Category Archives: Diet and Heart Disease

I Am A Keto-Friendly Cardiologist And I Love Keyto

The skeptical cardiologist has become more selective with regard to who he will accept as a new patient.  In practical terms this means I now call patients who want to see me and discuss with them why they want to see me, how they were referred or heard about me, and what their expectations are.

This might seem a little odd but turns out to be an excellent way for me to meet and smooth entrance for these newbies into my practice and gather important records and recordings prior to the first visit.

Recently, when I asked one of these potential patients why they had sought me as their cardiologist, the wife told me that through her internet research she had gleaned that I was a “Keto-friendly Cardiologist.”

Given that I have challenged conventional dogma on the dangers of dietary saturated fat and cholesterol and have written about ketosis (see here and here) a few times on this blog and defended Dr. Atkins I do actually consider myself “keto-friendly”.   However my prospective patient’s wife was not aware of the skeptical cardiologist as a blog writer.

How or why I was identified as Keto-friendly cardiologist was not clear.

I realized I needed to make it perfectly clear. It is now time to come out of the keto closet.

I am a “Keto-friendly cardiologist”!

I have dozens of patients who have been very successful using very low carb/high fat diets to help them lose weight and gain control of their diabetes and hypertension.

I don’t poo poo low carb high fat diets and I think they are vey compatible with a heart-healthy existence.

(I also advocate my version of a “plant-based diet“.)

In fact, lately I’ve gone back to dabbling with a Keto Diet myself.

To aid me in the dabbling I have found a device called Keyto to be the key to success and understanding of my ketosis.

Keyto: Breath Sensor for Ketosis and Weight Loss

When I went back to dabbling with ketosis in early 2019 I was using the Keto-Mojo finger prick device to measure my blood levels of beta hydroxybutyrate. I liked the precision this offered  compared to urine dip sticks but grew to dislike the need to prick my finger and create blood loss.

About a month ago I ordered I discovered the keto breath sensor KEYTO and have found since then that  it wonderfully simplifies  the process of being on a keto diet.

Keyto costs $99 and comes in a box the size of a video cassette  case.

In the box is the sensor device, four blowing mouthpieces, a very simple user manual, a AAA battery and a cute little bag for carrying the device

Ethan Weiss, MD, a highly respected preventative cardiologist and founder of Keyto includes a welcoming message for users which summarizes the mission of Keyto:

We designed the Keyto program to help you over-achieve your weight loss and health goals. With the Keyto Breath Sensor in this box, and the Keyto App on your phone, you have the key to unlocking success. You’ll be eating delicious foods, losing weight, and many  users even report an increase in energy and focus

Using Keyto Is Simple and Convenient

Getting started with Keyto is very easy: download the Keyto smartphone app, log in and follow the straightforward directions for pairing the breath sensor with the app.

Once paired via Bluetooth making measurements is easy. It’s important to understand the breathing technique needed and to facilitate this I strongly recommend watching the brief explanatory video Weiss has provided. Basically, you want to use a normal breath and blow for 10 seconds so that you are near the end of expiration when the device makes its recording.

To initiate a measurement you push the plus sign on the main “Journey” screen in the app then push the on button on the sensor.

Usually, if the sensor has been turned on and the app is activated the app immediately connects to the sensor, occasionally I have had to turn the sensor off and on again to initiated the connection.

At this point the sensor begins  warming up, reaching a temperature of 400 degrees Fahrenheit over a period of about 80 seconds.

The app displays the progress and offers you the option of answering some questions about how you are feeling and doing on the keto diet.

I often take my BP while this is going on. Sometimes I read the New Yorker. Frequently I listen to Radiohead (Climbing Up The Walls). It takes a while. Pay attention, though. You don’t want to miss your blowing window and have to repeat the process.

 

The app will give you a warning about 10 seconds prior to the time you need to blow. The graph to the right appears when it is time to blow and you can view the sensors output as it tracks the acetone it is seeing over the 10 seconds that you blow.

At the end of the blow you wait a few seconds, eagerly awaiting your score. Will you be in Ketosis?

 

Finally, your score is revealed. In this case I was congratulated for being in light ketosis with a fat burn of “medium high.” The highest score is an 8.

You can add notes to the record of your score

If you blow a 6 the app tells you that your fat burn is high and that you are in ketosis: “metabolizing fat like a champion.”

Accuracy of Keyto

When I first began using Keyto I checked the Keyto numbers versus the beta hydroxybutyrate (BOHB)  numbers I was simultaneously getting from my Keto-Mojo meter.

I found a Keyto 3 corresponded to 0.8 BOHB, a Keyto 4 to 0.9 BOHB, and a 5 to 1.0 BOHB.  That was enough to convince me that the device was accurate and useful in measuring my level of ketosis.

Given that it is so convenient compared to a finger stick I have stopped using the Keto-Mojo completely.

My observations confirm what Weiss and Ray Wu, MD, the cofounders of Keyto describe in very lucid prose here.

In extensive user testing, Keyto is directionally consistent with the more accurate commercially available blood meter. Keyto and blood β-hydroxybutyrate trend directionally the same in the majority of cases. Both go up and down in similar magnitude at different ranges of ketosis. There are some differences which are likely due to biology – the kinetics of clearance of acetone and β-hydroxybutyrate are not identical.

Some of the differences are also likely due to how we designed the Keyto program. Our primary goal was to develop a system that would give users the information they need to know i.e. if they are in ketosis, which would ultimately help promote healthy behavior change. Therefore, we chose not to report acetone concentrations in PPM or to attempt to convert PPM to blood β-hydroxybutyrate (mmol/L). The Keyto Level system was simply more effective, motivating, and fun without adding complexity and false precision.

I can make multiple measurements throughout the day without worrying about the cost or the discomfort of a finger stick. The ability to make multiple measurements means that I am getting very rapid and frequent feed back on how my dietary and lifestyle choices are effecting my level of ketosis.

Warning! Because the device is so convenient-literally you can have it with you at all times-you may find yourself blowing into it excessively. This may irritate your friends and loved ones, especially those that aren’t on a keto diet.

