Heart Attacks and E-cigarettes: Are America’s Teens Putting Themselves At Risk?

Many of the skeptical cardiologist’s patients managed to quit cigarette smoking by using e-cigarettes . They often continue to vape, prolonging their addiction to nicotine but overall I felt they were probably better off than smoking cigarettes. However,  a couple of recent articles have me very concerned about the overall effect of e-cigarettes on public health.

The first article came from the PR department at  UCSF with the headline:

Smoking E-Cigarettes Daily, Doubles Risk Of Heart Attacks”

It focused on an abstract presented in Baltimore in February 2018 by Stanton Glantz, UCSF professor of medicine and director of the UCSF Center for Tobacco Control Research and Education. The abstract (paper yet to be published) was an observational study of about 70,000 individuals. Since it was observational the causality implied by the headline is not justified but the findings are still worrisome:

When adjusted for other risk factors, daily e-cigarette use was associated with significantly increased odds (Odds Ratio: 1.79) of having had a heart attack (myocardial infarction), as was daily conventional cigarette smoking (OR: 2.72). Former and occasional e-cigarette use were not associated with significant changes in the odds of having had a heart attack, while the same categories of cigarette smoking were associated with smaller increases in risk than for current smokers.

So e-cigarettes might be safer than real cigarettes but if you don’t quit smoking you are worse off:

“E-cigarettes are widely promoted as a smoking cessation aid, but for most people, they actually make it harder to quit smoking, so most people end up as so-called ‘dual users’ who keep smoking while using e-cigarettes,” said Glantz. “The new study shows that the risks compound. Someone who continues to smoke daily while using e-cigarettes daily has an increased risk of a heart attack by a factor of five.

Juul and The Rise In Teenage Vaping

The second article was from The New Yorker and is fascinating. Entitled “The Promise of Vaping and the Rise of Juul.” ,  it details an alarming rise in teenage vaping which often involves a particular brand of e-cigarette, Juul,  which resembles a flash drive.

Screen Shot 2018-05-22 at 12.13.01 PM
“Smoking is gross,” a high schooler said. “Juuling is really what’s up.”Photograph by Elizabeth Renstrom for The New Yorker

To Juul (the brand has become a verb) is to inhale nicotine free from the seductively disgusting accoutrements of a cigarette: the tar, the carbon monoxide, the garbage mouth, the smell. It’s an uncanny simulacrum of smoking. An analyst at Wells Fargo projects that this year the American vaporizer market will grow to five and a half billion dollars, an increase of more than twenty-five per cent from 2017. In the latest data, sixty per cent of that market belongs to Juul.

Scientists Warn of E-cigarette Health Risks 

In March, a congressionally mandated report on the health effects of e-cigarettes  from the National Academies of Sciences, Engineering, and Medicine concluded:

Evidence suggests that while e-cigarettes are not without health risks, they are likely to be far less harmful than conventional cigarettes, the report says. They contain fewer numbers and lower levels of toxic substances than conventional cigarettes, and using e-cigarettes may help adults who smoke conventional cigarettes quit smoking.

With respect to cardiovascular diseases, their conclusions were:

  1. We don’t currently have evidence that e-cigarettes increase risk of stroke or heart attack or subclinical atherosclerosis
  2. There is good evidence that in the short term the nicotine in e-cigarettes raises systolic and diastolic blood pressure and heart rate
  3. There is limited evidence that e-cigarettes increase biomarkers of oxidative stress, increase endothelial dysfunction and arterial stiffness. All of these factors are known to contribute to the development of atherosclerosis.

Long term, it is anyone’s guess what the consequences of vaping on the cardiovascular system will be.

As the New Yorker article makes abundantly clear, however, the youth of America are taking up vaping and Juuling increasingly and the National Academies are appropriately worried:

However, their long-term health effects are not yet clear. Among youth — who use e-cigarettes at higher rates than adults do — there is substantial evidence that e-cigarette use increases the risk of transitioning to smoking conventional cigarettes

Are Your Kids Vaping?

In 2015 there was a 40% chance your middle school or high school child had used e-cigarettes. The chart below from the CDC shows how rapidly rates are climbing.

