Low Carb USA Recap

This past weekend, I had the pleasure of attending the Low Carb USA Conference in West Palm Beach.

I was blown away by the amazing community of providers and participants. Everyone I came across was very engaged and hungry for knowledge. There was also a special day devoted to the Spanish speaking audience. I was impressed by their growth from previous conferences.

Low Carb Spanish-Speaking Leader Ignacio Cuaranta

One leader in the Spanish speaking community is Ignacio Cuaranta, who is also a leader promoting low carb for the prevention and treatment of mental disorders. A big take home from his keynote was that that problems with our brains are not that different from the problems with our body. Metabolic derangements affect both, and low carb nutrition appears to be very beneficial for both.  I was lucky enough to record a podcast with him, so look for that in the near future! I don’t want to give away all the spoilers but suffice it to say, he is seeing outstanding success with Low Carb and Intermittent Fasting in his practice.

 

Dr. Robert Cywes on Carbohydrate Addiction

The headliner of the meeting was Dr. Robert Cywes. He is a weight loss bariatric surgeon, and the most unique surgeon I have ever met. He doesn’t want to operate. He would rather cure people of their underlying carbohydrate addiction and help them heal themselves. He has a refreshing perspective focusing on the emotional and psychological aspects of weight gain and recognizes that food choices alone won’t help if these aspects aren’t also addressed.  I also recorded a podcast with him so stay tuned for that!

 

Dr. Will Cole Spoke About Vegetarian Keto

Dr. Will Cole presented his case for Keto-tarians, essentially vegetarian ketosis. One of the predominate theories is that when we are in ketosis, our bodies require much less protein that we otherwise would. That way we can focus more on the non-animal fats and worry less about getting our 20+% of calories from protein. It is an interesting theory that he has had success with and highlights that a ketogenic diet can take many forms and mean different things to different people.

 

Dr. Ryan Lowery on Ketosis Being Protein Sparing

Florida’s own Dr. Ryan Lowery from ASPI echoed Dr. Cole’s theory that something about being in ketosis appears to be protein sparing, thus we don’t have to eat as much for muscle growth or maintenance. He also shared his research in rats that suggests lifelong ketosis promotes longevity. And guess what? That’s right, I filmed a podcast with him as well! This one was packed with information and I know you will love it as much as I did.

 

The food was fantastic!

Did I mention the food? WOW, the food was incredible! Some of the best conference keto buffets I have seen. The leg of lamb with onions on Friday night along with the spinach salad, avocado, and fat-soaked veggies were just what this doctor ordered (pun intended!)

I was in Keto heaven.

 

Learning from the conference overall

As usual the team from Low Carb USA did an incredible job and the event went off without a hitch. It inspired me to take away lessons on how they put together a successful conference for hundreds of people and adapt it to our upcoming intimate and personalized Low Carb Beach Retreat in April.

At this retreat, we will combine the benefits of didactic teaching with small group discussions and development of individualized low carb programs.  Due to its small size spots are limited so reserve your spot today!

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

Is LCHF Keto the right diet for you in the new year?

With New Year’s resolutions looming, many people are thinking about reinvigorating their health. In fact, 45% of people want to lose weight or get in shape as their New Year’s resolution.

The LCHF Keto diet has been quickly gaining momentum, and it is piquing a great deal of curiosity.

So, is this particular diet right for you? It may just be.

 

What are your diet goals?

Before selecting a diet, it’s important for you to define why you want to diet in the first place. Are your goals weight loss, general health, or a combination?

If you want to lose weight, reduce your hunger, enjoy your meals, and improve your metabolic health, then LCHF may be right for you.

 

Do you want to lose weight?

The primary reason most people go on a diet is to lose weight. As far as weight loss, low carb has you covered. Out of 60 studies comparing low carb to low fat diets, low carb had better weight loss in 30 and they were equal in 30. Low carb was inferior in exactly zero of these studies. That’s an impressive record, and definitely something to consider if weight loss is your primary goal.

But there is so much more to life and health than weight loss.

 

Do you want to reduce your hunger?