Keyto is Legitimate

The Keyto website has an excellent introduction to the keto diet (keto 101) and has numerous other very helpful resources for those who seek to lose weight using the diet.

In general I get a good feeling of integrity and legitimacy from every aspect of the Keyto operation.

I have a tremendous professional respect for Ethan Weiss, the cardiologist behind Keyto. He’s very active on Twitter and is typically spot on with his comments. He’s done a podcast with Peter Attia which serves as an excellent summary of atherosclerosis and coronary artery disease. He does really good basic science research involving growth hormone.

Weiss is now doing his own podcast called Best Known Method by Keyto which I highly recommend. It is not, surprisingly, focused on the keto diet or the keyto brand but interviews thought leaders in cardiology like Ron Krauss and Lisa Rosenbaum.

If you want to read more about how the Keyto breath sensor works see here. This is a very clear and concise description of the science behind the device and it is complete with references.

Ultimately, although I consider myself a keto-friendly cardiologist, I’m most interested in the diet that helps my patients achieve  and sustain their goals of weight loss and better health. For many this is the keto diet.

And for those who find the keto diet is optimal for their health I will be advising them to acquire a Keyto breath sensor and check out the programs Keyto offers to support their health goals.

Acetonely Yours,

-ACP

Is Dean Ornish’s Lifestyle Program “Scientifically Proven To Undo (Reverse) Heart Disease?”

Supporters of vegetarian/ultra low fat diets like to claim that there is solid scientific evidence of the cardiovascular benefits of their chosen diets.

To buttress these claims they will cite the studies of Esseslystn, Pritikin and Ornish.

I’ve previously discussed the bad science underlying the programs of Esselsystn and Pritikin but have only briefly touched on the inadequacy of Dean Ornish’s studies.

The Ornish website proclaims that their program is the first program “scientifically proven to undo (reverse) heart disease.” That’s a huge claim. If it were true, wouldn’t the Dietary Guidelines for Americans, the American Heart Association, and most cardiologists and nutrition experts be recommending it?

Who Is Dean Ornish?

Dean Ornish has an MD degree from Baylor University and trained in internal medicine but has no formal cardiology or nutrition training (although many internet sites including Wikipedia describe him as a cardiologist.)

Ornish, according to the Encyclopedia of World Biographies became depressed and suicidal in college and underwent psychotherapy “but it was only when he met the man who had helped his older sister overcome her debilitating migraine headaches that his own outlook vastly improved. Under the watch of his new mentor, Swami Satchidananda, Ornish began yoga, meditation, and a vegetarian diet, and even spent time at the Swami’s Virginia center.”

Can Ornish’s Program Reverse Heart Disease?

After his medical training Ornish founded the Preventive Medicine Research Institute and has has widely promoted his Ornish Lifestyle Program.  the website of which claims:

Dr. Ornish’s Program for Reversing Heart Disease® is the first program scientifically proven to “undo” (reverse) heart disease by making comprehensive lifestyle changes.

The Ornish claims are based on a study he performed between 1986 and 1992 which originally had 28 patients with coronary artery disease in an experimental arm and 20 in a control group. You can read the details of the one year results here.and the five year results here.

There are  so many limitations to this study that the mind boggles that it was published in a reputable journal.

-Recruitment of patients. 

193 patients with significant coronary lesions from coronary angiography were “identified” but only 93 “remained eligible.” These were “randomly” assigned to the experimental or control groups. Somehow , this randomization process assigned 53 to the experimental group and 40 to the usual-care control group.

If this were truly a 1:1 randomization the numbers would be equal and the baseline characteristics equal.

Only 23 of the 53 assigned to the experimental group agreed to participate and only 20 of the control group.

The control group was older, less likely to be employed and less educated.

“The primary reason for refusal in the experimental group was not wanting to undergo intensive lifestyle changes and/or not wanting a second coronary angiogram; control patients refused primarily because they did not want to undergo a second angiogram.”

In other words, all of the slackers were weeded out of the experimental group and all of the patients who were intensely motivated to change their lifestyle were weeded out of the control group. Gee, I wonder which group will do better?

-The Intervention.

The experimental patients received “intensive lifestyle changes (<10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support).
The control group had none of the above.

Needless to say this was not blinded and the researchers definitely knew which patients were in which group.

Control-group patients were “not asked to make lifestyle changes, although they were free to do so.”

There is very little known about the 20 slackers in the control group. I can’t find basic information about them-crucial things like how many smoked or quit smoking or how many were on statin drugs.

-The Measurement

Progression or regression of coronary artery lesions was assessed in both groups by quantitative coronary angiography (QCA) at baseline and after about a year.

QCA as a test for assessing coronary artery disease has a number of limitations and as a result is no longer utilized for this purpose in clinical trials. When investigators  want to know if an intervention is improving CAD they use techniques such as intravascular ultraound or coronary CT angiography (see here) which allow measurement of total atherosclerotic plaque burden.

Rather than burden the reader  with the details at this point I’ve included a discussion of this as an addendum.

-The Outcome

Ornish has widely promoted  this heavily flawed study as showing “reversal of heart disease” because at one year the average percent coronary artery stenosis by angiogram had dropped from 40% to 37.8% in the intensive lifestyle group and increased from 42.7% to 46.1% in the control patients.

The minimal diameter (meaning the tightest stenosis) changed from 1.64 mm at baseline in the experimental to 1.65 at one year. At 5 years the minimal diameter had increased another whopping .001 mm to 1.651. 

 

 

In other words even if we overlook the huge methodologic flaws in the study the  so-called  “reversal” was minuscule.


Utlimately, dropping coronary artery blockages by <5 % doesn’t really matter unless that is also helping to prevent heart attacks or death or strokes or some outcome that really matters.

There were no significant differences between the groups at 5 years in hard events such as heart attack or death.
In fact 2 of the experimental group died versus 1 of the control group by 5 years.

There were less stents and bypasses performed in the Ornish group but the decision to proceed to stent or bypass is notoriously capricious when performed outside the setting of acute MI. The patients in the experimental group under the guidance of Ornish and their Ornish counselors would be strongly motivated to do everything possible to avoid intervention.

