Tag Archives: cardiovascular disease

What You Should Know About Lipoprotein(a) And Heart Attack Risk

If you have had a heart attack at an early age or one of your parents did but your standard risk factors for coronary heart disease are normal you should consider getting tested for Lipoprotein(a) or Lp(a).

The standard lipid profile that most patients get checks LDL (bad) HDL (good) and total cholesterol along with  triglycerides. While these are useful, I have many patients who have normal standard values but have developed advanced coronary heart disease at an early age despite following a perfect lifestyle (not smoking, regular aerobic exercise, healthy diet.)

The skeptical cardiologist tests such patients for Lp(a) (pronounced LP little a)  and it is quite frequently elevated.

For patients, these are the facts to know about Lp(a)

  1. It is the strongest single inherited (monogenetic) risk factor for the early development of coronary artery disease, heart attacks and strokes.
  2. In addition to increasing risk of atherosclerosis, high Lp(a) is strongly associated with the development of calcific aortic valve disease which can result in narrowing of the aortic valve and aortic stenosis.
  3. Depending on the cut-off used  up to one in five individuals may have elevated Lp(a)
  4. Levels of Lp(a) can be measured with a simple blood test that should cost no more than 50 to 100$. This is not included in standard lipid or cholesterol testing.
  5. Risk for heart attack starts to rise with levels above 30 mg/dl and Canadian guidelines from 2016 (see here)) consider >30 mg/dl to be a risk factor and they recommend measuring Lp(a) in those with a family history of premature CAD or those at intermediate risk.
  6. The European Atherosclerosis Society (EAS, 2010), suggested levels of <50 mg/dl as optimal. The EAS advised measuring Lp(a) once in all patients with premature CVD.
  7. As levels get even higher risk also rises as these graphs show

 

 

 

 

Treatment For High Lp(a)

The lifestyle changes (both exercise and diet) that improve bad and good cholesterol levels have no effect on Lp(a). Our best drugs, the statins, for reducing risk of heart attack and stroke also don’t lower Lp(a) levels.

Only niacin has been shown to reduce Lp(a) across broad populations but there is no evidence that Lp(a) lowering by niacin lowers cardiovascular risk so it cannot be recommended for treatment.(In the AIM-HIGH study niacin did not reduce cardiovascular events in patients with Lp(a) with levels>50 mg/dl, despite achieving a mean Lp(a) reduction of 39%.)

Cholesteryl ester transfer protein inhibitors which raise HDL levels also reduce lipoprotein(a) concentrations, but three such inhibitors have not shown a clinical benefit.

In fact, currently there are no studies showing that lowering Lp(a) with any drug will effectively lower the associated risk of heart attack, stroke and aortic stenosis.

In the not too distant future, effective therapies may emerge. There are promising newer agents (antisense oligonucleotides or ASOs) currently in clinical trials and in limited populations the PCSK9 inhbitors, mipomersen and estrogen have lowered Lp(a) levels.

Why Test For Lp(a)?

If we have no effective therapies that work by lowering Lp(a) why recommend testing for it?

I test Lp(a) for  two reasons.

First, since it is inherited, patients with high levels should consider having first degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.

Second, I tend to recommend  more aggressive cholesterol lowering in patients who have evidence for early plaque build up for atherosclerotic events early in life than I otherwise would be.     I tend to agree with the approach diagrammed below:

 

With this approach for patients who have had events related to atherosclerosis or advanced CAC for age we work super aggressively on optimizing all risk factors. I try to lower LDL to <70 with statins and with the addition of ezetimibe or PCSK9 inhbitors if needed.

If the patient has more problems with atherosclerotic events despite optimizing risk factors and Lp(a) >60 mg/dl, some experts recommend using apheresis a technique which runs the patient’s blood through a filter which removes LDL and Lp(a). Personally, I have not sent any patients for apheresis and await better studies proving its benefit.

Antiproatherogenically Yours,

-ACP

For those patients seeking more detailed information and references I recommend Dr. Siggurdson’s excellent post on Lp(a)

There is a Lipoprotein(a) Foundation with reasonably informative and accurate website you can peruse here for more information.

Finally, if you want to delve deeply into the data check out this recent JACC review here.

The graphs above and this figure
showing the proposed pro-inflammatory, pro-atherogenic and pro-thrombotic pathways of Lp(a) are from that article.

 

Optimal Home Blood Pressure Monitoring: Must The Legs Be Uncrossed and The Feet Flat?

The new ACC/AHA guidelines for High Blood Pressure were published late last year and they were in favor of using home blood pressure measurement to aid in the management of hypertension.

I was happy to hear this as I am constantly advising my hypertensive patients to buy a home BP cuff, measure their BP once when they get up and again 12 hours later and report the values to me after two weeks.

I have not spent a lot of time instructing them on  exactly how to make the measurement but the new guidelines do specify in detail how this should be done:

• Remain still:

• Avoid smoking, caffeinated beverages, or exercise within 30 min before BP measurements.

• Ensure ≥5 min of quiet rest before BP measurements.

• Sit with back straight and supported (on a straight-backed dining chair, for example, rather than a sofa).

• Sit with feet flat on the floor and legs uncrossed.

• Keep arm supported on a flat surface (such as a table), with the upper arm at heart level.

• Bottom of the cuff should be placed directly above the antecubital fossa (bend of the elbow).

• Take at least 2 readings 1 min apart in morning before taking medications and in evening before supper. Optimally, measure and record BP daily. Ideally, obtain weekly BP readings beginning 2 weeks after a change in the treatment regimen and during the week before a clinic visit.

• Record all readings accurately:

• Monitors with built-in memory should be brought to all clinic appointments.

I monitor my own BP at home and often wonder whether there is scientific evidence to support such a rigid protocol.  Being a contrarian and a skeptic, I typically violate 3/4 of the recommendations that are listed.

It seems like all of the instructions are guaranteed to give you the lowest BP you are likely to experience during the day. The vast majority of the time I am not sitting quietly with my legs uncrossed, my bladder empty and my back straight so following these directions will underestimate my average daily BP.

I’ve spent some time looking into all the instructions and they generally have some scientific studies to support them. For example, the position of the upper arm in relation to the heart does  heavily influence BP readings (more on that in subsequent posts.)

The Mandate To Uncross The Legs

The instruction that most intrigued me was this one:

Sit with feet flat on the floor and legs uncrossed.

A number of questions came to the skeptical hypertensive:

What if you are on an exam table and your feet don’t reach the ground?

Does it really make a difference if your feet are flat on the ground versus slightly crooked?

Does any degree of leg crossing influence BP? Legs crossed at the ankles? Legs crossed at the knee?

And once I began thinking of leg crossing I realized that I spend a lot of my time with my legs crossed. Was this raising my blood pressure and my cardiovascular risk? Did I cross my legs because I liked the feel of a higher blood pressure?

The ACC/AHA guidelines are not alone in this recommendation-take a look at the British Health Service recommendation:

3.5. Measurements should be taken in silence when the patient is relaxed, with both feet flat on the floor and their back and arm supported. Many patients automatically cross their legs, which raises their blood pressure, so it is particularly important to emphasise the need for the patient to uncross their legs when taking their blood pressure.

Apparently the Brits believe that any ambient sound will alter the blood pressure. Talking is right out!

But if talking, ambient sounds and crossing your legs raises your blood pressure shouldn’t we be advising patients to spend their days wearing ear plugs in silence with their legs uncrossed?

Scientific Studies On Leg Crossing

It turns out there are good studies showing that leg crossing raises your blood pressure.

The first was published in 1999 and involved  53 hypertensive and 50 normotensive subjects.

Participants were randomly assigned, using a cross over design to having seated blood pressures measured with their leg in three different postures

  1. Feet flat on the floor and legs uncrossed

    Here I am demonstrating method 2 with my lateral malleolus carefully placed on my suprapatellar bursa. I actually prefer method 1 which is depicted below.
  2. Legs crossed , method 1-popliteal fossa of the dominant leg over the suprapatellar bursa of the non-dominant leg.
  3. Legs crossed, method 2- lateral malleolus (which the article spells mallelous) of the dominant leg over the suprapatellar bursa of the non-dominant leg.

I love the efforts these Calgarian investigators went to in this study to ensure blinding (although spelling is clearly not their forte’). They state “blood pressures were measured by one investigator who was behind a screen and blinded to the leg position of the patient while a second investighator (sic)  ensured that the subject assumed the proper leg position.”

