlled, randomized trial, lasting 20 weeks. Even more impressive, the study group provided all the food for participants, over 100,000 meals and snacks costing $12 million for the entire study! This eliminated an important variable in nutrition studies — did the subjects actually comply with the diet — and shows the power of philanthropy and partnerships in supporting high-quality science.

After a run-in period where all subjects lost the same amount of weight, participants were randomized to one of three diets: 20% carbs, 40% carb, or 60% carbs, with the protein remaining fixed at 20%. Importantly, calories were adjusted to stabilize weight and halt further weight loss, thus making it much more likely that any observed difference in calorie expenditure was not from weight loss, but rather from the types of food consumed.

After five months, those on the low-carb diet increased their resting energy expenditure by over 200 calories per day, whereas the high-carb group initially decreased their resting energy expenditure, exposing a clear difference between the groups. In addition, those who had the highest baseline insulin levels saw an even more impressive 308-calorie increase on the low-carb diet, suggesting a subset that may benefit even more from carbohydrate restriction.

Why is this important? It shows why the conventional wisdom to eat less, move more and count your calories is not the best path to weight loss. Numerous studies show better weight loss with low-carb diets compared to low-fat diets, and now studies like this one help us understand why.

Our bodies are not simple calorimeters keeping track of how much we eat and how much we burn. Instead, we have intricate hormonal responses to the types of food we eat. It’s time to accept this and get rid of the outdated calories in-calories, calories-out model, thus allowing for more effective and sustainable long-term weight loss.

Originally Posted on the Diet Doctor Blog 

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