I’ve gotten a lot of flack for humorously suggesting that Nathan Pritikin killed himself as a result of the austere no fat diet he consumed but the bottom line on any lifestyle change is both quality and quantity of life.

If you are miserable most days due to your rigid diet you might consider that life is no longer worth living

Ornish’s Lifestyle Intervention Is Not A Trial Of Diet …And Other Points

 

Although often cited as justification of ultralow fat diet, the Ornish Lifestyle trial doesn’t test diet alone.

It is a trial of multiple different interventions with frequent counseling and meetings to reinforce and guide patients.

The interventions included things that we know are really important for long term health-regular exercise, smoking cessation, and weight management. These factors alone could account for any differences in the outcome but they are easily adopted without becoming a vegetarian.

The patients who agreed to the experimental arm were a clearly highly motivated bunch who agreed to this really strict regimen. Even in this population there was a 25% drop out rate.

Since investigators clearly knew who the “experimental patients” were and they were clearly interested in good outcomes in these patients there is a high possibility of bias in reporting outcomes and referring for interventions.

Despite all the limitations the study does raise an interesting hypothesis. Should we all be eating vegan diets?

 if Ornish really wanted to scientifically prove his approach he should have repeated it with much better methodology and much larger numbers.

Finally, this tiny study has never been reproduced at any other center.

Because of the small numbers, lack of true blinding, lack of hard outcomes and use of multiple modalities for lifestyle intervention, this study cannot be used to support the Ornish/Esselstyn/Pritikin dietary approach.

It most certainly doesn’t show that the Ornish Lifestyle Program “reverses heart disease.” Consequently, you will not find any evidence-based source of nutritional information or guideline (unless it has a vegan/vegetarian philosophy or is being funded by the Ornish/Pritikin lifestyle money-making machines) recommending these diets.

Skeptically Yours,

-ACP

N.B.1 A recent paper on noninvasive assessment of atherosclerotic plaque has a great infographic which shows how coronary artery disease progresses and how and when in the progression various imaging modalities are able to detect plaque:

I’ve inserted a vertical red arrow which shows how IVUS detects very early atheroma whereas angiography (ICA, green line) only detects later plaque when it has started protruding into the lumen of the artery.

The paper notes that “Intravascular ultrasound (IVUS)  constitutes the current gold standard for plaque quantification. Multiple studies using IVUS and other techniques have revealed a robust relation between statin therapy and plaque regression. In the ASTEROID trial coronary atheroma volume regressed by 6.8% during 24 months of high-intensity lipid therapy. A meta-analysis of IVUS trials including 7864 patients showed an association between plaque regression and decreased cardiovascular events.”

While I believe Ornish started off as a legitimate scientist several authors have pointed out that he has joined the ranks of pseudoscientific practiioners.

Here’s one analysis from Science Blogs :

In the end, the problem is that Dr. Ornish has yoked his science to advocates of pseudoscience, such as Deepak Chopra and Rustum Roy. Why he’s done this, I don’t know. The reason could be common philosophy. It could be expedience. It could be any number of things. By doing so, however, Dr. Ornish has made a Faustian deal with the devil that may give him short-term notoriety now but virtually guarantees serious problems with his ultimately being taken seriously scientifically, as he is tainted by this association. Let me yet again reemphasize that this relabeling of diet, exercise, and lifestyle as somehow being “alternative” is nothing more than a Trojan Horse. Inside the horse is a whole lot of woo, pseudoscience and quackery such as homepathy, reiki, Hoxsey therapy, acid-base pseudoscience, Hulda Clark’s “zapper,” and many others,

Feel Free To Skip Breakfast Again And Again And Again

It seems like every 2 years the skeptical cardiologist has to defend skipping breakfast.

I first described how irritating and puzzling I find the concept that skipping breakfast causes obesity and heart disease in a 2013 post entitled “Breakfast is not the most important meal of the day: feel free to skip it.” When I’m irritated with a ridiculous concept I ask lots of questions:

Why would I eat breakfast if I am not hungry in order to lose weight? What constitutes breakfast? Is it the first meal you eat after sleeping? If so, wouldn’t any meal eaten after sleeping qualify even it is eaten in the afternoon? Is eating a donut first thing in the morning really healthier than eating nothing? Why would your first meal be more important than the last? isn’t it the content of what we eat that is important more than the timing?

Most of the studies on the proposed effect of breakfast on obesity (PEBO), I pointed out, are observational studies which cannot prove causality and the few, small prospective randomized studies don’t clearly support the hypothesis.

I suggested that PEBO comes from the breakfast food and cereal industry and should be ignored.



Writing an update on my post in 2015 I referenced Melanie Warner’s excellent book on the methods of the food industry entitled “Pandora’s Lunchbox”

“Walk down a cereal aisle today or go onto a brand’s Web site, and you will quickly learn that breakfast cereal is one of the healthiest ways to start the day, chock full of nutrients and containing minimal fat. “Made with wholesome grains,” says Kellogg’s on its Web site. “Kellogg’s cereals help your family start the morning with energy by delivering a number of vital, take-on-the-day nutrients—nutrients that many of us, especially children, otherwise might miss.” It sounds fantastic. But what you don’t often hear is that most of these “take-on-the-day” nutrients are synthetic versions added to the product, often sprayed on after processing. It’s nearly impossible to find a box of cereal in the supermarket that doesn’t have an alphabet soup of manufactured vitamins and minerals, unless you’re in the natural section, where about half the boxes are fortified.”

The Kellogg’s and General Mills of the world strongly promoted the concept that you shouldn’t skip breakfast because they had developed products that stayed fresh on shelves for incredibly long periods of time. They could be mixed with easily accessible (low-fat, no doubt) milk to create inexpensive,  very quickly and easily made, ostensibly healthy breakfasts.

Unfortunately, the processing required to make these cereals last forever involved removing the healthy components.