Systolic blood pressure in patients with hypertension increased by 8 mm Hg by method 1 leg crossing and 10 mm Hg by method 2.

Figure from Adiyaman, et al. demonstrating method 1 on the left.

Another study demonstrated that although crossing the legs at the knees influenced blood pressure, crossing them at the ankles had no effect.

A recent review identified 7 studies which support the influence of leg crossing on BP.

 An Inconvenient Truth
If leg crossing raises the systolic blood pressure  8 to 10 mm Hg why aren’t we doctors recommending patients sit with leg uncrossed the majority of the time. Personally, I had never heard there were any health complications to sitting with my legs crossed.
Apparently the myriad health information sources on the internet are near unanimous in their condemnation of leg crossing but the hypertensive effect of this maneuver is usually not cited.
My favorite title condemning the practice was “The surprising and inconvenient truth of crossing your legs.”
I must admit since doing this bit of research I have substantially reduced the amount of time I sit with my legs crossed. And I’ve pondered extensively whether sitting with legs crossed makes me feel any different and why I suddenly and seemingly randomly decide to cross my legs.
I’ve also started asking  friends and colleagues and medical residents how much of the day they spend with legs crossed.
On teaching rounds one morning recently we tested a volunteer resident’s blood pressure with legs crossed and uncrossed. Sure enough, the systolic BP was 10 mm Hg higher with legs crossed.
Chiasmically Yours,
-ACP

 

For those of you itching to read more about BP and leg crossing here are the references:

 

Pinar R, Ataalkin S, Watson R. The effect of crossing legs on blood pressure in hypertensive patients. J Clin Nurs 2010; 19:1284–1288. [PubMed]
Adiyaman A, Tosun N, Elving LD, Deinum J, Lenders JWM, Thien T. The effect of crossing legs on blood pressure. Blood Press Monit 2007; 12:189–193. [PubMed]
Pinar R, Sabuncu N, Oksay A. Effects of crossed leg on blood pressure. Blood Press 2004; 13:252–254. [PubMed]
Avvampato CS. Effect of one leg crossed over the other at the knee on blood pressure in hypertensive patients. Nephrol Nurs J 2001; 28:325–328. [PubMed]
Keele-Smith R, Price-Daniel C. Effects of crossing legs on blood pressure measurement. Clin Nurs Res 2001; 10:202–213. [PubMed]
Foster-Fitzpatrick L, Ortiz A, Sibilano H, Marcantonio R, Braun LT. The effects of crossed leg on blood pressure measurement. Nurs Res 1999; 48:105–108. [PubMed]
Peters GL, Binder SK, Campbell NR. The effect of crossing legs on blood pressure: a randomized single-blind cross-over study. Blood Press Monit 1999; 4:97–101. [PubMed]

Dear Dr. Gottlieb, Full Fat Dairy is “Healthy”. Why Are You Pushing Low-Fat Dairy?

By all accounts, Scott Gottlieb, the Trump appointed director of the FDA is doing a good job.

Vox points out, he has announced substantial FDA moves to reduce cigarette consumption and is committed to improving competition in generic drugs.

However, he gave a recent speech at the National Food Policy Conference  on “Reducing the Burden of Chronic Disease” which indicates he is misinformed on crucial aspects of nutritional science.

Gottlieb indicated he wanted the FDA to play a bigger role in guiding Americans to eat a healthier diet to reduce the burden of chronic disease.

To facilitate this he is looking to define what foods are “healthy”:

We’re keeping all these considerations in mind as we pursue rulemaking to update the definition of “healthy” so it’s based on nutrition criteria and food considerations that are more up-to-date than those being used for the current definition….

Once updating the definition, Gottlieb wants to label food as “healthy” In a way that makes it easier for consumers to understand:

To address this, we’ve had discussions about whether there should be a standard icon or symbol for the word “healthy” that everyone could use on food packages.

Gottlieb goes on to bemoan a focus on nutrients rather than foods but in the very  next sentence recommends a food, dairy, in a form that has one important nutrient stripped from it-fat.

Traditionally, we’ve focused primarily on the nutrients contained in food in considering what is healthy. But people eat foods, not nutrients.

This is why we’re asking the important question of whether a modernized definition of “healthy” should go beyond nutrients to better reflect dietary patterns and food groups, like whole grains, low fat dairy, fruits and vegetables and healthy oils?

Obviously, the first step in getting Americans to eat healthier is to make sure you are doling out the correct advise and in his speech Dr. Gottlieb indicates he has bought into  long-standing fundamental errors. I wrote him the following letter hoping to correct these errors.


Dear Dr. Gottlieb,

Congratulations on your recent appointment as FDA director and kudos for your fine work to date. I read your recent comments on developing an updated definition of “healthy” and the importance of  conveying that information to American consumers  I applaud your efforts in this area as well as your ongoing efforts to limit cigarette smoking and improve generic competition.

I am fine with guiding consumers to healthy foods but I beg of you, let this determination of what is healthy be guided by the actual science, not prior dogma.

In your recent speech you indicate that Americans are not consuming enough dairy and you recommend low-fat dairy which implies that you and the FDA believe that scientific studies have demonstrated that dairy fat is unhealthy.

Five years ago I, too , thought dairy fat was unhealthy and recommended my patients avoid butter, full-fat yogurt and cheese. However, when challenged on this belief, I reviewed the scientific literature on dairy fat and cardiovascular disease.

It turns out when objectively analyzed (as I have written about here and here ) there is no scientific evidence that supports the concept that dairy processed to remove dairy fat is healthier than the original unadulterated product.

In fact, evidence suggests full fat dairy reduces central obesity, diabetes, cardiovascular disease and atherosclerosis in general.

As a result of misguided recommendations to avoid dairy fat, it is virtually impossible in most grocery stores to find full fat yogurt or milk. The vast majority of the dairy aisle is devoted to various low or non fat concoctions which have had loads of sugar and chemicals added and are arguably worse than a Snickers bar.

Dr. Gottlieb ,I am not cherry-picking the data here or relying on out of date studies. I’ve reviewed everything I can find on this issue and reviewed it without bias. Evidence continues to accumulate supporting the healthiness of full fat dairy.

For example, here’s a 2018 review from researchers totally unaffiliated with the dairy industry which asks the question “Dairy Fats and Cardiovascular Disease: Do We Really Need to Be Concerned?”

After a exhaustive review they conclude the answer is no.

recent research and meta-analyses have demonstrated the benefits of full-fat dairy consumption, based on higher bioavailability of high-value nutrients and anti-inflammatory properties. … In general, evidence suggests that milk has a neutral effect on cardiovascular outcomes but fermented dairy products, such as yoghurt, kefir and cheese may have a positive or neutral effect.

Flawed Reasons for Low Fat Dairy Recommendations

As I have written previously, I believe there are three reasons for the failure of major nutritional recommendations such as the 2015  Dietary Guidelines For Americans  to correct previously  flawed advice to choose  non or low-fat dairy over full fat:

1. In  few randomized dietary studies showing benefits of a particular diet over another, non fat or low fat dairy was recommended along with a portfolio of other healthy dietary changes.

The overall benefit of the superior diet had nothing to do with lowering the dairy fat but was due to multiple other changes.

2. The dairy industry has no motivation to promote full fat dairy. In fact, they do better financially when they can take the fat out of milk and sell it for other purposes such as butter, cheese, and cream. (Please read my interview with a plastic surgeon dairy farmer on the skim milk scam here.)

3. Saturated fat is still mistakenly being treated as a monolithic nutritional element.  Although dairy fat is mostly saturated, the individual saturated fats vary widely in their effects on atherogenic lipids and atherosclerosis. In addition, the nature of the saturated fat changes depending on the diet of the cow.

4. Since authorities have been making this low fat dairy recommendation for so long they are extremely reluctant to reverse their advice. It lowers their credibility.

There Is No Scientific Consensus On What Constitutes A Healthy Oil

Finallly, Dr. Gottlieb, I would like to briefly point out that there is considerable ongoing scientific debate about what constitutes a “healthy oil.”

I summarized this last year on a post on coconut oil (which I fear you will also pronounce “unhealthy”).

In many respects, the vilification of coconut oil by federal dietary guidelines and the AHA resembles the inappropriate attack on dairy fat and is emblematic of the whole misguided war on dietary fat. In fact, the new AHA advisory  after singling out coconut oil goes on to cherry-pick the data on dairy fat and cardiovascular disease in order to  support their faulty recommendations for choosing low or nonfat dairy.