The surgeon general/CDC issued a warning in 2016, writing:

E-cigarette use among U.S. youth and young adults is now a major public health concern. E-cigarette use has increased considerably in recent years, growing an astounding 900% among high school students from 2011 to 2015. These products are now the most commonly used form of tobacco among youth in the United States, surpassing conventional tobacco products, including cigarettes, cigars, chewing tobacco, and hookahs. Most e-cigarettes contain nicotine, which can cause addiction and can harm the developing adolescent brain.

Compared with older adults, the brain of youth and young adults is more vulnerable to the nega- tive consequences of nicotine exposure. The effects include addiction, priming for use of other addic- tive substances, reduced impulse control, deficits in attention and cognition, and mood disorders. Furthermore, fetal exposure to nicotine during pregnancy can result in multiple adverse consequences, including sudden infant death syndrome, altered corpus callosum, auditory processing deficits, effects on behaviors and obesity, and deficits in attention and cognition. Ingestion of e-cigarette liquids con- taining nicotine can also cause acute toxicity and possibly death if the contents of refill cartridges or bottles containing nicotine are consumed.

Stealth Vaping Devices

Vaping devices no longer clearly look like cigarettes. Here are some examples from the CDC report.

 

 

 

 

 

 

 

 

Note, however, that the Juul is not depicted.

By Mylesclark96 [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)%5D, from Wikimedia Commons
It doesn’t look like a cigarette or a device that would be facilitating your child’s addiction to nicotine. And it has a USB port so it can be recharged from a laptop.

 

 

This wasn’t an issue as far as I can tell when my children were teens but I’m pretty sure if I had teenagers I would ban vaping and would confiscate anything that resembled an e-cigarette including  flash or thumb drives that aren’t flash or thumb drives.

Skeptically Yours,

-ACP

US Health Care: Spending More But Getting Less Than Peer Countries Since 1980

Austin Frackt has a good article up at The incidental Economist discussing this graph:

life-spend

Why did the US become such an outlier; spending lots more per capita on health care but without demonstrable benefit?

A second graph shows how US longevity has not kept up with improvements noted in peer countrieslife-expectancy-1.jpg

Frakt touches on many of the proposed mechanisms for America’s divergence from the pack and the article is well worth a few minutes of your time.

Skeptically Yours,

-ACP

 

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 Skeptical Cardiologist Answers Good Questions: Retesting For Symptomatic Benign PVCs?

One of the many things I enjoy about writing this blog is the interesting comments and questions that readers post. Many of them stimulate me to better answer and inform my patients.

Here’s one such question (about premature ventricular contractions):

Wondering your opinion on retesting. I’ve had PVCs since I was 15 (63 now) and they have come and gone over the years, attributed to hormones, low potassium, stress, and dehydration/bad diet. Recently they started again and are driving me insane and none of the usual fixes are working. Two ER visits with normal EKGs and my cardiologist all say no worries. I’m thinking maybe I should have another ultrasound, buy MD doesn’t think it’s necessary. I had a perfectly normal cath in 2015 but no tests since. Your thoughts? Thank you.

This was the response I typed off the top of my head:

Good question. I consider retesting for patients who have not had documentation of “structurally normal heart” for some time and who have a significant change in their symptoms. You would qualify since no testing in 3 years and worsened symptoms.
Typically I would order a stress echocardiogram which allows a reassessment of both LV structure and function and for any blockage in the coronary arteries and I would consider some kind of monitor-a 24 hour Holter would be fine if you are having daily symptoms.
You might also consider acquiring an AliveCor device to monitor your rhythm with symptoms. I’ve written a lot about this elsewhere on this site. Unfortunately AliveCor does not identify PVCs but if you connect via KardiaPro with your physician your recordings can be viewed and interpreted by him/her.

The answer reflects my clinical practice, which is based on 30 years of experience taking care of patients with PVCs, in conjunction with regularly reading papers, reviews and guidelines in this area.

Periodically, both for specific patient problems and for blog questions, I will search the medical/scientific literature and review guideline publications to see if there is any new information that I am unaware of to ensure that my recommendations are scientifically grounded.

In this case, a more prolonged search of the literature did not yield precise guidance on the frequency of retesting of patients with benign PVCs.

This 2014 guideline comments briefly on the evaluation and treatment of PVCs without structural heart disease (SHD):

In the absence of SHD, the most common indication for treating PVCs remains the presence of symptoms that are not improved by explanation of their benign nature and reassurance from the physician.