As Warner writes about W.K. Kellogg:

“In 1905, he changed the Corn Flakes recipe in a critical way, eliminating the problematic corn germ, as well as the bran. He used only the starchy center, what he referred to as “the sweetheart of the corn,” personified on boxes by a farm girl clutching a freshly picked sheaf. This served to lengthen significantly the amount of time Corn Flakes could sit in warehouses or on grocers’ shelves but compromised the vitamins housed in the germ and the fiber residing in the bran”



In 2017 I felt compelled to revisit the topic when a New York Times piece made the case for making breakfast a feast:

The writer, Roni Rabin (who has a degree in journalism from Columbia University)  struggles to support her sense that there is a “growing body of research” suggesting we should all modify our current dietary habits in order to eat a  breakfast and make breakfast the largest meal of the day

My post entitled  “Ignore The New York Times and The American Heart Association and Feel Free to Skip Breakfast” examined the weak evidence for benefits of “mindful” eating and harms of skipping breakfast.


A new study has popped up and, of course, been widely publicized as supporting eating breakfast. Fortunately, it caught the eye of Peter Attia thus saving me from having to read the article.

Below are some of his scathing comments, taken from one of his non-lame weekly emails:

You’ve probably heard that breakfast is the most important meal of the day. “What is less commonly mentioned,” writes Alex Mayyasi in The Atlantic, “is the origin of this ode to breakfast: a 1944 marketing campaign launched by General Foods, the manufacturer of Grape Nuts, to sell more cereal.”

Seventy-five years later, here’s the latest report from the April issue of the Journal of the American College of Cardiology: “Taken together, these studies [showing a positive association between skipping breakfast and CVD and CVD risk factors] as well as our findings underscore the importance of eating breakfast as a simple way to promote cardiovascular health and prevent cardiovascular morbidity and mortality.”
What were the findings? Let’s look at a few newspapers:

  • “Want to Lower Your Risk for Heart Disease? Eat Breakfast Every Morning” (Healthline)
  • “Eating breakfast? Skipping a morning meal has higher risk of heart-related death, study says” (USA TODAY)
  • “Study: Skipping breakfast increases risk of heart disease mortality by 87 percent (FOX)”

(You may notice that all three headlines imply causality.)

Looks like General Foods was right. Time to reach for the Lucky Charms? Perhaps it’s time to put on our critical thinking cap instead. The actual study, and the media coverage of it, is a part of the Groundhog Day that is observational epidemiology (for more on the limitations of this type of research, check out Studying Studies: Part II). This was a prospective cohort study pulling data from NHANES III, looking at people who reportedly eat breakfast every day to people who never eat breakfast, and then following up with them (about 19 years later on average), tallying up the deaths from CVD and deaths from all causes.

One question to ask about the population studied is: was eating breakfast or not eating breakfast the only difference between these two groups? In other words, were there any confounding factors (for more on confounding, see Studying Studies: Part IV)? The authors reported that, “participants who never consumed breakfast were more likely to be non-Hispanic black, former smokers, heavy drinkers, unmarried, physically inactive, and with less family income, lower total energy intake, and poorer dietary quality, when compared with those who regularly ate breakfast.” Not only that, “participants who never consumed breakfast were more likely to have obesity, and higher total blood cholesterol level than those who consumed breakfast regularly.” They also had a higher reported incidence of diabetes and dyslipidemia. Read that again, please.

While the study used statistical models to “adjust for” many of these potential confounders, it’s extremely difficult (actually, it’s impossible) to accurately and appropriately adjust for what amounts to fundamentally different people. The healthy user bias (or the inverse, an unhealthy user bias) is virtually impossible to tease out of these studies (the healthy user bias is covered in more depth in Studying Studies: Part I). Not only that, you never really know what you’re not looking for. This is typically referred to as residual confounding in the literature, where other factors may be playing a role that go unmeasured by the investigators.

I haven’t even yet mentioned the misleading nature of reporting relative risk — in this case, an associated 87% (reported in the study as a hazard ratio of 1.87) — without reporting absolute risk. The question you should always ask is, 87% greater than what? To get an idea of the associated absolute risk, the number of CVD deaths in the “every day” breakfast group were 415 out of a total of 3,862 people over 16.7 years (that’s an unadjusted rate of 10.7%) while the numbers for the “never” breakfast folks were 41 CVD deaths out of a total of 336 people over 16.7 years (unadjusted rate of 12.2%). That’s an absolute difference of 1.5% over almost 17 years (annually, this is an absolute difference of 0.09%). Granted, this is before adjustment of the myriad confounders (including the biggest “risk factor” for CVD death, age, in which the “never” breakfast group was younger on average at baseline), but it gives you an idea that we’re looking at small differences even over the course of a couple of decades. This looks a lot difference on paper than an associated 87% increased risk of CVD death. (For more on absolute risk and relative risk, see Studying Studies: Part I.)

There’s more:

  • What were the participants actually eating for breakfast? We don’t know. The investigators didn’t have information about what foods and beverages they consumed.
  • Did participants change their breakfast eating (or abstaining) habits over the course of almost 20 years? We don’t know. Information on breakfast eating was only collected at baseline.
  • Could there be errors in the classification of the causes of death in the participants? It’s possible.
  • What constitutes skipping breakfast? Was it the timing of the first meal of the day? We don’t know. Participants were asked, “How often do you eat breakfast?” but there was no definition of what that means, exactly.

What’s more likely: reported skipping breakfast was a marker for a lifestyle and environment that may have predisposed these people to a higher risk of CVD death or that skipping breakfast itself causes CVD death?

Go ahead and skip all the breakfasts you want. And please forward this to the next 10 people who tell you it’s unhealthy to do so.

And ditto for this post.

Breakfastingly Yours,

-ACP

Is It Time To Stop Eating Deadly Eggs Or Time To Stop Putting Nutritional Epidemiology In The Headlines?

After carefully ingesting the new JAMA egg study that has gotten the media and many patients in a tizzy I consumed a three egg (of course with yolk) omelette.

I am happy to report that I survived the incident and am not concerned at all that my longevity has been compromised.

My 2013 summary of eggs, dietary cholesterol and heart disease (see here) is still valid and I highly recommend patients and readers read that post plus my updates on eggs with newer data (see here and here) rather than information related to the new egg study.

Although CNN and other news outlets lead with an inflammatory headline suggesting that eating those 3 eggs increased my risk of heart disease the new egg study could not possibly prove causation because it was an observational study.

