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Author: Bret Scher

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 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

 

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!

A 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.

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 

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

More False Claims About Keto- Bias and Lack of Evidence Beware!

There is a lot of “Fake Science” out there. It’s clear that we live in an age of misinformation and sensationalized headlines, and it’s often difficult to discern what contains real evidence, and what is lacking. This week, I’m motivated by a particular article by a “reputable” source. Aside from pointing out the specifics of this particular article, I want the larger lesson to be to understand how to read between the lines of an article and search for evidence, regardless of how credible a source may seem.

 

Who’s the Culprit?

 

Harvard Health strikes again with ignorance and false claims. I try not to respond negatively too often, but I couldn’t let this one go.

 

Does talking about an awful publication give it more attention than it deserves? Or is it more important to point out the fallacies for all to see? I don’t know that there is a “right” answer to that question, but in this case the critic and vocal dissenter won out. We can’t let flat out wrong claims perpetuate and become “truth” as happens too often in medicine.

 

Bias in Language

 

  • It starts right off the bat by the language use in this article. “The keto diet aims to force your body into using a different fuel.” Force your body? That assumes your body doesn’t want to burn fat, so we have to force it against its will to do so. That is certainly a “carb centric” view point!

 

Why not say “allow your body to use a different fuel.” The clear assumption/bias is that we are meant to be carbohydrate eating, glucose burning machines. But is that true? Is that how we were meant to be? Snackwells, Nabisco and Tony the Tiger sure think so, but I think evolutionary biology may differ.

 

  • “It requires that you deprive yourself of carbohydrates.” Deprive? There is certainly no deprivation on a wonderful array of veggies like cabbage, Brussels sprouts, cauliflower, broccoli, peppers, green beans, and so on. I also don’t think anyone would complain about the health risks of depriving ourselves of white bread, bagels, candy, cookies, cakes etc. Would Harvard also talk about how vegans deprive themselves the nutrient density found in eggs, fish and meat? I think not.

 

 

Lacking Evidence

 

Next comes the section on “Keto Risks.”

 

 

  • Saturated fat is the obvious one, and I have written enough about that one to not address it in this post. You can read more here, here, and here. The article also seemingly adds a source with what sounds like evidence, but provides no link to the study.

 

  • Liver problems. How could they reference “liver problems” with no references or specifics and fail to mention that LCHF is one of the best nutritional interventions to treat fatty liver, the fastest growing cause of liver disease in the country. And what does “liver problems” even mean? It seems clear that there is a clear lack of understanding here.

  • Kidney problems. The only concern of too much protein is in individuals with complete kidney failure. In healthy individuals, high protein consumption can increase the renal filtration rate, but there is no evidence to show resulting kidney damage. And where did they get the current recommendations for protein intake? 46 grams per day for women and 56 for men? Even using the lower estimates of 0.5 grams per pound would make this 90 grams per day for the average 180-pound man. And this is a minimum recommendation.

 

  • Fuzzy thinking and mood swings- This one is my favorite. Actually, LCHF keto diets are phenomenal at treating “fuzzy thinking and mood swings.” The article claims, “the brain needs sugar from healthy carbohydrates to function.” That could not be further from the truth. No matter how low our carbohydrate intake, glucose levels never drop to zero. I hope they have heard the term gluconeogenesis at Harvard because it is something our bodies have been doing for a few years. Well, maybe a few thousand years but let’s not be too picky. Yes, our brains require glucose. By no means do we need to eat that glucose.

 

  • Last, they get one more jab in to say how “restrictive” the diet is.

Eating all the meat and veggies you want is restrictive? I like how they don’t refer to vegetarian or vegan diets as restrictive. Bias is very hard to overcome.

 

Also, you have to love the part about the weight returning when you resume a “normal” diet. Let me get this right. We shouldn’t change from a standard American diet to a low carb diet because the weight will come back if we go back to a SAD diet? So, we shouldn’t even try? Great rationale. How’s that working for our country?

 

The Danger of These Biased Articles

 

Now let’s look at the bigger picture. An institution with a reputable name publishes this paper.  This paper has no scientific references, it is clearly biased, and has many statements that are blatantly false.

 

How are most people going to respond? I am afraid most people will accept it at face value. I mean, it’s Harvard for Pete’s sake!

 

My guess is most of my readers (you!) will say, “No way. People won’t fall for this garbage.”  And for that I am thankful. But the problem is that my readers (you!) tend to be more astute and more interested in these topics and by habit critically analyze what they read. My fear is that does not translate to the rest of the population.