In addition, some patients may require treatment for frequent asymptomatic PVCs if longitudinal imaging surveillance reveals an interval decline in LV systolic function or an increase in chamber volume.

For patients with  >10,000 PVCs/24 h, follow-up with repeat echocardiography and Holter monitoring should be considered.

In patients with fewer PVCs, further investigation is only necessary should symptoms increase.

It should also be recognized that PVC burden often fluctuates over time.

This initial testing approach corresponds closely to what I wrote in my post on benign PVCs here.

Retesting with echocardiography and Holter monitoring is advised for those few patients who have lots of PVCs, but the frequency of this retesting is not specified and cardiologists have to use their best judgement, balancing the cost (to patient and to society) and patient safety.  Most cardiologists will err on the side of more frequent repeat testing for a variety of reasons.

Personally, I will advise an annual echocardiogram to such patients since they are at a higher risk of developing a cardiomyopathy.

In the absence of really frequent PVCs (>10,000 per 24 hours is a nice round number, but the precise cut-off is debatable), we should probably only repeat testing if the patient recognizes a significant change in their symptoms.

The reader clearly fits into that category, and retesting in her will provide reassurance that all is still good with her heart. This, in turn, should help with managing symptoms and preventing recurrent ER visits.

The final question (and the toughest) that we could pose related to retesting is “What is the time interval that one should wait before retesting in a patient with worsened symptoms?”

For example, if the reader had a normal echocardiogram 6 months ago should we repeat it when symptoms worsen? My reflex answer would be no, but at some time interval depending on the individual characteristics of the case-patient risks for heart disease, patient anxiety levels, patient symptom severity and frequency, the answer would become yes.

Cardiologists have to answer dozens of questions like this daily.  There is no science to inform a precise answer, consequently the answers will vary wildly from one cardiologist to another depending on a variety of factors specific to the cardiologist.

Those cardiologist-specific factors are complex and sometimes controversial. Part of this makes up the art of medicine and part reflects the business of medicine. They are definitely worthy of another post when time permits.

Questioningly Yours,

-ACP

N.B. The Eternal Fiancee’ (my layperson surrogate) expressed surprise that one could have 10 000 PVCs per day. I told her that if your heart beats roughly once per second (6o beats per minute) since there are  60 x 60 x 24 = 86400 seconds in a day, your heart beats almost 90 000 times in 24 hours.

Thus, roughly  1 in 9 beats is a PVC.

Thoughts On Prolonged Bleeding Whilst Taking Baby Aspirin

I was hurriedly shaving the other day and felt a sharp stinging sensation in my philtrum.  Shortly thereafter, blood began pouring forth from the area and dribbling into my mouth.

I don’t typically name-check the area between the nose and the margin of the upper lip, but if one cuts the area (and wants to write about the experience), it is useful to have a single noun that describes it precisely.

This is not my philtrum but the graphic nicely demonstrates why the area is often called “cupid’s bow”. Courtesy of Wkipedia

The human philtrum is apparently vestigial; per Wikipedia

The philtrum (Latin: philtrum, Greek: φίλτρονphiltron, lit. “love charm”[2]), or medial cleft, is a vertical groove in the middle area of the upper lip, common to many mammals, extending in humans from the nasal septum to the tubercle of the upper lip. Together with a glandular rhinarium and slit-like nostrils, it is believed[by whom?] to constitute the primitive condition for mammals in general.

Although lacking function, it does cause a protrusion in the otherwise smooth facade of the face, and as a consequence, is at an increased risk for cuts.

Despite holding pressure on the cut for many minutes and daubing it with toilet paper, it continued to bleed. The bleeding continued on for much longer than I am use to, and after a while I realized that my bleeding was prolonged due to the aspirin I have been taking.

I’ve been following my own advice to those with documented significant atherosclerotic plaque, and have been taking 81mg aspirin daily. I began chewing daily my chewable aspirin after writing my post on the best form of baby aspirin to take. Prior to that it was only intermittently.

BARCing Up the Willow Tree

As a cardiologist I commonly hear patients complain about the nuisance of bruising and bleeding caused by the aspirin and other blood thinners I have prescribed them. Now I had joined their ranks.