One main struggle in health and weight loss is how hungry we are and how much we need to think about food during the day. Studies show that following a LCHF diet reduces our hunger in the long-term. That means less worry about constant snacks, and less concern with needing to eat every few hours. In fact, LCHF works so well at curbing appetite that more people can practice time-restricted eating by compressing eating into a 6-8 hour window, which has indicated potential beneficial effects for longevity.

 

Do you want to improve your focus?

Food, especially the wrong food, can make us feel lethargic and unfocused. Many people report thinking more clearly and having better mental performance when on a low carb diet. The brain loves ketones, whereas carbs can cloud your thinking. Why not switch to low carb and see if your brain fog lifts?

 

Do you want to improve metabolic health?

A recent study showed that only 12% of Americans are metabolically healthy. Low carb diets are one of the fastest and best ways to improve metabolic health. Studies show it puts type 2 diabetes in remission, improves insulin resistance, reduces visceral fat, and improves overall metabolic health.

 

Do you want to decrease your cardiovascular risk?

Fat phobia is gone. Limiting carbs to real food veggies and eating plenty of healthy fats improves our cardiovascular risk profile. It reduces BP, reduces TG, increases HDL and improves the size and density of LDL, which all add up to a net improvement in cardiovascular health.

 

The main reason you should consider LCHF/Keto in the new year

You will love it!

No counting calories, no feeling hungry, no wild glucose swings and post meal crashes, no afternoon slump. With all of this research backing this diet, it’s definitely worth a try.

 

One last consideration

A note of caution, most people will do great. But not everyone reacts to this diet the same way, so you may want to consult a doctor experienced in low carb nutrition.

If you don’t already have a doctor to consult with or want to speak with one who specializes in Keto, I’m a professional who has extensive experience with LCHF diets and how they affect your health. If you’re just getting started, I recommend downloading my free LCHF/Keto starter tips e-book to get you on the right track:

 

 

 

If we can be of any additional service, please let us know!

Thanks for reading,

Bret Scher, MD FACC

Eating red meat increases TMAO levels. Should we care?

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 herehereherehere 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

 

Originally Posted on the Diet Doctor Blog 

Blood pressure medications — friend or foe?

The medical world experienced yet another guideline update in 2018 telling doctors more medication is better. This guideline for treating hypertension was put out by the American College of Cardiology and the American Heart Association, and effectively lowered the definition of hypertension from 140/90 down to 130/80. The organizations also recommended drug treatment for all individuals with blood pressure greater than 140/90, regardless of underlying risk.

Unfortunately, this seems like a common scenario — medical guidelines recommend more aggressive medication use for minimal potential benefit despite potential harm. A new study published in the Journal of the American Medical Association (JAMA), suggests the blood pressure guidelines go too far for low risk individuals, and the risk of harm outweighs the potential benefits.

JAMA: Benefits and harms of antihypertensive treatment in low-risk patients with mild hypertension

The JAMA study was an extensive chart review of over 38,000 patients at low risk for heart disease who had stage two hypertension (blood pressure between 149/90 and 159/99) and were treated with blood pressure medications. Over an average follow-up time of almost six years, they found no reduction in the risk of cardiovascular disease events or risk of death with medication use. They did, however, find an increased risk for low blood pressure, fainting, and acute kidney injury among those treated with medications.

Based on these results, treating stage two hypertension in low risk patients tends to cause more harm than good.

What makes this study valuable is that it documents real world experience. Guidelines are frequently made from trials conducted with more aggressive follow-up and monitoring than is typical in usual care. That fuels the medical community’s perspective that drug interventions are the best course of care, which is why we need more studies like this one from Dr. Sheppard et. al. showing us how low risk patients probably do not benefit from drug therapy in real world scenarios.

Instead of reaching for drugs, we should continue to find the most effective lifestyle interventions to help lower blood pressure and reduce cardiovascular risk without a laundry list of side effects. Unless, of course, you consider losing weight, having more energy, and feeling great as side effects — those are the type of side effects (from low-carb eating) that we all can embrace!

Thanks for reading,
Bret Scher, MD FACC

 

Originally Posted on the Diet Doctor Blog 

High LDL cholesterol may protect against dementia – don’t tell the statin pushers!

