Dr. Scher’s six-month program has been helping me make progress on my health journey. I started the program five months ago after I decided to get more serious about my health and reduce my coronary heart disease (CHD) risk by making healthy diet and lifestyle changes.

The program is not only providing me with excellent video and written content that helps me progressively realize my health goals with effective plans of action, but also individualized attention via email and with monthly video calls with Dr. Scher. I’m grateful for this individualized attention and for Dr. Scher’s insights and suggestions. His advice has honored my preference to continue following a low-carbohydrate lifestyle and has helped me select appropriate macronutrient targets such as daily intake of carbohydrates and protein based on my goals and his review of my medical history and lab test results.

Ken Carrillo
Chemical Engineer

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

Did you know changing the way you eat may be able to normalize your blood pressure completely? For many people it’s true. But what’s surprising is that it isn’t changing to the diet that most doctors and dieticians recommend.

The DASH diet, Dietary Approach to Stop Hypertension, has long been the “go-to” diet for reducing blood pressure. The DASH diet is a high carbohydrate, low fat diet that recommendseating plenty of fruits, veggies, whole grains, and limiting salt and saturated fat. And while that works for some people, many others can normalize their blood pressure with a nearly opposite approach.

A 2023 study published in The Annals of Family Medicine, demonstrated that a very low carbohydrate diet with no limitations on the amount of salt or the amount or type of fat eaten was better at lowering blood pressure compared to the DASH diet.

Many wonder how this could be, but the answer is pretty straightforward.

Poor metabolic health, from insulin resistance to type 2 diabetes, is a leading cause of high blood pressure. And low carb diets are one of the best lifestyle approaches for improving or even normalizing metabolic health. Therefore, it makes complete sense that a low carb diet would be highly effective at normalizing blood pressure.

Of course there are many other ways to improve blood pressure, such as quitting drugs, tobacco and alcohol, getting regular exercise, managing stress, etc. And these are very important. But since everyone has to eat, it is powerful to eat in a way that can normalize blood pressure.

Let’s explore four ways how low carb diets can help blood pressure.

1- Weight loss
Having overweight or obesity is a strong contributing factor to high blood pressure. And while low-carb eating isn’t the only way to lose weight, it tends to be as good as or even better than low fat eating for weight loss. Some publications even demonstrate weight loss on par with highly effective GLP1 weight loss drugs like Ozemipic and Wegovy.

2- improved metabolic health
As mentioned, metabolic dysfunction is a clear trigger for elevated blood pressure. And while low carb eating isn’t the only way to improve metabolic health, it is likely the most effective dietary pattern for improving metabolic health, and can even do so with or without weight loss.

3- Ketosis
If someone lowers their carbohydrate intake enough, they can enter a state of ketosis, a normal physiologic state where we burn primarily fat for energy instead of carbohydrates. When this occurs, our insulin levels drop to a normal level and we have a natural diuresis, meaning we eliminate sodium and water more than usual. This can help lower blood pressure above and beyond weight loss.

4- Avoiding processed foods
Most well formulated low carb diets avoid highly processed junk foods like potato chips, candy, doughnuts, etc. that can lead to high blood pressure. So, simply eliminating these foods can also contribute to lower blood pressure.

What about salt?

One of the big misconceptions about blood pressure is that we all need to lower our salt intake for better blood pressure. However, this appears to be a gross over-generalization. There’s a growing understanding that a minority of individuals have “salt sensitive” hypertension. This means that the majority are unlikely to affect their blood pressure by altering their salt intake.

Furthermore, where we get our salt likely makes a difference. For insurance, if someone is getting their salt from highly processed foods like chips, pretzels, etc, they are hit with an ultra-processed combination of salt, calories, carbs, and sugars that is bound to raise blood pressure.

But what if someone is eating whole foods like broccoli, cauliflower, steak, and avocado, and they add salt to that meal? Clinical experience suggests our bodies react much differently to this type of salt exposure, and people can dramatically lower their blood pressure despite adding salt to their diet.

Low Carb Eating Works

So while it may not be the right approach for everyone, it is increasingly clear that eating a well-formulated low carb diet is a safe and effective way to lower blood pressure. It’s time to include low carb diets as a first line treatment option for normalizing blood pressure.

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

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