Doctors mostly worry about major bleeding caused by aspirin; things like bleeding from the gastrointestinal (GI) tract, or into the head. A recent review found that baby aspirin doubles the risk of bleeding from the upper GI tract, and increases the risk of intracranial hemorrhage by a factor of 1.4.

There is relatively little concern about the type of minor bleeding I experienced. However, beginning in 2010, the Bleeding Academic Research Consortium (BARC) investigators came up with a more precise way of categorizing bleeding events, the BARC bleeding types.

By far, the most common bleeding on aspirin is the kind I had: Type 1 BARC.

Type 1: bleeding that is not actionable and does not cause the patient to seek unscheduled performance of studies, hospitalization, or treatment by a healthcare professional. Examples include, but are not limited to, bruising, hematoma, nosebleeds, or hemorrhoidal bleeding for which the patient does not seek medical attention. Type 1 bleeding may include episodes that lead to discontinuation of medications by the patient because of bleeding without visiting a healthcare provider.

Indeed, my Type 1 bleeding prompted me to skip my aspirin doses for the next few days.

Many patients do the same thing. Just this morning a patient told she had stopped taking her aspirin because she thought it was causing “little red spots” on her arms.

Does Prolonged Bleeding Mean You Are Taking Too Much Aspirin?

My philtrum persisted in bleeding, and as I felt the need to use my hands for something other than holding pressure, I put a band-aid on the area (actually a Nexcare), which temporarily stemmed the bleeding tide: I began pondering if I was taking too much aspirin.

Since aspirin is so widely used to prevent heart attacks and strokes caused by sticky platelets, why isn’t there a way to see how effective it is at making sticky platelets less sticky?  We have such methods for blood pressure meds (blood pressure levels) and cholesterol lowering drugs (cholesterol levels).

And for the older blood thinner warfarin, we have a blood test which helps us make sure the dosage of medication is keeping the blood thinning in a range that maximizes  effectiveness and minimizes bleeding risk.

It turns out there are lots of ways to measure how effective aspirin is in an individual, but no consensus on which particular method should be used, and authorities don’t recommend we make such measurements.

This article on platelet function tests lists 13 different platelet function tests, ranging from the mostly historical “bleeding time” to sophisticated tests of platelet aggregation.

The  Verify Now test (not available in the US) of platelet reactivity predicted in one study which patients would have BARC type I bleeding like mine.  The test did not predict major bleeding complications, things like GI bleeding and intracranial hemorrhage.

Those patients who had minor bleeding problems were more likely to be noncompliant, stopping their aspirin therapy.

I could easily visualize the following  scenario as the blood began pooling underneath my band-aid and progressing down my philtrum.

Let’s say I’ve just had a heart attack and had a drug-eluting stent placed in one of my coronary arteries. I’ve been started on aspirin and another anti-platelet drug. I cut myself and bleed excessively and prolongedly. I decide that the aspirin is the reason, and start skipping doses. The lower aspirin levels subsequently allow my platelets to become sticky again. As a result a clot forms in my coronary stent and a heart attack ensues.

Thus, prolonged bleeding from a cut, considered a minor side effect of aspirin therapy, could increase heart attack risk.

There is a clinically available test for aspirin effect called AspirinWorks.

The AspirinWorks Test Kit is an enzyme-linked immunoassay (ELISA) to determine levels of 11-dehydrothromboxane B2 (11dhTxB2) in human urine, which aids in the qualitative detection of aspirin effect in apparently healthy individuals post ingestion. Unlike platelet aggregation tests, which require freshly drawn blood that must be evaluated within at least four hours, the AspirinWorks Test is performed on a random urine sample that can easily be obtained in any doctor’s office.

AspirinWorks points out the putative benefits of testing for aspirin effect:

An increasing body of evidence in the medical literature overwhelmingly supports clinically significant variability in aspirin effect, which has been well-established in findings from trials, including the Heart Outcomes Prevention Evaluation (HOPE) Study and the CHARISMA trial published in Circulation (Journal) (2002 and 2008). These trials have demonstrated that:

  1. Increased levels of urinary 11dhTxB2 are associated with as much as a four fold increased risk for adverse cardiovascular events or death.
  2. Statin treatment is associated with lower concentrations of 11dhTxB2
  3. 11dhTxB2 is an independent, modifiable predictor of risk for stroke, heart attack and cardiac death (CHARISMA).