Nutritional epidemiology has come under considerable criticism in the last few years for churning out these weak observational studies .John Ionaddis has been particularly vocal about these limitations, writing:

A large majority of human nutrition research uses nonrandomized observational designs, but this has led to little reliable progress. This is mostly due to many epistemologic problems, the most important of which are as follows: difficulty detecting small (or even tiny) effect sizes reliably for nutritional risk factors and nutrition-related interventions; difficulty properly accounting for massive confounding among many nutrients, clinical outcomes, and other variables; difficulty measuring diet accurately; and suboptimal research reporting. Tiny effect sizes and massive confounding are largely unfixable problems that narrowly confine the scenarios in which nonrandomized observational research is useful

This egg study contains the usual flaws that render it inconclusive:

First, the study relies on data collected from a food frequency questionnaire. Have you ever sat down and tried to recall exactly what you ate in the previous week? How accurate do you think your estimate of specific food items would be?

Ed Archer has written about the inaccuracy of the food frequency questionairres extensively. Here’s a sample from one of his devastating critiques;

In lieu of measuring actual dietary intake, epidemiologists collected millions of unverified verbal and textual reports of memories of perceptions of dietary intake. Given that actual dietary intake and reported memories of perceptions of intake are not in the same ontological category, epidemiologists committed the logical fallacy of “Misplaced Concreteness.” This error was exacerbated when the anecdotal (self-reported) data were impermissibly transformed (i.e., pseudo-quantified) into proxy-estimates of nutrient and caloric consumption via the assignment of “reference” values from databases of questionable validity and comprehensiveness. These errors were further compounded when statistical analyses of diet-disease relations were performed using the pseudo-quantified anecdotal data. These fatal measurement, analytic, and inferential flaws were obscured when epidemiologists failed to cite decades of research demonstrating that the proxy-estimates they created were often physiologically implausible (i.e., meaningless) and had no verifiable quantitative relation to the actual nutrient or caloric consumption of participants.

In addition to unreliable initial data the subjects were followed up to 30 years without any update on their food consumption. Has your food consumption remained constant over the last 30 years? Mine hasn’t. I went from avoiding eggs to eating them ad lib and without concern for my cardiovascular health about 5 years ago after looking at the science related to dietary cholesterol.

It’s Hard To Get Around Confounding Variables

Observational studies like this one try to take into account as many factors as they can which might influence outcomes. Invariably, however, there are factors which are unaccounted for, indeed unknowable, which could be influencing the results.

Individuals who were avidly trying to follow a healthy lifestyle in 1985 likely had drummed into their heads the message when these questionnaires were filled out that they needed to limit egg consumption. These individuals were also likely following other healthy habits, including exercising more, smoking less, and eating more fruits and vegetables and less junk food.

Observational studies cannot account for all these confounding variables.

At science-media centre.org they do a fantastic job of having independent experts in the field present their evaluation of scientific studies which have been popularized in the media. For the JAMA egg study their analyses can be found here.

Prof Kevin McConway, Emeritus Professor of Applied Statistics, The Open University emphasized the problem with residual confounding :

That’s because, for instance, there will be many other differences between people that eat many eggs and people that eat few other than their egg consumption.  These other differences might be what’s causing higher death rates in people who eat a lot of eggs, rather than anything to do with the eggs themselves.  The researchers point out that this has been a particular problem in some previous studies, and that this may have been a reason for inconsistency in the results of those studies.  They have made considerable efforts to allow statistically for other differences in the new study.  But they, correctly, point out that their own study is still not immune from this problem (known as residual confounding), and that therefore it’s impossible to conclude from this new study that eating eggs, or consuming more cholesterol in the diet, is the cause of the differences in cardiovascular disease rates and overall death rates that they observed.

For observational epidemiological studies like this egg study which show increased risks that are only “modest” it is highly likely that the next such study will find something different.

Eggs Are Not Eaten In Isolation

Finally, It’s important to remember that eggs, like most foods, are rarely consumed without accompanying food. This accompaniment is often bacon in the US. Eggs are often cooked in oil or butter and unless you cook them yourself you are unlikely to know the nature of the oil.

Eggs are frequently components of recipes.

We have no idea how these factors play into the results of the egg study.

So, rather than drastically cutting egg consumption I propose that there be a drastic cut in the production of weak observational nutrition studies and a moratorium on inflammatory media coverage of meaningless nutritional studies.

Eggsponentially Yours,

-ACP

N.B. For a good article on this topic read Julia Volluz of Vox on why nutritional science is so messy

The Peter Attia Drive Podcast: Longevity, Lipidology, Fructose, and How To Keep Your Face And Joints Young

Lately while exercising I’ve been binge-listening to podcasts from Peter Attia, a cancer surgeon turned “longevity” doctor.

I first encountered his writing while researching ketosis, the Atkins diet and low carb diets in 2012 and found his writing to be incredibly well-researched, detailed and helpful.

I appreciate how he never opts for oversimplification of a topic as this disclaimer at the begining of his post on ketosis indicates:

If you want to actually understand this topic, you must invest the time and mental energy to do so.  You really have to get into the details.  Obviously, I love the details and probably read 5 or 6 scientific papers every week on this topic (and others).  I don’t expect the casual reader to want to do this, and I view it as my role to synthesize this information and present it to you. But this is not a bumper-sticker issue.  I know it’s trendy to make blanket statements – ketosis is “unnatural,” for example, or ketosis is “superior” – but such statements mean nothing if you don’t understand the biochemistry and evolution of our species.

When I first came across his writing he was obsessively monitoring his beta-hydroxy butyrate levels on a ketogenic diet and was partnering with Gary Taubes to launch “the Manhattan project of nutrition”, the Nutritional Science Institute. (NUSI) . Designed to help fund good nutritional research with the ultimate goal of reducing obesity and testing the hypothesis that “all calories are equal” NUSI, unfortunately has floundered (see here.)

He’s always been very rigorous in his thinking and writing in the areas of nutrition, diet and longevity and he is quite brilliant and knowledgeable down to very basic areas of biology and metabolism.