Canola and corn oil, the products of extensive factory processing techniques, contain mostly mono or polyunsaturated fats which have been deemed “heart-healthy” on the flimsiest of evidence.

The most recent data we have on replacing saturated fat in the diet with polyunsaturated fat comes from the Minnesota Coronary Experiment performed from 1968 to 1973, but published in 2016 in the BMJ.

Data from this study, which substituted liquid corn oil in place of the usual hospital cooking fats, replaced corn oil margarine for butter and added corn oil to numerous food items, showed no overall benefit in reducing mortality. In fact, individuals over age 65 were more likely to die from cardiovascular disease if they got the corn oil diet.

So, Dr. Gottlieb, please continue your efforts to make Americans healthier but make sure the current scientific evidence actually supports your recommendations. Keep in mind, the disastrous public health experiments of previous decades.


Skeptically Yours,

-ACP

N.B. Some of my posts on dairy fat are below.

Dairy Fat Makes You Thinner

The Skim Milk Scam

More Evidence That Diary Fat is associated with a lower risk of heart disease

What happens to cholesterol levels when you switch to low or non fat dairy?

Dietary Guidelines 2015: Why Lift Fat and cholesterol limits but still promote low fat dairy?

In defense of real cheese.


h/t to the always excellent Conscien Health for bringing Gottlieb’s speech to my attention.


Credit for the featured image of dairy cows from the wonderful Trader’s Point Creamery

The Bad Food Bible: A Well-Written, Sensible and Science-Based Approach To Diet

The skeptical cardiologist has been searching for some time for a book on diet that he can recommend to his patients. While I can find books which have a lot of useful content, usually the books mix in some totally unsubstantiated advice with which I disagree.

I recently discovered a food/diet/nutrition book which with I almost completely agree. The author is Aaron Carroll,  a pediatrician, blogger on health care research (The incidental Economist) and a Professor of Pediatrics and Associate Dean for Research Mentoring at Indiana University School of Medicine.

He writes a regular column for the New York Times and covers various topics in health care. His articles are interesting,  very well written and researched and he often challenges accepted dogma.

Like the skeptical cardiologist, he approaches his topics from an unbiased perspective and utilizes a good understanding of the scientific technique along with a research background to bring fresh perspective to health-related topics.

Last last year he wrote a column, within which I found the following:

Studies of diets show that many of them succeed at first. But results slow, and often reverse over time. No one diet substantially outperforms another. The evidence does not favor any one greatly over any other.

That has not slowed experts from declaring otherwise. Doctors, weight-loss gurus, personal trainers and bloggers all push radically different opinions about what we should be eating, and why. We should eat the way cave men did. We should avoid gluten completely. We should eat only organic. No dairy. No fats. No meat. These different waves of advice push us in one direction, then another. More often than not, we end up right where we started, but with thinner wallets and thicker waistlines.

I couldn’t agree more with this assessment and as I surveyed the top diet books on Amazon recently, I saw one gimmicky, pseudoscientific  diet after another. From the Whole30 approach (which illogically  completely eliminates any beans and legumes, dairy products,  alcohol, all grains, and starchy vegetables like potatoes (see how absurd this diet is here)) to Dr. Gundry’s Plant Paradox (aka lectin is the new gluten (see here for James Hambling’s wonderful Atlantic article on the huckster’s latest attempt to scare you into buying his useless supplements).

It turns out Carroll published a useful book recently, The Bad Food Bible which critically examines diet and I agree with the vast majority of what is in it.

The first three chapters are on butter, meat, eggs and salt. His conclusions on how we should approach these 4 are similar to ones I have reached and written about on this site (see here for dairy, here for meat, here for eggs and here for salt).  Essentially, the message is that the dangers of these four foods have been exaggerated or nonexistent, and that consuming them in moderation is fine.

The remaining chapters cover topics I have pondered extensively,  but have not written about: including gluten, GMOs, alcohol, coffee, diet-soda and non-organic foods.

I agree with his assessments on these topics. Below, I’ll present his viewpoint along with some of my own thoughts in these areas.

Gluten

Carroll does a good job of providing a scientific, but lay-person friendly background to understanding the infrequent (1 of 141 Americans), but quite serious gluten-related disorder, celiac disease.

However, surveys show that up to one-third of Americans, the vast majority of whom don’t have celiac disease, are seeking “gluten-free” foods, convinced that this is a healthier way of eating. Carroll points out that there is little scientific support for this; there are some individuals who are sensitive to wheat/gluten, but these are rare.

He concludes:

“If you have celiac disease, you need to be on a gluten-free diet. If you have a proven wheat allergy, you need to avoid wheat. But if you think you have gluten sensitivity? You’d probably be better off putting your energy and your dollars toward a different diet. Simply put, most people who think they have gluten sensitivity just don’t.

I do agree with him that the “gluten-free” explosion of foods (gluten-free sales have doubled from 2010 to 2014) is not justified.

However, I must point out that my 92 year old father has recently discovered that he has something that resembles gluten sensitivity. About a year ago, he noted that about one hour after eating a sandwich he would feel very weak and develop abdominal discomfort/bloating. He began suspecting these symptoms were due to the bread and experimented with different bread types without any symptom relief.

Finally, he tried gluten-free bread and the symptoms resolved.

If you have engaged in this type of observation and experimentation on your self, and noted improved symptoms when not consuming gluten, then I think you’re justified in diagnosing gluten sensitivity, and by all means consider minimizing/avoiding wheat.

GMOS

Carroll begins his chapter on genetically modified organisms (GMOs) with a description of the droughts that plagued India in the 1960s and the efforts of Norman Borlaug to breed strains of wheat that were resistant to fungus and yielded more grain. By crossbreeding various strains of wheat he was able to develop a “semi-dwarf” strain that increased what was produced in Mexico by six-fold.

Despite the fact that numerous scientific and health organizations around the world have examined the evidence regarding the safety of genetically modified organisms (GMOs) and found them to be completely safe, there remains a public controversy on this topic. In fact a Pew Poll found that while 88% of AAAS scientists believe that GMOs are safe for human consumption, only 37% of the public do – a 51% gap, the largest in the survey.

This gap is largely due to an aggressive anti-GMO propaganda campaign by certain environmental groups and the organic food industry, a competitor which stands to profit from anti-GMO sentiments. There is also a certain amount of generic discomfort with a new and complex technology involving our food.

The National Academy of Sciences analyzed in detail the health effects of GMOs in 2016. Their report concludes:

While recognizing the inherent difficulty of detecting subtle or long-term effects in health or the environment, the study committee found no substantiated evidence of a difference in risks to human health between currently commercialized genetically engi-neered (GE) crops and conventionally bred crops, nor did it find conclusive cause-and-effect evidence of environmental problems from the GE crops. GE crops have generally had favorable economic outcomes for producers in early years of adoption, but enduring and widespread gains will depend on institutional support and access to profitable local and global markets, especially for resource-poor farmers

Carroll does a good job of looking at the GMO issue from all sides. He touches on environmental downsides related to herbicide-resistant GMO crops and the problems created by patenting GMO seeds, but asserts that “these are the result of imperfect farming and the laws that regular agribusiness, not of GMOS themselves.”

Ultimately, despite these concerns, I agree with Carroll’s conclusion that:

“Foods that contain GMOs aren’t inherently unhealthy, any more are  than foods that don’t contain them. The companies that are trying to see you foods by declaring them ‘GMO-free” are using the absence of GMOs to their advantage–not yours.”

Alcohol, Coffee, and Diet-Soda

Carroll does a good job of summarizing and analyzing the research for these three topics and reaches the same conclusions I have reached in regard to coffee, alcohol and diet-soda:

-alcohol in moderation lowers your risk of  dying, primarily by reducing cardiovascular death

-coffee, although widely perceived as unhealthy, is actually good for the vast majority of people

For those seeking more details a few quotes


on alcohol:

“Taken together, all of this evidence points to a few conclusions. First, the majority of the research suggests that moderate alcohol consumption is associated with decreased rates of cardiovascular disease, diabetes, and death. Second, it also seems to be associated with increased rates of some cancers (especially breast cancer), cirrhosis, chronic pancreatitis, and accidents, although this negative impact from alcohol seems to be smaller than its positive impact on cardiovascular health. Indeed, the gains in cardiovascular disease seem to outweigh the losses in all the other diseases combined. The most recent report of the USDA Scientific Advisory Panel agrees that “moderate alcohol consumption can be incorporated into the calorie limits of most healthy eating patterns.”