I have never ordered this test and am unaware of any other physicians ordering it on their patients.

Doctors don’t test for aspirin effect in individual patients because it is expensive and it won’t change our approach in most cases.
Taking  81 mg aspirin daily might be too high a dose to optimize the balance between bleeding and clotting in me.  If I took it every other day I might have less Type I BARC episodes. However, we don’t have any good evidence that adjusting the dosage based on aspirin effectiveness testing will improve my outcomes.
Thus, we bleeders on baby aspirin (the BOBA) of the world must find better ways of dealing with minor bleeding.
When I changed the band-aid on my philtrum several hours after the initial cut, I began actively bleeding again. This time I decided to apply ice to the area to vasoconstrict the arteries. This, plus more pressure and time, almost completely stopped the bleeding.
Another Nexcare was applied to the area, and when it was removed the next morning, the bleeding did not resume.
There are a variety of other measures that can be tried with varying degrees of success, as described here (deodorant, lip balm, listerine, Visine) and here (styptic pencils and powders, cayenne pepper, tea bag, sugar, alum-ironically this article mentions making a paste out of aspirin and applying it to the cut).
There also appears to be a thriving industry devoted to commercial  products for stopping bleeding from minor cuts outlined here.
Should We Worry About Minor Bleeding?
Ultimately, the seemingly excessive bleeding one experiences upon incidentally cutting oneself while taking aspirin is best viewed as a reassuring sign that the drug is doing its job: Your platelets are less sticky, less likely to cause bad clots that cause strokes and heart attacks.
Platelets don’t know bad from good clots, they just react indiscriminately.
The small amount of blood that exudes from superficial cuts can be scary but it can be controlled with fairly simple measures.
The little red dots my patient experiences, although unattractive, are benign.
Styptically Yours,
-ACP

AliveCor Mobile ECG : Ways To Minimize Low Voltage and Unclassified Recordings

Sometimes AliveCor’s Mobile ECG device yields unclassified interpretations of recordings. Understandably if you want to know whether your rhythm is normal or atrial fibrillation, the unclassified  classification can be very frustrating.

There are various caues of an unclassified tracing with different solutions.  Some unclassified recordings are due to a heart rate over 100 BPM or under 50 BPM and cannot be fixed. Similarly, some patients with ectopic beats like PVCS may consistently generate unclassified interpretations (see my discussion here).

Artifacts induced by poor recording techniques are common as a cause and almost always can be fixed.

These can be reduced by minimizing motion, extraneous noise, and maximizing contact with the electrodes.  Follow all the steps AliveCor lists here.

For me, the following step is crucial

  • If your fingers are dry, try moistening them with antibacterial wipes or a bit of lotion

And be aware the device needs to be near the microphone of your iPad or smartphone.

Low Voltage As Cause of Unclassified Kardia Recordings

Another cause of unclassified interpretations is a low voltage recording (which I initially discussed here.).

At the recent ACC meeting I asked Alivecor inventor and CEO David  Albert if he had any solutions to offer for those who obtain unclassified low voltage AliveCor tracings.

He told me that the cause is often a vertically oriented heart and that recording using the lead II technique can often solve the problem.

Lead II involves putting one electrode on your left knee and one your right fingers as described in this video:

Reader “J”  recently sent me a series of Kardia ECG recordings,  some of which were unclassified , some normal and one read as possible atrial fibrillation.

The unclassified and possible AF tracings looked like this:

 

They were very regular with a rate between 80 and 100 BPM but they totally lacked p waves. It was not clear to me what the rhythm was on these tracings.

Other tracings had lowish voltage but the p waves were  clearly visible  and Kardia easily classified them as normal

Lowish voltage with p waves (Type B)

 

Good QRS voltage with clear p waves ( Type B

 

Still others had improved QRS voltage with clear p waves and were also classified  appropriately as normal

 

After some back and forth emails we discovered that the ECG recordings with no p waves were always  made using the chest lead recording.   AliveCor-describes this as follows:

  • For an Anterior Precordial Lead, the device can be placed on the lower left side of the chest, just below the pectoral muscle. The bottom of the smartphone or tablet should be pointing towards the center of the body.

Mystery solved!