He has started  a podcast in the last year that has featured in depth conversations with some really interesting physicians and scientists. It’s described thusly : “The Peter Attia Drive is a weekly, ultra-deep-dive podcast focusing on maximizing health, longevity, critical thinking…and a few other things. Topics include fasting, ketosis, Alzheimer’s disease, cancer, mental health, and much more.”

The first one that I listened to was with Thomas Dayspring, M.D., FACP, FNLA, a world-renowned expert in lipidology and a fantastic teacher.  If you’d like to dive deeply into cholesterol metabolism, lipid biomarkers, the mechanism of atherosclerosis and cholesterol treatment options, this is a great way to start. 

It’s a five part, 7 hour series of podcasts with the first one here

Some Eye-opening Thoughts About Processed Foods, Sugar and Fructose

Most patients are not going to be up for deep dives into lipidology but I highly recommend Attia’s discussion with Robert Lustig.

I quoted Lustig in a 2015 post entitled “Fructose and the Ubiquity of Added Sugar”

Robert Lustig, a pediatric endocrinologist has talked and written extensively about fructose as a “toxin.” You can watch him here. He’s also published a lot of books on the topic including one which identifies the 56 names under which sugar masquerades.

Lustig is a passionate, articulate and compelling speaker who has contributed significant research in this area. Most recently he has retired from clinical practice and obtained a law degree with the goal of trying to change US food policy.

Attia does a great job of interviewing him as he helps clarify points and guides  Lustig into specific real world problems such as what to feed your children.

In addition, Attia’s staff do a great job of providing “show notes” which summarize the important points, adding helpful context and links and summarizing the content.

Lustig firmly believes:

‘Fructose and glucose are not the same: the food industry would have you believe a calorie is a calorie, a sugar is a sugar…and it is absolute garbage: they are quite different, and it does matter’

Fructose is a monosaccharide that combines with the monosaccharide glucose to form sucrose, which is what most people recognize as table sugar. Processed foods commonly contain a lot of added fructose-containing sugar but also, increasingly they contain high fructose corn syrup (HFCS) which contains up to 65% fructose.

High intake of fructose goes hand in hand with consumption of processed foods. Approximately 75% of all foods and beverages in the US contain added sugars. Consumption of added sugar by Americans increased from 4 lbs per person per year to 120 lbs per person per year between 1776 and 1994. Thanks to a dramatic increase in sugar-sweetened beverages, American teenagers consume about 72 grams of fructose daily.

There are a substantial amount of observational, short-term basic science, and clinical trial data suggesting that all this added sugar, especially fructose, are posing a serious public health problem and Lustig lays out a compelling narrative in this podcast.

Lustig discusses the  fundamental biochemical differences between glucose and fructose- whereas glucose is the energy of life for all animals, fructose is “vesitigial to all animal life” and is basically a storage form of energy for plants.

Your gut bacteria are more adept at metabolizing fructose than you are

Ludwig points out that fructose accelerates the Amadori rearrangement: the browning of your body tissues and potentially contributing to aging. Fructose does not suppress the hunger hormone ghrelin as glucose dose thus “When you consume a lot of fructose your brain doesn’t know you’ve eaten and so you end up consuming more”.

Finally, Ludwig notes, fructose in contrast to glucose behaves like cocaine on the brain. Fructose specifically lights up the reward center ‘and now has been shown to induce the same physiology in the brain that cocaine, heroin, nicotine, alcohol, or any hedonic substance also generates’

There is not a clear scientific consensus on many of Lustig’s points to be honest but he is a very convincing advocate of avoiding sugar in general and fructose in particular from non-real food sources.

There’s a whole lot more in this discussion that is important to at least think about:

-A detailed discussion of NASH and NAFLD (fatty liver disease that is becoming common in obese Americans.)

-Why you need both soluble and insoluble fiber together as opposed to added soluble fiber in a supplement or processed food adition.

-How to change the food system in which 10 companies control almost 90% of the calories consumed in the US

-the importance of eliminating government food subsidies which make junk food cheap. 

-How eliminating food subsidies wouldn’t change the price of wheat or soy, only corn and sugar which where most of our dietary sugar comes from.

Maintaining Youthful Appearance And Function-The Face and The Joints

Attia’s other podcasts touch on many other issues related to longevity. I found his interview with Brett Kotlus, a New York City oculofacial plastic surgeon who specializes in both non-surgical and surgical cosmetic and reconstructive procedures of the eyes and face (How to look younger while we live longer) to be surprisingly enlightening and engrossing.

Attia’s website and podcasts are refreshingly free of advertising and any annoying teasers. This description of the Kotlus podcast is about as close to a mass-market teaser as you will see:

“Using these powerful basics, I’ve seen amazing changes.” —Brett Kotlus, referring to the 3 simple tools people can utilize to protect and rejuvenate their skin

I will not reveal the “3 simple tools” here but the show notes indicate you can skip to the 46 minute mark to hear about them.

Most recently I’ve been listening to his podcast with Dr. Eric Chehab, orthopedic surgeon and sports medicine specialist (Eric Chehab, M.D.: Extending healthspan and preserving quality of life (EP.36).)  As Attia points out, longevity is related to both healthspan and lifespan and our joint health is a major contributor to healthspan.

In this episode, Chebab “explains the measures we can take to live better and maintain our physical health through exercise and the avoidance of common injuries that prove to be the downfall for many. He also provides valuable insight for those weighing their treatment options from physical therapy to surgery to stem cells.”

Because the show notes are so detailed you can read exactly what is discussed in these podcasts and when. For example, if you wanted to skip the early discussion on Eric’s training, fellowship with the New York Giants, and the risk vs. reward of playing football (39:15) and listen to the discssion on The knee joint: common injuries, knee replacements, and proper exercise ” you know to skip to [1:00:00].

Personally, I found all of the preliminary discussion on Springsteen, Pearl Jam  and Chebab’s pre-medical school adventures fascinating.

I highly recommend recommend Attia’s podcasts: they are always enlightening, unbiased, objective and mentally stimulating.

In the world of longevity doctors he is unique in offering solid science-based recommendations and information free of hype,  bias and woo.