Keep in mind that moderate consumption is up to one drink per day for women, and two drinks for men (my apologies to women in general and the Eternal Fiancee’ of the Skeptical Cardiologist in particular) and be aware of what constitutes “one drink.”

Also keep in mind that any alcohol consumption raises the risk of atrial fibrillation (see here) and that if you have a cardiomyopathy caused by alcohol you should avoid it altogether.


on coffee:

“It’s time people stopped viewing coffee as something to be limited or avoided. It’s a completely reasonable part of a healthy diet, and it appears to have more potential benefits than almost any other beverage we consume.
Coffee is more than my favorite breakfast drink; it’s usually my breakfast, period. And I feel better about that now than ever before. It’s time we started treating coffee as the wonderful elixir it is, not the witch’s brew that C. W. Post made it out to be.”

Strangely enough, coffee is usually my breakfast as well (although I recommend against adding titanium oxide to your morning java).  Why am I not compelled to consume food in the morning?  Because breakfast is not the most important meal of the day and I don’t eat until I’m hungry.


on diet-soda:

Carroll notes that many Americans are convinced that artificial sweeteners are highly toxic:

“no article I’ve written has been met with as much anger and vitriol as the first piece I wrote on this subject for the New York Times, in July 2015, in which I admitted, “My wife and I limit our children’s consumption of soda to around four to five times a week. When we let them have soda, it’s . . . almost always sugar-free.”

He notes, as I have done, that added sugar is the real public enemy number one in our diets. He reviews the scientific studies that look at toxicity of the various artificial sweeteners and finds that they don’t convincingly prove any significant health effects in humans.

Some believe that artificial sweeteners contribute to obesity, but the only evidence supporting this idea comes from observational studies. For many reasons, we should not highly value observational studies but one factor, “reverse causation,” is highly likely to be present in studies of diet sodas. If diet soda consumption is associated with obesity, is it the cause, or do those who are obese tend to drink diet soda. Observational studies cannot answer this question but randomized studies can.

Carroll points out that:

the randomized controlled trials (which are almost always better and can show causality) showed that diet drinks significantly reduced weight, BMI, fat, and waist circumference.”

Simple Rules For Healthy Eating

Carroll concludes with some overall advice for healthy eating:

-Get as much of your nutrition as possible from a variety of completely unprocessed foods

-Eat lightly processed foods less often

-Eat heavily processed foods even less often

-Eat as much home-cooked food as possible, preparing it according to rules 1, 2, and 3

-Use salt and fats, including butter and oil, as needed in food preparation

-When you do eat out, try to eat at restaurants that follow the same rules

-Drink mostly water, but some alcohol, coffee, and other beverages are fine

-Treat all calorie-containing beverages as you would alcohol

-Eat with other people, especially people you care about, as often as possible

These are solid, albeit not shocking or book-selling, rules that  correspond closely to what I have adopted in my own diet.

In comparison to the bizarre advice from nutrition books which dominate the best-selling diet books, I found The Bad Food Bible to be a consistent, well-written, extensively researched, scientifically-based, unbiased guide to diet and can highly recommend it to my readers and patients.

Semibiblically Yours,

-ACP

Still More Evidence That Fish Oil Supplements Do Not Prevent Cardiovascular Disease

Avid readers of the skeptical cardiologist know that he is not an advocate of fish oil supplements.

One of my first posts (1/2013) was devoted to taking down the mammoth OTC fish oil industry because recent scientific evidence was clearly showing no benefit for fish oil pills.

I concluded:

", the bottom line on fish oil supplements is that  the most 
recent scientific evidence does not support any role for them  inpreventing heart attack, stroke, or death. There are potential 
down sides to taking them, including contaminants and the impact on the marine ecosystem. I don’t take them and I advise my
patients to avoid them (unless they have triglyceride levels 
over 500.)"

Despite a lack of evidence supporting taking them, the fish oil business continues to grow,  buttressed by multiple internet sites promoting various types of fish oil (and more recently krill oil)  for any and all ailments and a belief in the power of “omega-3 fatty acids”.

Another Meta-Analysis Concludes No Benefit To Fish Oil Supplements

A publication this month evaluated the 10 randomized controlled trials involving 77 917 thousand individuals that have studied fish oil supplements in preventing heart disease. The writers concluded that fish oil supplements do not significantly prevent any cardiovascular outcomes under any scenario.

It was written by a group with the ominous title of “The Omega-3 Treatment Trialists’ Collaboration.”

The Omega-3 Treatment Trialists’ Collaboration was established to conduct a collaborative meta-analysis based on aggregated study-level data obtained from the principal investigators of all large randomized clinical trials of omega-3 FA supplements for the prevention of cardiovascular disease, using a prespecified protocol and analysis plan. The aims of this meta-analysis were to assess the associations of supplementation with omega-3 FAs on (1) fatal CHD, nonfatal MI, stroke, major vascular events, and all-cause mortality and (2) major vascular events in prespecified subgroups.

The authors conclusions:

. Randomization to omega-3 fatty acid supplementation (eicosapentaenoic acid dose range, 226-1800 mg/d) had no significant associations with coronary heart disease death (rate ratio [RR], 0.93; 99% CI, 0.83-1.03; P = .05), nonfatal myocardial infarction (RR, 0.97; 99% CI, 0.87-1.08; P = .43) or any coronary heart disease events (RR, 0.96; 95% CI, 0.90-1.01; P = .12). Neither did randomization to omega-3 fatty acid supplementation have any significant associations with major vascular events (RR, 0.97; 95% CI, 0.93-1.01; P = .10), overall or in any subgroups, including subgroups composed of persons with prior coronary heart disease, diabetes, lipid levels greater than a given cutoff level, or statin use.

Nothing. Nada. No benefit.

There is clearly no reason to take fish oil supplements to prevent cardiovascular disease!

American Heart Association Sheepishly Recommends Fish Oil Supplements

If the science was conclusive on this in 2013 why did the American Heart Association (AHA) issue an “advisory” in 2017  suggesting that the use of omega-3 FAs for prevention of coronary heart disease (CHD) is probably justified in individuals with prior CHD and those with heart failure and reduced ejection fractions?

The AHA advisory is clearly misguided and relies heavily in its discussion on a 2012 meta-analysis from Rizos, et al. published in 2012.

Oddly, this is the study that prompted me to write my first fish oil post in 2013

The AHA advisory totally distorts the completely negative conclusions of the Rizos meta-analysis, writing:

A meta-analysis published in 2012 examined the effects of omega-3 PUFA supplementation and dietary intake in 20 RCTs that enrolled patients at high CVD risk or prevalent CHD and patients with an implantable cardioverter-defibrillator (total n=68 680). That meta-analysis demonstrated a reduction in CHD death (RR, 0.91; 95% CI, 0.85–0.98), possibly as the result of a lower risk of SCD (RR, 0.87; 95% CI, 0.75–1.01).11

Strangely enough, if you look at the conclusions of Rizos, et al. they are

No statistically significant association was observed with all-cause mortality (RR, 0.96; 95% CI, 0.91 to 1.02; risk reduction [RD] -0.004, 95% CI, -0.01 to 0.02), cardiac death (RR, 0.91; 95% CI, 0.85 to 0.98; RD, -0.01; 95% CI, -0.02 to 0.00), sudden death (RR, 0.87; 95% CI, 0.75 to 1.01; RD, -0.003; 95% CI, -0.012 to 0.006), myocardial infarction (RR, 0.89; 95% CI, 0.76 to 1.04; RD, -0.002; 95% CI, -0.007 to 0.002), and stroke (RR, 1.05; 95% CI, 0.93 to 1.18; RD, 0.001; 95% CI, -0.002 to 0.004) when all supplement studies were considered.

Nothing. Nada. No significant benefit!

The AHA was so confused by their own advisory that in the AHA news release on the article they quote Dr. Robert Eckel, a past AHA president as saying he remains “underwhelmed” by the current clinical trials.

“In the present environment of evidence-based risk reduction, I don’t think the data really indicate that fish oil supplementation is needed under most  circumstances.”

The end of the AHA news article goes on to quote Eckel as indicating he doesn’t prescribe fish oil supplements and the science advisory won’t change his practice:

Eckel said he doesn’t prescribe fish oil supplements to people who have had coronary events, and the new science advisory won’t change that. “It’s reasonable, but reasonable isn’t a solid take-home message that you should do it,” he said.