There is an abnormal cardiac rhythm that is regular between 80 and 100 BPM with no p waves and normal QRS called junctional tachycardia but in J’s case the absent p waves are related to the recording site.

Also, note that for this young woman the lead II voltage (Type B tracing) is much higher than the standard, lead I voltage (type A tracing).

Lead II With Pants On

After Dr. Albert told me of the advantages of Lead II I responded that it seemed somewhat awkward to take one’s pants off in order to make an ECG recording.

He immediately reached in his suit pocket and pulled out a pen-shaped device and began spraying a liquid on his left knee.

To my surprise he was able to make a perfect Lead II recording without taking his pants off!

Lessons learned from reader J and Dr. A:

  • Consider trying different leads if the standard Lead I (left hand, right hand) is consistently yielding unclassified ECG recordings
  • Try Lead II (left knee, right hand) to improve voltage and recording quality
  • You can record off your knee even with your pants on if you are prepared to spray liquids on your pants

Pantsonically Yours,

-ACP

Joe’s Cafe: A Cornucopia of Visual and Musical Delights

The coolest music venue in St. Louis in my opinion is Joe’s Cafe.

Fortunately, for the skeptical cardiologist, the venue remains fairly obscure, even to music lover’s who reside in Saint Louis.

For example, last Thursday the Eternal Fiancee’ and I, along with Doug, the Guitarist of the Band of the skeptical cardiologist (GOBOSC) and his wife were able to sit within a couple of feet of Spencer Bohren as he played roots, blues, folk and Americana on a banjo, a lap steel or two, and an acoustic guitar.

Bohren, based out of New Orleans, also sang and told stories, often at the same time.

The GOBOSC and I, being musicians, appreciated the proximity which allowed us to observe closely what Bohren did with his non-finger-pick covered fingers and thumb.

You can watch a video of Bohren relating the history of a Blues song using five guitars here:

I’ve also seen Kinky Freidman at Joe’s. I’ve been a fan of Kinky’s since I heard “Get Your Biscuits In The Oven And Your Buns In The Bed” from his 1973 album Sold American. His wikipedia entry pretty accurately summarizes his career as follows:

American singer, songwriter, novelist, humorist, politician, and former columnist for Texas Monthly who styles himself in the mold of popular American satiristsWill Rogers and Mark Twain.[2] He was one of two independent candidates in the 2006 election for the office of Governor of Texas. Receiving 12.6% of the vote, Friedman placed fourth in the six-person race.

I had forgotten about the Kinkster since reading one of his (18) detective novels a few decades ago; I figured he had retired from the music business. To my surprise one day last year, I received an email from Joe’s Cafe indicating he would be playing there on an upcoming Thursday night.

I don’t usually allow semi-celebrities to have their pictures taken with me but since I love Kinky Freidman, I made an exception for him

Bill Christman, Impresario And Connoisseur Of Signs

Joe’s Cafe is the brain child of Bill Christman, a one time sign painter, now fine artist, and lover of good live music.

Bill decides who will perform, and introduces the acts, always with a quirky sense of humor, but a stern warning that we audience members should be listening when the artist is performing, and not talking or playing on iphones.

Bill Christman (right) introducing band. I forget why he had the arab headgear and why the man is playing the trumpet on the left. It’s always interesting at Joe’s Cafe!

Christman’s studio, Ars Populi sits next to Joe’s Cafe. According to the RFT:

Christman quit the sign-painting business more than two decades ago in order to devote himself full-time to fine art — Ars Populi doubles as his studio — and today St. Louisans can find his handiwork all over town, perhaps most famously at Beatnik Bob’s Museum of Mirth, Mystery & Mayhem inside the City Museum. His homage to bohemia, Joe’s Café, is the stuff of legend in Christman’s Skinker-Debaliviere neighborhood and beyond; its sporadic schedule of music events and invite-only policy have combined to create a speakeasy vibe that — improbable as it might seem in this day and age — is uncontrived and genuine.

Arrive early to Joe’s Cafe for the best seats (although there are no “bad” seats-some do require a climb up a wooden ladder to the balcony) so you can wander through the wonder of the back yard.

The view from the balcony is quite good. Be aware, however, that the only air conditioner in the place will be blowing cold air directly on you if you sit in these particular seats. Up in the balcony you may feel sufficiently distant to chat with your friends during the performance but please don’t. Music is King at Joe’s! Go to a bar (?TGI Friday’s)  if you want to chat with your friends when musicians are playing nearby.