Skeptically Yours,

-ACP

Are Probiotics A Panacea Or Pure Hype?: The Gullible Gastroenterologist Weighs In

Please allow me to introduce myself.  I am the Gullible Gastroenterologist.  I’ve been around for a long long year, and today I have been given the opportunity by my good friend, the Skeptical Cardiologist (SC), to guest-blog on issues involving the GI tract.

As opposed to my skeptical friend, I had been very trusting by nature. But the SC has opened my eyes to the importance of fact-based medicine.  Seems to be a pretty good way to treat patients while making informed decisions based on the facts.

When the SC approached me to comment about probiotics, I jumped at the chance.  What could possibly be easier than discussing the obviously positive effects associated with ingesting good bacteria?  I mean, it says “good” right there in the description!  But then I remembered the SC’s insistence on giving weight to the facts.  And that’s when things started to get a more problematic.

What Are Probiotics?

Probiotics are defined by the World Health Organization as “live microorganisms that when administered in adequate amounts confer a health benefit on the host.”  The hope is that these ingested microorganisms will somehow affect the bacterial environment (the flora or microbiota) that already exists in our digestive tract.  This sounds great in theory, but it is important to realize that this issue is far from straight forward.

Go look in the mirror right now.  No seriously.  Do it.  I’ll wait.  I’m going to guess that you saw a human being in front of you (I hope).  Think about all the cells that made up what you saw.  All the cells in all the tissues that make up you.  It has been estimated that the total number of cells in an average 70 kg male equals 3.0 x 1013.  Now we know that bacteria normally reside in our body, but how many?  This has actually been estimated to equal approximately 3.8 x 1013 cells.  So you are made up of MORE bacterial cells than “you” cells.  Think about that for a second.  These bacterial cells are an intrinsic part of us.  Some have even gone so far as to call our gut flora a separate organ or even, when combined with our immune system, another sense akin to sight, smell, or touch.

So it is clear that the gut flora should be looked upon with respect, and we have known this for some time.  When animals are raised within isolators to create germ-free animals, we can see evidence that the gut microbiota influences normal neurological development and cognition, digestion, immune response, growth, and metabolism.  So somehow changing the gut microbiota might be effective in treating disease or alleviating certain symptoms, right?  Well, that is the idea behind many sources which claim that probiotics boost immune response, improve the health of your digestive tract, relieve dermatological conditions, cure or prevent autism, treat erectile dysfunction, and so on.

But there is a huge gap between the actual science of attempting to alter the gut microbiome and these unsupported ever-growing claims.  The main issue is that the gut microbiome is extremely complicated.  There is great individual variability between the types and concentrations of bacteria that live in my gut, and those that live in your gut.  Even the Great SC has his own unique concoction of gut flora.  In fact researchers have shown that the DNA makeup of the bacteria in an individual’s intestine is like a fingerprint and is remarkably stable in each individual.  Even after a year, these researchers were able to identify participants in their study just from the analysis of their unique gut flora.

So if we all have our unique gut flora, how can we determine what strains of bacteria to use to treat a patient for whatever ailment we are trying to cure?  What dosage or concentration should we use?  By what route should we introduce our special concoction?  Maybe more importantly, is any of this safe for us?  Can probiotics actually do us harm?

This becomes even more problematic due to the under regulation of the sources of these probiotics.  When we obtain these probiotics from various sources, it’s hard to know exactly what is in these products.  Multiple studies have found discrepancies between what we see on the label and what is actually in the bottle.  In 2015, an analysis of 16 probiotic products found that only one of them matched the bacterial species reported on the label.  Furthermore, if we are trying to somehow alter our bacteria microbiota, we would optimally want live bacteria in the product, and we know that this is not always the case.

Gastrointestinal Benefits Of Probiotics

So from a gastrointestinal perspective, what are the scientifically proven health benefits of probiotics?  These appear to be few and far between.  The majority of the studies have failed to reveal any benefits in individuals that are already healthy.  There seems to be no evidence that people with normal gastrointestinal tracts benefits from these products.

What about folks that are not healthy?  Can probiotics cure a gastrointestinal disease or a condition?  

Many people with irritable bowel syndrome (IBS) come to see the Gullible Gastroenterologist every day.  Although some individual studies have shown some positive effect from probiotics on the symptoms that can be associated with IBS, there is not enough data to recommend any particular strain of bacteria for this condition, and these studies are even more problematic given that even the placebo rate for treatment of IBS averages approximately 40%.

For patients with ulcerative colitis, a disease that causes abnormal inflammation in the large intestine, some small studies have suggested some potential benefits, but combining the results of these studies together does not prove any reliable benefit.

There has been no proven benefit regarding the use of probiotics in Crohn’s disease, a condition similar to ulcerative colitis that can affect anywhere in the gastrointestinal tract.

Small controlled studies do suggest that a probiotic preparation called VSL#3 can be effective in a condition called Pouchitis.  This is a specific condition that can affect patients with ulcerative colitis that have undergone a certain surgery to treat the disease.

There is no evidence to suggest that probiotics are effective in treating celiac disease.

Probiotics And C. difficile Infection

And now we get to the intriguing topic of Clostridium difficile associated colitis.  Clostridium difficile infection typically occurs in patients who have received antibiotics for therapy for bacterial infections elsewhere in the body, pneumonia for example.  The antibiotics can alter the bacterial flora of the gut leading to overgrowth of the C. difficile bacteria.  This overgrowth leads to production of a toxin and subsequent inflammation of the colon.  This bacteria can form spores and so in some patients this condition can be very difficult to treat, resulting in multiple recurrences. 

One of the treatments for recurrent C. difficile infection involves fecal transplantation: transferring stool from a healthy patient to the affected individual. 

The Gullible Gastroenterologist had the opportunity to participate in a fecal transplantation procedure.  The stool from a related donor was prepared in a blender by an infectious disease specialist colleague of mine (this is the reason I absolutely do not attend cocktail parties hosted by that particular physician).  I performed a colonoscopy on the patient and the stool mixture was instilled into the patient’s colon. 