AHA: Wrong On Coconut Oil and Fish Oil

It’s hard for me to understand why the AHA gets so many things wrong in their scientific advisories. In the case of the recent misguided attack on coconut oil , their ongoing vilification of all saturated fats, and their support for fish oil supplements I don’t see evidence for industry influence. The authors of the fish oil supplement advisory do not report any financial conflicts of interest.

There is, however, one bias that is very hard to measure which could be playing a role: that is the bias to agree with what one has previously recommended.  The AHA issued an advisory in 2002 recommending that people take fish oil. Changing that recommendation would mean admitting that they were wrong and that they had contributed to the growth of a 12 billion dollar industry serving no purpose.

Personally, I am aware of this kind of bias in my own writing and strive to be open to new data and publications that challenge what I personally believe or have publicly recommended.

In the case of fish oil supplements for preventing cardiovascular disease, however, the most recent data supports strongly what I wrote in 2013:

Don’t take fish oil supplements to prevent heart disease.

Americans want a “magic-bullet” type pill to take to ward off aging and the diseases associated with it. There isn’t one. Instead of buying pills and foods manipulated and processed by the food industry which promise better health, eat real food (including fish) eat a lot of plants and don’t eat too much.

Piscinely Yours,

-ACP

N.B. I have no patients on the two prescription fish oil supplements available, Lovaza and Vascepa. I wrote about Vascepa here

Below is an excerpt:

Like the first prescription fish oil available in the US, Lovaza, VASCEPA is only approved by the FDA for treatment of very high triglycerides (>500 mg/dl).

This is a very small market compared to the millions of individuals taking fish oil thinking that  it is preventing heart disease.

The company that makes Vascepa (Amrin;$AMRN)would also like to have physicians prescribe it to their patients who have mildly or moderatelyelevated triglycerides between 200 and 500 which some estimate as up to 1/3 of the population.

The company has a study that shows that Vascepa lowers triglycerides in patients with such mildly to moderately elevated triglycerides but the FDA did not approve it for that indication.

Given the huge numbers of patients with trigs slightly above normal, before approving an expensive new drug, the FDA thought, it would be nice to know that the drug is actually helping prevent heart attacks and strokes or prolonging life.

After all, we don’t really care about high triglycerides unless they are causing problems and we don’t care about lowering them unless we can show we are reducing the frequency of those problems.

Data do not exist to say that lowering triglycerides in the mild to moderate range  by any drug lowers heart attack risk.

In the past if a company promoted their drug for off-label usage they could be fined by the FDA but Amarin went to court and obtained the right to promote Vascepa to physicians for triglycerides between 200 and 500.

Consequently, you may find your doctor prescribing this drug to you. If you do, I suggest you ask him if he recently had a free lunch or dinner provided by Amarin, has stock in the company (Vascepa is the sole drug made by Amrin and its stock price fluctuates wildly depending on sales and news about Vascepa) or gives talks for Amarin.

If he answers no to all of the above then, hopefully, your triglycerides are over 500.

.

 

 

 

 

Should You Take An Antioxidant (Supplement or Vitamin) To Prevent Or Treat Heart Disease

Antioxidant-rich foods, vitamins and supplements are incessantly promoted to Americans as effective and safe means to stave off the chronic diseases of aging and even aging itself.

The simple concept that sells billions of dollars of these  products seems logical and seems to be supported by science: damaging and disease-causing  free radicals  are neutralized by super hero antioxidants.  All you have to do to benefit from these disease-fighting agents is identify foods with the highest level of antioxidants or take supplements with super antioxidant vitamins or chemicals.

To remain young  and free of heart disease, cancer and dementia, the glowing marketing material for antioxidant products proclaims,  eat this magical Italian fruit or drink this fruit juice or take this concentrated substance that we have carefully extracted from a super fruit.

Unfortunately, the early hopes that antioxidant therapy would reduce heart disease,in particular, and other chronic diseases of aging in general have been dashed by excellent scientific studies  performed in the 1990s.

For antioxidant vitamins, in particular, which continue to be heavily promoted for heart disease and cancer prevention, over the last 20 years a wealth of studies have accumulated which clearly demonstrate a lack of efficacy.

Despite data clearly showing no benefit in well done randomized trials (and in some cases evidence for harm) sales of antioxidant vitamins C, E and beta-carotene continue to thrive.

Why did scientists strongly believe in the idea that antioxidants in pure and concentrated form would prevent heart disease?

Antioxidants: Free Radical Scavengers

Laboratory and animal studies beginning in the 1950s suggested that excess free radicals generated by oxidative processes could be responsible for the chronic degenerative diseases of aging.

Oxygen, which is essential to animal life, undergoes processing in cells which creates unstable free radicals. Free radicals are short an electron and seek other molecules which can donate an electron and make them more stable. This process is termed oxidation.

The molecules produced by oxidation play an important role in a a number of biological processes such as the killing of bacteria and in cell signaling. These same unstable molecules, however,  have been implicated in a number of deleterious processes as they can participate in unwanted side reactions and create cell damage.

Thus, too many free radicals have been implicated as potentially causal in diseases ranging from cancer to cardiovascular disease to dementia.

Antioxidants can reduce damage from free radical reactions because they can donate electrons to neutralize free radicals or their offspring without forming another free radical.

This observation logically lead to the theory that large amounts of antioxidants taken as an oral supplement or within (either naturally or added artificially)  food and beverages can prevent the free radical damage presumably causing chronic disease  and aging.

Investigators early on identified three vitamins as the most important cellular antioxidants:

  • Vitamin E or  d-alpha tocopherol is a fat soluble vitamin.
  • Vitamin C or ascorbic acid. is a water soluble vitamin, deficiency of which leads to scurvy
  • Beta-carotene is a precursor to vitamin A (retinol)

Early Observational Studies Suggest  Taking An Antioxidant Prevents Heart Disease 

Based on laboratory, animal and human clinical trials many investigators by the early 1990s were convinced that oxidation of LDL cholesterol was the major cause of atherosclerosis and that antioxidant supplementation , in particular Vitamin E, could prevent the heart attacks and strokes caused by atherosclerosis.

The introduction to the landmark Nurses Health Study  summarizes the seemingly compelling evidence leading to these conclusions:

Rapidly growing evidence suggests that oxidation of low-density lipoprotein (LDL) plays an important part in atherosclerosis. As Steinberg et al. have found,1-3 oxidized LDL is taken up more readily than native LDL by macrophages to create foam cells. Also, oxidized LDL is chemotactic for circulating monocytes,4 and it inhibits the motility of tissue macrophages5. It may also be cytotoxic to endothelial cells6 and may increase vasoconstriction in arteries7. Oxidized LDL has been identified in atherosclerotic lesions,8-10 and elevated titers of circulating autoantibodies to epitopes of oxidized LDL are found in patients with atherosclerosis11. Lipid peroxide concentrations have been found to be higher in patients with atherosclerosis12. In addition, the susceptibility of LDL to oxidation was correlated with the severity of atherosclerosis13.

Vitamin E is a potent lipid-soluble antioxidant carried in LDL14,15. It inhibits the proliferation of smooth-muscle cells in vitro,16 and when added to plasma, it increases the resistance of LDL to oxidation17. LDL from volunteers given alpha-tocopherol supplements showed increased resistance to oxidation18

Starting in 1980  the Nurses Healthy Study began gathering information on diet and supplement use in 87,245 female nurses 34 to 59 years of age who were free of diagnosed cardiovascular disease and cancer. Information on diet was assessed every two years  and the participants were monitored for cardiovascular outcomes for 8 years.

High consumers of Vitamin E compared to lower consumers had a 34% lower risk of major coronary disease. Those who took Vitamin E for more than 2 years had a 41% reduction in risk which was significant after adjustment for age, smoking status, risk factors for coronary disease, and use of other antioxidant nutrients (including multivitamins).

After reading this study I and many of my colleagues began recommending that our patients take Vitamin E. These observational trials, however, could only show an association between antioxidants and disease, they didn’t prove causality.

Good Quality Randomized Trials Fail To Show Any Benefit of Antioxidants and Raise Concerns of Possible Danger

Given the strong evidence for antioxidants in reducing heart disease from the observational and laboratory studies the theory that antioxidant supplementation would reduce heart disease needed to be tested in randomized trials.

Fortunately, multiple well done randomized studies have tested whether supplementation with the major proposed antioxidants will reduce heart disease, cancer or mortality.