 

That is why the publishers at Harvard Health should be ashamed of themselves to allow their name on such an obviously biased and tainted article. Whether you believe in a low carb diet or not should have nothing to do with recognizing the falsehoods in their article.

 

In the end, I hope this will serve as a cautionary tale to remind us that everyone has a bias. Some hide it better than others. Some can be more objective than others. And as Harvard has proven, notoriety has nothing to do with it.

 

Let’s strive to be better.

 

 Thanks for reading,

Bret Scher MD FACC

Is Aspirin Dangerous? New Evidence Sheds New Light

Is Aspirin Dangerous?

 

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

 

Now that needs to change.

 

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

 

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

 

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

 

Does Aspirin Increase Risk of Cancer?

 

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

 

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

 

Is Aspirin Beneficial?

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

 

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

 

 

Importance of Randomized Studies Over Observational Trials

 

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

 

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

 

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

 

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

 

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

 

May Aspirin for primary prevention rest in peace.

 

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

 

Thanks for reading,

Bret Scher MD FACC

 

Food Appreciation through Fasting on Yom Kippur

I still remember Yom Kippur 2013. The year I had to fast.

 

I know I am “supposed” to fast every year, but in my mind that ship had sailed long ago. I am not the best rule follower, especially when I don’t see the purpose of the rule. What does not eating have to do with being a good person?

 

But in 2013, my son was old enough to ask, “Why isn’t daddy fasting for Yom Kippur like we are supposed to?” That was the end for me. I had to lead by example, and fast. Back then fasting was a four-letter word. It was something I was forced to do. It was uncomfortable, it made me grouchy, and it seemed like a waste of a day.

 

How times have changed. Now I practice intermittent fasting on a regular basis. I regularly experience the physical and psychological benefits, and I know that science supports even greater long-term benefits. Plus, it’s easy now. 

 

This year I learned that like with most things, I have started take fasting for granted.

 

A good friend of mine unknowingly reminded me of this when we met for lunch the day after Yom Kippur. He does not fast regularly, so the Yom Kippur fast is a big deal for him. I was fascinated listening to him describe his experience. His focus wasn’t the hunger, or lack of energy, or the headaches some people experience. Rather, his was the appreciation he had for cold, crisp water. The joy of his first taste of food in 24 hours. The smell, the texture, the flavors. He had taken food for granted and fasting helped him appreciate it all over again.

 

I felt the same appreciation as my friend when I did my five-day fasting mimicking diet. But on a regular day of fasting, I don’t experience the same appreciation. It made me wonder, why not? Why had I lost that heightened appreciation?

 

I eat high quality, minimally processed, real food that comes from the ground or from an animal. It is food as nature intended it to be. It nourishes my body and is delicious. I should celebrate it every day.

 

Yet, I learned that I can sometimes take my food for granted.

 

A prolonged period without it is a stark reminder of how much I should appreciate my food. But why don’t I appreciate it to the same degree every day?

 

This reminds me of the comedian, Louis CK, who tells the story of someone sitting next to him on the plane complaining that the WiFi wasn’t working at 30,000 feet in the air. The comedian responded that every time a plane takes off and is in the air, we should all scream “Holy $&!% we are flying! I mean literally flying!! Can you believe that?!?!?” Again, that is a perfect example of something we easily take for granted.

 

So, what is the secret? How do we not take for granted the things we experience every day, regardless of how amazing or awe inspiring they may be? How do we appreciate what can easily become mundane?

 

In our family, we say a short prayer every meal. Maybe prayer is the wrong word. It is more of a thank you. We try to remember to thank God for growing the food, the field workers for harvesting it, me or my wife for cooking it, and all of us for appreciating it. But I would be lying if I said that we did that at every meal.

 

We are quick to point out when something is from a factory or packaged in a box or bag.  That helps us recognize the simplicity and pleasure of eating real food (in fact, my kids were freaked out when they saw me eating food from a box during my 5-day FMD).

 

Yet I feel like there should be more. I feel like I still underappreciate the treasure that is our food. Is that setting too high of an expectation? Or should I strive for a greater appreciation?

 

What are your thoughts? What are your rituals? How to you remember to appreciate what you have? It doesn’t have to be just food either.  We should be thankful for anything we are fortunate enough to have. Please comment below so we all can benefit from our collective knowledge and experience.

 

For now, I am going to appreciate my freshly steamed veggies and my grass-fed steak. I don’t want to have to wait for my next FMD to appreciate that!

 

Thanks for reading

Bret Scher, MD FACC

 

 

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