Don’t tell the statin brigade, but elevated LDL cholesterol may actually help us as we age!

new study from China suggests that those with higher levels of LDL-C have a lower incidence of dementia. They evaluated 3,800 subjects with a mean age of 69 years, performing extensive neuropsychological and cognitive ability testing. They found that the diagnosis of dementia and cognitive impairment correlated with increasing age, decreasing education level, diagnosis of type 2 diabetes, and being an ApoE4 carrier. After controlling for all these factors, they also found that those in the highest tertile of LDL-C (>142 mg/dL or 3.7 mmol/L) had a 50% lower incidence of dementia than those in the lowest tertile (<110 mg/dL or 2.9 mmol/L).

Frontiers in Neurology: High low-density lipoprotein cholesterol inversely relates to dementia in community-dwelling older adults: The Shanghai aging study

These findings are consistent with a prior study (also observational) examining the Framingham Heart Study data that found lower risk of dementia in those over 85 years old with higher cholesterol levels.

In fairness, these studies were observational studies, so they do not prove higher LDL-C directly protected against dementia. We can hypothesize why higher levels of LDL-C are associated with lower incidence of dementia. It could be a marker of overall health or nutritional status, it could be that LDL-C directly improves the health of neurons and prevents brain atrophy, or it could be more related to lack of diabetes or ApoE4 status for which a study may not always completely control.

Even without proving causation, these studies are wonderful reminders that we can easily get caught up in one specific disease processes (i.e. cardiovascular disease) and forget about the rest of the patient. The old joke is that when the surgeon talks to the family after a complicated and risky coronary bypass surgery, he says, “The surgery was a great success. The grafts were perfect, and the anastomosis were flawless, some of the best I have ever done. I’m sorry the patient died, but the surgery was wonderful.”

This is a fictional over-exaggeration, but it makes my point.

Cholesterol’s effects on our health are far too intricate to simply label LDL-C as “bad” and leave it at that. Such oversimplifications harm our overall understanding and eventually harms our health.

Instead, we need to focus on the whole patient, not one specific outcome. Trials should focus on all-cause mortality and overall morbidity rather than one or two specific outcomes. It doesn’t do us much good to lower heart attack risk by 0.5% over five years if we are also increasing the risk of dementia, cancer or other complications.

Thanks for reading,
Bret Scher MD FACC

 

Originally Posted on the Diet Doctor Blog 

New Major Study: A Calorie Is Not A Calorie

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

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 

Management of blood cholesterol just got personal

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 

Does Eating Fat Make Us Fat?

Does eating fat make us fat? According to a new article in The New York Times, it just might. With a heavy emphasis on “might.”

The New York Times: Which kinds of foods make us fat? (Paywall)

The article is based on a trial published in Cell Metabolism over the summer, which concluded that feeding mice up to 80% calories from fat causes weight gain. The same was not seen with higher levels of carbs or sugar intake.

Does this end the debate on what make us fat? Does this prove Gary Taubes and all the low-carb pioneers wrong?

Of course not. For starters, this was a study of mice. So, if you have pet mice, then you should definitely pay attention.

The bigger question, however, is does this trial apply to humans? I would argue absolutely not.

Here is what they found. The mice that ate a higher percentage of fat calories ate more total calories and gained more weight. They also found changes in the mice brains with increased gene expression of serotonin, dopamine and opioid receptors — the so-called “reward” receptors. Simply put, that means the mice found the fat so pleasurable, they ate more calories than any of the other mice and they even increased their reward-signaling pathways to match the pleasure they were experiencing.

Here’s the crux of the problem. Humans do the opposite. That’s right. The exact opposite. A review of 23 randomized trials showed that low-carb, high-fat subjects lost more weight than low-fat subjects, plus trials show low-carb, high-fat subjects experienced less hunger and ate fewer calories than low-fat subjects.

What about the reward center upregulation? In humans, that clearly happens in response to sugar, not fat. Once again, the exact opposite of the findings in the mice study.

The biggest take home from this study, therefore, should be the cautionary tale of using a mice study to predict human behaviors. This is especially true when we already have human studies showing the opposite effect. Low-carb diets help us eat less and lose more weight, and sugar lights up our reward centers like a Christmas tree. We don’t need mice studies to tell us that.

Thanks for reading,
Bret Scher, MD FACC

Originally Posted on the Diet Doctor Blog 

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

Bret Scher, MD FACC

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