Sadly, the consensus assessment is that they are useless and in some cases antioxidant vitamin supplementation may increase risks.

The Physicians’ Health Study II is a great example:

Published in 2008, This study randomly assigned 14,641 physicians without heart disease to treatment with vitamin E 400 international units every other daily, vitamin C 500 mg daily, both, or neither; After  eight years, treatment with vitamin E  and Vitamin C either alone or in combination had no effect on major cardiovascular events or all-cause mortality.

Those participants taking Vitamin E had a significant 70% increased risk of hemorrhagic stroke compared to those taking placebo.

After this trial was published I took all my patients off Vitamin E.

Multiple good quality randomized controlled studies of Vitamin E, Vitamin C and beta-carotene in various combinations have also been done on patients who have established coronary heart disease and have shown no benefit in reducing cardiovascular events or mortality. This 2003 Lancet meta-analysis nicely summarizes the data.

These studies strongly called into question the theory that supplementation with antioxidants reduce chronic disease and by 2003 there was a broad consensus among serious scientists, cardiologists and nutritionists that Vitamin E and Vitamin C in various doses and in diverse populations had no benefit in reducing mortality, cardiovascular disease or cancer.

In fact, Vitamin E may increase hemorrhagic stroke and high-dose vitamin E supplementation (≥400 international units/day) may be associated with an increase in all-cause mortality

Studies with beta-carotene overall suggested an increase in overall mortality and one study has shown an increased risk of lung cancer in male smokers who received supplementation.

More recently, a 2012 BMJ meta-analysis   concluded that there was no benefit for any vitamin or antioxidant supplement in reducing cardiovascular risk or mortality.

 

Despite Scientific Studies Showing No Benefit, Antioxidant Sales Continue To Grow

You might conclude that based on high quality studies showing no benefits and potential harm that sales of antioxidants would taper off. Unfortunately, the opposite has occurred.

Nutraceuticals World reported that sales of antioxidant supplements are growing steadily, reaching all time highs.

Combining top antioxidant ingredient sales such as green tea, dark chocolate, superfruit juice and dietary supplements, Euromonitor estimated the combined global sales in these categories totaled $34 billion in 2010. According to Euromonitor, the top antioxidant markets are Japan, the U.S. and China, with sales growing steadily in all five ranked product areas in the past five years. Growth from 2005 to 2010 was 43% in current terms. As a point of comparison, the global organic packaged food and beverage market was only $27 billion.

The Sneakiness of the Nutraceutical Snake Oil Salesmen

The quacks and charlatans that make their living selling useless vitamins, minerals, supplement and nutraceuticals are masters at creating the appearance of a scientific basis for buying their snake oil.

Their promotional material always features references to scientific studies.  Almost invariably, these references do not prove any health benefit for the product being sold.

In cases like antioxidants where initial studies suggest a benefit and subsequent higher quality studies have shown no benefit, only the earlier studies will be quoted.

If relevant negatives studies for an antioxidant are referenced, the talented snake oil salesman will explain to his gullible audience that the lack of efficacy was because the wrong form of the antioxidant was utilized.

Fortunately, for you, the snake oil salesman has developed his own special formulation which is superior. Such formulations are typically described as containing additional ingredients that enhance efficacy. Often, the special formulation is described as somehow better at getting into the body or being absorbed.

None of these special formulations has any scientific support for treating or preventing any disease.

Dr. Mercola, A Master of Pseudoscientific Support For Selling Useless Vitamins

The most successful marketers of useless antioxidant supplements and vitamins convince their audience that they alone have the insight and wisdom to provide the consumer with the knowledge and products they need to be healthy.  To accomplish this, they must create mistrust of standard medical advice and prescription medications, often portraying doctors as ignorant of proper nutrition and hostile to allegedly superior “natural” or alternative cures.

Doctors, in this portrayal, are the enemy, pushing dangerous prescription medications along with unneeded procedures like coronary stents and bypass surgery because we are in the pay of the pharmaceutical and medical device industries.

Joseph Mercola, an osteopath, has created an alternative medicine internet empire by convincing millions to follow his advice and buy his useless supplements. He is arguably the master of alternative medicine misinformation. (See this article to fully understand how dangerous Mercola’s ideas are.)

Hoovers reports that Mercola makes 9.8 million dollars per year selling useless stuff and Alexa describes his website as the top “alternative medicine” website. Mercola sells so much snake oil it is mind-numbing.

Mercola (or more likely his marketing department)  has  an astonishingly long and  detailed  list of reasons why you should buy only his own special formulation of Vitamin E. None of them are supported by scientific references.

-His form is natural versus synthetic.

-Other natural forms of vitamin E come from soy which you should avoid because it is genetically engineered.

-You need all 8 forms of natural vitamin E and they must be balanced in the way that he deems most healthy. His form comes from sunflower seeds.

-Science has ignored the tocotrienol form of Vitamin E but has “started to wake up to the potential benefits.”

-Tocotrienols potentially “help support normal cholesterol levels., protect again  free radical damage and the normal effects of aging” and promote brain health.”

Mercola vitamin E

The average consumer reading this long and complicated discussion is likely to be impressed with the pseudoscientific language, the complicated chemical names, and  the appeal to a more natural approach and has no way of knowing that it is all unsubstantiated marketing hype.

The average consumer is not likely to see buried in small print at the bottom of the page the truth:

*These statements have not been evaluated by the Food and Drug Administration.

These products are not intended to diagnose, treat, cure, or prevent any disease.

Don’t Buy Antioxidant Supplements and Vitamins

What have we learned?

  1. Although early research suggested a role for antioxidant vitamins in preventing heart disease when high quality randomized controlled rials were performed they showed no benefit and in some cases increased risk.
  2. Despite this, antioxidant sales are booming.
  3. Supplement marketers are brilliant at confusing consumers with pseudoscience and sell billions of dollars of useless product.

There is minimal regulation of the nutraceutical/supplement industry. The snake oil purveyors get away with their lies and escape (for the most party) FDA scrutiny by admitting that their products don’t “treat, cure or prevent any disease.”

Rather than hiding this information, at a minimum, they should be forced to put it in large, bold letters at the beginning of every page on their website.

THESE PRODUCTS ARE NOT INTENDED TO TREAT, CURE OR PREVENT ANY DISEASE!

Please don’t buy them any more.

Uncleoxidantly Yours,

-ACP

 

Which Kind of Baby Aspirin Should I Take To Prevent Heart Attack? Chewable Versus Enteric Coated Versus Regular

The skeptical cardiologist recently asked his Eternal Fiancée to grab a bottle of baby aspirin  while she was at the local Walgreen’s. Aspirin or acetyl salicylic acid (ASA) comes in either a 325 mg dose or in a low dose which can be between 75 to 100 mg and is often called “baby” aspirin.

However, since a link between aspirin use and a potentially lethal disease called Reye’s syndrome was identified in the 1980s, no authorities recommend aspirin in children or babies, and the low dose ASA (LDASA) is primarily marketed and used for prevention of cardiovascular disease.

Although Bayer and Dr. Oz would have us believe that all individuals over the age of 55 should be taking LDASA, as I pointed out here in 2014, the FDA no longer recommends it for prevention of cardiovascular disease.

The US Preventive Services Task Force, on the other hand, recognizes certain individuals without heart disease who benefit from LDASA:

The USPSTF recommends initiating low-dose aspirin use for the primary prevention of cardiovascular disease (CVD) and colorectal cancer (CRC) in adults aged 50 to 59 years who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years.
I’m 63  years old, so the USPTF recommendation for me to take LDASA is a little less enthusiastic:
The decision to initiate low-dose aspirin use for the primary prevention of CVD and CRC in adults aged 60 to 69 years who have a 10% or greater 10-year CVD risk should be an individual one. Persons who are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit. Persons who place a higher value on the potential benefits than the potential harms may choose to initiate low-dose aspirin.
Following my own advice (see here), I have started taking 81mg of aspirin regularly (well, when I remember) in order to prevent stroke and heart attack. I do have subclinical atherosclerosis with a plaque in my LAD, and I think the aspirin will make my platelets less sticky and less likely to form clots if my plaque ruptures, thereby reducing my chances of an acute heart attack.
I am willing to accept the increased risk of bleeding from the gastrointestinal tract and hemorrhagic stroke associated with LDASA use.

Previous to this I had been taking ASA from little sample bottles that Bayer sends to my office. These bottles are quite annoying as they are stuffed with cotton and contain very few pills making extrication of the tiny pills an exercise in futility (I am using this as an excuse for my lack of regularity in taking them).