Words are insufficient to describe what one encounters either inside or outside Joe’s Cafe, so let’s savor some snapshots of both.

First, some relatively random shots from outside:

It has been said of the interior:

at Joe’s, you enter another dimension, a place lit by red neon and dusty yellow incandescent marquee bulbs

The Eternal Fiancee’ describes the decoration as “the interior of Joe’s Cafe is the reality of what TGI Friday’s does a bad job of imitating.”

Spencer Bohren playing one of his lap steel guitars and singing Dylan’s “Ring Them Bells” (Ring them bells for the time that flies For the child that cries When innocence dies) a mere meter away from my table. The popcorn on the table is the only food or beverage one can purchase at Joe’s and it costs one (or two) bucks.

If you end up going to Joe’s Cafe be sure and tell them the skeptical cardiologist sent you. And please, don’t tell your friends and neighbors how cool it is.

Sonically Yours,

-ACP

N.B. Here’s the info Joe’s Cafe emails provide about performances.

Here’s the Joe’s Mostly Official Facebook page https://www.facebook.com/stlouisjoescafe/
which often has better information than these emails.

Joe’s is a BYOB, BYOF music club.
Admission: $10
Doors open around 7:00
Music starts at 8:00
Alcohol consumption ends at 10:15
Recycle your own stuff
Smoking outside only
Park on Des Peres Ave. Thou shalt not annoy our neighbors.

 

Low-Fat Versus Low-Carb Diet: DIETFITS Show Both Can Work If They Are “Healthy”

In the ongoing nutritional war between adherents of low-fat and low-carb diets, the skeptical cardiologist has generally weighed in on the side of lower carbs for weight loss and cardiovascular health.

I’ve questioned the vilification of saturated fat and emphasized the dangers of added sugar. I’ve even dabbled in nutritional ketosis.

The science in  nutrition is gradually advancing and the DIETFITS study recently published in JAMA is a welcome addition.

DIETFITS is a  really well done study which provides important insights into three huge questions about optimal diet:

  1. Should we choose a low-fat or a  low-carb diet for  weight loss and cardiovascular health?
  2. Do baseline insulin dynamics predict who will respond to low-fat versus low-carb diet?
  3. Can we predict who will respond to low-fat versus low-carb by genetic testing?

The Details Of DIETFITS

Stanford investigators recruited 609 San Francisco area individuals between the ages of 18 to 50 years with BMI of 28 to 40  and randomized them to a “healthy” low-fat diet or a “healthy” low-carb diet.

During the first 8 weeks of the study, low-fat participants were instructed to reduce fat consumption to <20 gm/ day while the low carb participants were instructed to reduce digestible carbohydrate to <20 gms/day.

Then individuals were allowed to add back fats or carbs back to their diets in increments of 5 to 15 g/d per week until “they reached the lowest level of intake they believed could be maintained indefinitely.”  Importantly no explicit instructions for energy restriction were given.

The “healthy” instructions for both groups were as follows

  1. maximize vegetable intake
  2. minimize intake of added sugar, refined flours and trans-fats
  3. focus on whole foods that are minimally processed, nutrient dense and prepared at home whenever possible

Dietfits Outcomes-Diet And Weight

Major findings

  1. Total energy intake was reduced by 500-600 kcal/d for both groups
  2. The low-fat vs the low-carb intake at 12 months was 48% versus 30% for carbs, 29 vs 43% for fat and 21 vs 23% for protein.
  3. Mean 12 months weight change was -5.3 kg for low-fat vs 6-6.0 kg for low-carb which was not significantly different
  4. There was no difference between groups in body fat percentage or waist circumference
  5. Both diets improved lipid profiles and lowered blood pressure, insulin and glucose levels
  6. LDL (bad cholesterol) declined more in the low-fat group whereas HDL (good cholesterol) increased more and triglycerides declined more in the low-carb group.

Thus both diets were successful for weight loss and both improved risk markers for cardiovascular disease after a year.

DIETFITS- Can Genes and Insulin resistance Predict Best Diet?

Surprisingly, the study found no significant diet-genotype interaction and no diet-insulin secretion interaction with weight loss.