There’s no reason to pay the premium for Bayer ASA despite the company’s advertising attempts to link inextricably their name with ASA.  Aspirin is aspirin, whether Bayer made it or Walgreens. In Bayer’s defense, their website has reasonable information on heart attacks and they appear to be giving aspirin away to people named Smith.

But what type of aspirin should you get? Enteric-coated, safety-coated, delayed release, chewable?

Chewable Aspirin

I asked the Eternal Fiancée to buy the cheapest baby aspirin possible.

She ended up buying a chewable formulation with orange flavoring, presumably aimed at children:

When I put one of these in my mouth I tasted the sickly sweet taste of an artificial sweetener. The ingredients are listed as: Dextrates, Ethyl Cellulose, FD&C Yellow 6 Aluminum Lake, Orange Flavor, Sodium Saccharin, Starch. Saccharine! Yikes!

The only reason to chew ASA is if you are having an acute heart attack.

In this situation, chew 4 of the LDASA or one regular 325 mg aspirin.  Chewing the aspirin makes the levels rise faster in your blood stream and can help dissolve the clot causing your heart attack more rapidly.

How do you know if you are having a heart attack? This is actually a very difficult question to answer with certainty. See here for a reasonable discussion.

Low Dose Aspirin: Enteric-Coated versus Non-coated

It is very difficult (perhaps impossible) to find low dose, non-chewable ASA that has not been “safety-coated” or “enteric-coated.” These formulations have become popular by promoting the idea that they are less likely to cause stomach pain or bleeding.

The concept is that the coating leads to delaying the aborption of the ASA until it reaches the small intestines where, presumably, it will do less damage. However, there is no good evidence to support lower bleeding risk with enteric-coasted (EC) ASA.

There is, on the other hand, very good evidence that therapeutic levels of aspirin in the bloodstream, and therefore the speed and efficacy of ASA in preventing heart attacks, is reduced by these “safety” formulations.

The most recent study showing this was published in 2017.

Volunteers were given either 325mg regular ASA or 325mg EC ASA and researchers looked at how each formulation effected platelet activity.  The onset of antiplatelet activity was determined by the rate and extent of inhibition of serum thromboxane B2(TXB2) generation.

The EC ASA took longer and was less effective at blocking platelet activity than plain ASA. Presumably, this translates into lower efficacy in preventing heart attacks and strokes.

Therefore,  if you feel like you are having a heart attack, chew ASA which is not enteric or safety-coated. Yes, you can chew a regular 325 mg ASA pill. Or you can chew 4 of the LDASA, preferably uncoated but still helpful if coated.

If it turns out you weren’t having a heart attack there is no down side to having chewed 325 mg ASA.

I just spent a fair amount of time trying to find non EC, non-chewable LDASA online and failed.

For the time being I will be swallowing daily the orange chewable LDASA and I will carry a bottle around in my satchel for emergency use.

Salicylically Yours,

-ACP

N.B. Aspirin is generally recommended in secondary prevention of cardiovascular disease, ie. for those who have had heart attacks, stents or bypass surgery . For a good review of the evidence for this see here.

Donald Trump Has Moderate Coronary Plaque: This Is Normal For His Age And We Already Knew It

In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 .  At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.

Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .

Yesterday it was revealed by the White House doctor , Ronny Jackson, that Trump’s repeat score  was 133.

I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.

I pointed out that his previous  score was average for white men his age and his repeat score is also similar to the average white male of 71 years.

Entering Trump’s numbers into the MESA coronary calculator shows us he is at the 46th percentile, meaning that 46% of white men his age have less calcium.We can also calculate Trump’s 10 year risk of heart attack and stroke using the app from the ACC (the ASCVD calculator) and entering in the following information obtained from the White House press briefing:

Total Cholesterol          223

LDL Cholesterol            143

HDL Cholesterol              67

Systolic Blood Pressure 122

Never Smoked Cigarettes

Taking aspirin 81 mg and rosuvastatin (Crestor) 10 mg.

His 10 year risk of heart attack or stroke is 16.7%.

Given that his calcium score is average it doesn’t change his predicted risk and the conclusion is that his risk is identical to the average 71 year old white man-moderate.

We also know that Trump had an exercise stress echocardiogram which was totally normal and therefore can be reasonably certain that the moderate plaque build up in his arteries is not restricting the blood flow to his heart.

Here is what Dr. Jackson said about the stress echo:

He had an exercise stress echocardiogram done, which demonstrated above-average exercise capacity based on age and sex, and a normal heart rate, blood pressure, and cardiac output response to exercise.  He had no evidence of ischemia, and his wall motion was normal in all images. the stress echo:

The New York Times article on this issue, entitled “Trump’s Physical Revealed Serious Heart Concerns, Outside Experts Say”  however, presents a dramatically worrisome and misleading narrative.

It quotes several cardiologists who were very concerned about Trump’s high LDL level, weight and diet.

It’s interesting that some of the experts quoted in the NY Times piece feel that Trump’s Crestor dose should be increased in light of the recent NY  Times piece questioning whether the elderly should take statins at all.

If we have serious concerns about Trump’s heart then we should have the same concerns about every 71 year old white man because he is totally average with regard to cardiac risk. In addition he is on a statin and on aspirin, the appropriate drugs to reduce risk.

In contrast to the average 71 year old male he has had a battery of cardiac tests which show exactly where he stands cardiac wise.

Most of these cardiac tests we would not recommend to an asymptomatic individual of any age. Jackson revealed that Trump had an EKG and an echocardiogram.

His ECG, or commonly EKG, was normal sinus rhythm with a rate of 71, had a normal axis, and no other significant findings.

He had a transthoracic echocardiogram done, which demonstrated normal left ventricular systolic function, an ejected fraction of 60 to 65 percent, normal left ventricular chamber size and wall thickness, no wall motion abnormalities, his right ventricle was normal, his atria were grossly normal, and all valves were normal.

So our President has a normal heart for a 71 year old white male. This automatically puts him at moderate risk for heart attack and stroke over the next 10 years but he is being closely monitored and appropriately treated and should do well.

Nonalarmingly Yours,

-ACP

N.B. I see that Trump’s LDL was reported previously as 93. The current LDL of 143 suggests to me that he has not been taking his Crestor.

N.B. Below is an excerpt from my prior post which explains coronary calcium

Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now.  I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain  patient’s risk of sudden death and heart attacks.

coronary calcium
Image from a patient with a large amount of calcium in the widowmaker or LAD coronary artery (LAD CA).

The CAC scan utilizes computed tomography (CT)  X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.

Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.

Are You A Victim of Excessive Daytime Sleepiness?

The Skeptical Cardiologist has been analyzing the data on sleep apnea (OSA) and cardiovascular disease, utilizing his spectacular skeptical skills.

Recent guidelines from the American Academy of Sleep Medicine suggest that 30 million adults in the US have OSA and that OSA is causing all manner of problems.

I note patient awareness of the possibility of OSA is rising exponentially and many of my patient’s are being subjected to sleep studies because their wives are bothered by their excessive snoring.

The AASM guidelines state that

Increased risk of moderate to severe OSA is indicated by the presence of excessive daytime sleepiness and at least two of the following three criteria: habitual loud snoring; witnessed apnea or gasping or choking; or diagnosed hypertension

Although I have no reason to suspect that I have sleep disordered breathing (SDB-I feel like this term is becoming popular as it avoids the stigma of apnea), I decided to determine my  Epworth Sleepiness Scale which is often utilized   to measure excessive daytime sleepiness.

Developed by Dr. Murray Johns, this scale has its own website where you will learn that:

Johns (2002) introduced the term somnificity to describe the effects of different postures and activities on sleep propensity.

The somnificity of any particular posture, activity and situation is a measure of its ability to facilitate or impede sleep onset in the majority of people. It is not a characteristic of individual people or their sleep disorders.

and (no doubt after years of intense sleepiness research) Dr. Johns has discovered that:

Simply to lie down rather than stand up increases one’s likelihood of falling asleep – the change of posture increases one’s sleep propensity at the time.

After stumbling up on this revelation I have decided to test my hypothesis that playing electric guitar while standing has extremely  low somnificity. (I also hope to use the word somnificity in a normal daily conversation without biting my tongue.)

This self-administered questionnaire asks you to rate how likely you are (on a scale of 0=never to 3=high chance of dozing)  to doze off or fall asleep in certain situations. What follows are the situations with my observations and my self-rated score.