This means that they could not predict (as many believed based on earlier studies) who will benefit from a low carb diet based on either currently available genetic testing or a generally accepted measure of insulin resistance.

As the authors point out, these findings “highlight the importance of conducting large, appropriately powered trials such as DIETFITS for validating early exploratory analyses.”

DIETFITS-Perspectives

As you can imagine this study has led to quite an uproar and backlash from dedicated combatants in the macronutrient wars.

A reasoned summary and response from Andreas Eenfeldt, a low carb proponent can be found on his excellent low carb/keto Diet Doctor site here.

Eenfeldt concludes

If I’m allowed to speculate, the reason that we did not see any major additional benefit from low carb in this study is that the groups ended up so similar when it came to bad carbs. The low-fat group ended up eating fewer carbs too (!) and significantly less sugar, while the low-carb group ended with a somewhat weak low-carb diet, reporting 130 grams of carbs per day.

Eenfeldt emphasizes that low-fat diets never “win” these macronutrient dietary skirmishes:

On the whole, this study adds to the 57 earlier studies (RCTs) comparing low carb and low fat for weight loss.

From a standing of 29 wins for low carb, zero for low fat and 28 draws, we now have 29 wins for low carb and 29 draws. The wins for low fat stay at zero.

Larry Husten at Cardiobrief.org in his analysis of the study quotes a number of experts including Gary Taubes, the low carb pioneering journalist

Taubes speculates “that the weight loss may have been similar not because any diet works if you stick with it and cut calories (one possible interpretation) but because of what these diets had in common — avoid sugar, refined grains, processed foods. Whether the low-carb arm would have done even better had Gardner kept their carbohydrates low is something this study can’t say. (And Ornish [low-fat diet proponent] would probably say the same thing about fat consumption.)”

The low-fat or vegan disciples seem to have had a muted response to this study. I can’t find anything from John McDougal , Dean Ornish, Caldwell Esselstyn or Joel Fuhrman.

Readers feel free to leave comments which  link to relevant analysis from the low-fat proponents.

Dietfits-Perspective Of The Participants

Julia Volluz at Vox wrote a fascinating piece recently which involved interviewing some of the participants in this study.

She points out that although the average DIETFITS participant lost over 10 pounds, “Some people lost more than 60 pounds, and others gained more than 20 during the year.”

LOW_FAT_LOW_CARBS_DIETS1__1_

She obtained permission from the lead author, Christopher Gardner  and interviewed  “Dawn, Denis, Elizabeth*, and Todd — two low-fat dieters and two low-carb dieters — about their experiences of succeeding or faltering in trying to slim down”

LOW_FAT_LOW_CARBS_DIETS1

I highly recommend reading the entire article for details but Volluz concludes

And that leads us to one of the burning mysteries of diets: how to explain why some people fail where others succeed — or the extreme variation in responses. Right now, science doesn’t have compelling answers, but the unifying theme from the four study participants should be instructive: The particulars of their diets — how many carbs or how much fat they were eating — were almost afterthoughts. Instead, it was their jobs, life circumstances, and where they lived that nudged them toward better health or crashing.

DIETFITS-Importance of “Healthy” Diet

Most likely the success of both of these diets is due to the instruction that both groups received on following a “healthy” diet. This guidance is remarkably similar to what I advocate and is something that combatants in the diet wars ranging from paleo to vegan can agree on.

The JAMA paper only provides the description I listed above but Volluz adds that participants were instructed to:

… focus on whole, real foods that were mostly prepared at home when possible, and specifically included as many vegetables as possible, every day … choose lean grass-fed and pasture-raised animal foods as well as sustainable fish ... eliminate, as much as possible, processed food products, including those with added sugars, refined white flour products, or trans-fats … prepare as much of their own food as possible. …

Indeed, if you want to see a very detailed description of the instructional process for participants check out the very detailed description of the methods here.

Yours in Health,

-ACP

N.B. I was searching for a reasoned response to this study from the low fat camp and to my surprise came across this fascinating video featuring the lead author of the study, Christopher Gardner, on (no fat/vegan) John McDougal’s YouTube site. Gardner is clearly on the side of sustainable, local , ethical food consumption but to his credit, his research , publications and comments on DIETFITS don’t reveal this.

Unbiased, evidence-based discussion of the effects of diet, drugs, and procedures on heart disease

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