Sitting and reading    (Principles of Nuclear Medicine=3, Brave New World=0)                          1

Watching TV   1

Sitting, inactive in a public place (theatre or a meeting)     1

As a passenger in a car for an hour without a break     2

Lying down to rest in the afternoon when circumstances permit 3

sitting and talking to someone               1

sitting quietly after a lunch without alcohol      1

In a car while stopped for a few minutes in the traffic   2

They don’t ask about falling asleep while driving which seems much more important than the other situations. I’ve done that a lot.

The biggest soporific situation for me is sitting in a barber’s chair. No matter what small talk the hairdresser throws at me, I am asleep within 5 minutes. My bobbing head requires the rare skill of trimming a moving target.

My total score was 12 which puts me solidly in the land of sleep disordered breathing. In the original study by Johns  the patient’s with sleep apnea  (OSA-line 3 in below chart) had an  average score of 11.7.

The AASM guidelines indicate that I could have gotten into some OSA studies with my score, especially if I add in that I have been caught snoring, gasping and choking (sometimes all three simultaneously!) and I have hypertension.

The Eternal fiancée got a respectable score of 7. Apparently she never falls asleep at traffic lights, watching TV/movie or sitting after lunch and believes these are masculine traits. However, I think she should get double points for taking long, intentional naps throughout the day.

Somnificitically Yours,

-ACP

 

 

Why Did I Go Into Atrial Fibrillation?

The skeptical cardiologist is asked this  question or  variations of it (such as  what caused me to go out of rhythm?) on a daily basis.

Most patients would like to have a reason for why their atria suddenly decided to fibrillate.  It’s understandable. If they could identify the reason perhaps they could stop it from happening again.

There are two variations on this question:

For the patient who has just been diagnosed with afib the question is really “what is the underlying reason for me developing this condition?”

For the patient who has had afib for a while and it comes and goes seemingly randomly the question is “what caused the afib at this time? i.e. what triggers my episodes?”

For most patients, there is no straighforward and simple answer to either one of these questions

The Underlying Cause of Atrial Fibrillation

My stock response to this first question goes like this:

“Atrial fibrillation is associated with getting older and having high blood pressure. 10 % of individual >/= 80 years have atrial fibrillation. 90% of patients with afib have hypertension.

Aging and hypertension may increase scarring or damage in the left atrium or pulmonary veins that drain into the left atrium setting up abnormal electrical signals.

There are some specific things that cause afib and we will be doing a complete history and physical and some testing to check for the most common. We’ll check you for thyroid or electrolyte abnormalities and we will do an echocardiogram to look for any structural problems with your heart.

If we do find a treatable cause such as hyperthyroidism or a cardiac valve problem we will fix that and the afib may go away, however chances are we won’t find a specific reason why you developed atrial fibrillation.

Finally, and possibly most importantly, let’s take a close look at your lifestyle. Are you overweight? If so, losing 10% of your body weight will substantially lower your risk of recurrent atrial fibrillation. Let’s get you exercising regularly and eating a healthy diet, Make sure your sleep is optimized and your stress minimized.”

If you’d like a more sophisticated look into what causes afib take a look at this graphic from a recent paper.

Current theory has it that factors that we know are associated with atrial fibrillation  including obesity, hypertension and sleep apnea cause atrial structural abnormalities or remodeling which then create various atrial electrical abnormalities.

 

Exhaustive List of Causes

If you’d like an exhaustive list of factors associated with atrial fibrillation, you can memorize the acronym P.I.R.A.T.E.S. which is sometimes used by medical students to remember the causes of atrial fibrillation which include:

  • Pulmonary disease (COPD, PE)/Phaeochromocytoma
  • Ischemia (ACS)
  • Rheumatic heart disease (mitral stenosis)
  • Anemia (high output failure/tachycardia)/Atrial myxoma/Acid-base disturbance
  • Thyrotoxicosis (tachycardia)
  • Ethanol/Endocarditis/Electrolyte disturbance (hypokalaemia, hypomagnesaemia)/Elevated BP
  • Sepsis/Sick Sinus Syndrome/Sympathomimetics (Drugs)

And here’s a cute  mnemonic from the Family Practice Notebook using ATRIAL FIB itself (although you have to use the ph of pheochromocytoma to make the f of fib)

  1. Alcohol Abuse
  2. Thyroid Disease
  3. Rheumatic Heart Disease
  4. Ischemic Heart Disease
  5. Atrial Myxoma
  6. Lung (Pulmonary Embolism, Emphysema)
  7. Pheochromocytoma
  8. Idiopathic
  9. Blood Pressure (Hypertension)

Both of these mnemonics are a little outdated. For example, rheumatic mitral stenosis is quite rare as a cause of afib in the US but  degenerative and functional mitral regurgitation is a common cause.

Ischemic heart disease (aka coronary heart disease) isn’t felt to cause atrial fibrillation unless it results in a myocardial infarction and subsequent heart failure. Way too many cardiac catheterizations are performed on patients who present with atrial fibrillation by doctors who don’t know this.

Congenital heart defects (not mentioned in either mnemonic) especially atrial septal defects often are associated with afib

There may be case reports of pheochromocytoma (a catecholamine-secreting neuroendocrine tumor) causing afib but they are few and far between.

Finally, genetics clearly play a role in the younger patient with afib without any known risk factors. One of my patients and his twin brother both developed symptomatic afib in their 40s.

In The Chronic Afibber What Triggers An Episode?

Alas, for most afibbers we won’t identify specific reasons why you go in and out of afib although there are some triggers you should definitely avoid such as excessive alcohol.

Some of the “causes” listed in the mnemonic are acute triggers of afib episodes.

For example low potassium or magnesium (typically induced by diuretics, diarrhea or vomiting) can bring on episodes .(See my discussion on potassium and PVCS here-much of it is relevant to afib.)

And I  have definitely seen patients go  into atrial fibrillation who have acute pulmonary problems such as pneumonia, pulmonary embolism or exacerbation of COPD.  In these cases, it is felt that the lung process raises pressure in the pulmonary arteries thereby  putting strain on the right heart leading to higher right atrial pressures.

Sleep apnea is associated with afib and I have had a few cases where after identifying that a patient’s  afib always began during sleep we were able to substantially lower episodes by treatment of sleep apnea.

Pericarditis with inflammation adjacent to the left atrium not uncommonly causes  afib. This is the likely mechanism for the afib that occurs frequently after cardiac surgery. Since pericarditis may never recur (especially in the cardiac surgery patient) we think the risk of afib recurring is low in these patients.

Anything that raises stress and stimulates the sympathomimetic nervous system can be a trigger. For example, a young and otherwise healthy patient of mine went into afib after encountering a car in flames along the side of the road. We found that beta-blockers (which block the sympathetic nervous system) helped prevent her episodes.

Some patients have odd but reproducible triggers. One of my patients routinely went into afib when he ate ice cream. I had a simple , very effective treatment plan for him.

Caffeine and Chocolate

Many afibbers have been told to avoid caffeine but a recent study of 34,000 women found that there was no increased risk of afib with increasing caffeine content and no sign that any of the individual contributors to caffeine in the diet (coffee, tea, cola, and chocolate) were more likely to cause afib.

Higher chocolate consumption, in fact, has recently been linked to a lower rate of afib. An observational  study of 55 thousand Danish men and women found that those who consumed 2 to 6 servings per week of 1 oz (30 grams) of chocolate had a 20% lower rate of clinically apparent afib.

Alcohol and Atrial Fibrillation

Binge drinking has long been known to cause acute atrial fibrillation.

However, it appears that even light to moderate chronic alcohol consumption increases the risk of going into atrial fibrillation.

This graphic from an excellent recent review of the topic gives the potential mechanisms:

The review concludes that although light to moderate alcohol consumption lowers your risk of dying, any alcohol consumption increases your risk of afib.

This graph shows the relationship between dying from heart disease (red line) and risk of going into afib (blue line) and amount of alcohol consumed.

Looking at the 15 drinks per week point on the x-axis (about 2 drinks per day) we see that your CV mortality is reduced by 20% whereas your risk of afib has increased by 20%.

A better point on the x-axis is 7 (1 drink per day) which has a 25% lower CV mortality but only a 10% higher risk of afib.

Whatever caused you to go into afib the good news is that with lifestyle changes and the care of a good cardiologist chances are excellent that you can live a normal, happy, healthy , long and active life.

Etiologically Yours,

ACP