The patient did well with no recurrences, and fecal transplant does appear to be a promising tool in the armamentarium in treatment of recurring C. difficile infection.  That being said, there is insufficient data to support routine use of probiotics for prevention of C. difficile colitis or for treatment of active C. difficile colitis.

Why Are Probiotics Ineffective?

So there is little convincing evidence that probiotics positively effect gastrointestinal disorders.  One reason might be that bacteria from a probiotic supplement might not actually succeed in colonizing the human intestinal tract.  A recent study concluded that in some patients, probiotic strains could be identified in samples obtained from some study participants, but in others, those probiotic strains were undetectable. 

In another study, researchers looked at the fecal microbiome in patients that had received antibiotics.  Normally, a person’s microbiome will recover on its own over time after receiving antibiotics.  This usually takes about 21 days without any intervention.  Surprisingly, administering probiotics to these subjects actually delayed recovery of the microbiome to the pre-antibiotic state to greater than five months.  What does this mean?  Is this good?  Is this bad?  The answer is that we just don’t know.  Yet.

Harm From Probiotics?

Can probiotics do harm?  Although these agents are generally felt to be safe in healthy individuals, we don’t know the long term consequences.  Furthermore, probiotics should be used with caution in patients with chronic disease, are immunocompromised, or are otherwise vulnerable (such as elderly patients).

Bottom Line: More Research Needed Before Usefulness Of Probiotics Proven

So the bottom line?  Research on the fecal microbiome is certainly exciting.  This area of study definitely has the potential to be very important and likely holds the key to discovering the underlying pathophysiology to many conditions. 

But in the year 2019, we just do not have enough information to determine which preparations may be helpful, which patients should be targeted, and how. 

Although I am hopeful that someday probiotics might be an effective tool in treating some of the diseases and conditions that my patients suffer from today, I am just not gullible enough to buy into the hype associated with unsubstantiated claims regarding their usefulness until we learn much much more.

Gullibly yours,

DSL


The Gullible Gastroenterologist,

Dave Lotsoff,  lives south of Delmar in University City, Missouri  and when he’s not singing like Jim Morrison for the skeptical cardiologist’s band he practices gullible clinical gastroenterology  in St. Louis.

-ACP

N.B. Probiotics have also been promoted for lowering blood pressure and reducing risk of cardiovascular disease but the proof of benefit is similar to that for GI problems-severely lacking.

It’s far too early to recommend probiotics  for preventing or treating any chronic diseases.

Is Trump’s USDA Making School Lunches Great Again?: Not Until They Stop Mandating Low Fat or Non Fat Milk

In 2010 President Obama signed into law the “Healthy, Hunger-free kids  act (HHKA) of 2010” which funded child nutrition programs and free school lunch programs in schools. New nutrition standards for schools were a point initiative of then First Lady Michelle Obama as part of her fight against childhood obesity and her “Let’s Move” initiative.

In May of 2017, President Trumps’s new secretary of agriculture, Scotty Perdue, issued a proclamation (Entitled Ag Secretary Perdue Moves To Make School Meals Great Again) which pledgee to loosen some of Obama’s school nutrition standards with respect to whole grains, salt and milk.

These changes have been finalized recently and have received considerable criticism. For example, Vox’s Julia Belluz wrote a piece entitled  “The Trump administration’s tone-deaf school lunch move” with a subtitle implying that the USDA’s loosening of standards would contribute to already soaring childhood obesity rates.

Belluz summarized the changes

That means 99,000 schools, feeding 30 million kids, can offer 1 percent chocolate and strawberry milk again, more refined white flour products, and, most importantly, freeze sodium levels in school lunches instead of reducing them further.

Criticism of the loosening implies that the original school lunch standards were appropriate and based on state of the art nutritional science, but were they?

The HHKA relied on guidance from the Institute of Medicine which established a committee to put together its report which was published in 2009 and was heavily based on the scientific guidance provided in the 2005 Dietary Guidelines for Americans and the IOM’s Dietary Reference Intake books”

Unfortunately, the 2005 Dietary Guidelines for Americans were not privy to  dramatic changes in our understanding of nutritional science which have occurred in the 13 years since they were written.

The IOM report copied the 2005 DGA in recommending the consumption of low fat or non fat dairy and defined low fat as 1%.

To achieve its aim of reducing saturated fat intake to <10% the IOM chose to force schools to only utilize low fat or skim milk.

 

The IOM and school lunch program recommended eliminating whole milk entirely and only allowing

-fat-free (plain or flavored) or

-plain low-fat (meaning 1%) milk

In 2018 it is very clear to anyone who examines the relevant data (see here, here and here) that dairy fat, despite being predominantly saturated fat is not associated with higher rates of cardiovascular disease, obesity, diabetes or total mortality.

A 2013 editorial in JAMA Pediatrics from Ludwig and Willet challenged recommendations for children to consume 3 glasses of low fat or non fat milk daily and noted:

Remarkably few randomized clinical trials have examined the effects of reduced-fat milk (0% to 2% fat content) compared with whole milk on weight gain or other health outcomes. Lacking high-quality interventional data, beverage guidelines presume that the lower calo rie content of reduced-fat milk will decrease total calorie intake and excessive weight gain.. However, a primary focus on reducing fat intake does not facilitate weight loss compared with other dietary strategies, as shown in observational studies and clinical trials, perhaps because reduced-fat foods tend to have lower satiety value.

Therefore, one of the key components of the HHK is misguided and not science-based.  It has in effect committed all of our children to a vast experiment with unknown health consequences.

How Do New USDA Guidelines Effect Dairy?

The change the USDA recently announced is to allow flavoring in 1% milk. Perdue is quoted as saying:

Because milk is a critical component of school meals, and providing schools with the discretion to serve flavored, 1 percent fat milk provides more options for students selecting milk as part of their lunch or breakfast, I am directing USDA to begin the regulatory process to provide that discretion to schools.

Prior to the mandated changes, the IOM report noted that dairy intake in children was predominantly from milk with >1% dairy fat.

17 percent of the total milk intake was from unflavored 2 percent milk, 16 percent from unflavored whole milk, and 9 percent from flavored milk

The dairy industry basically demanded the right to flavor 1% milk because the mandate to force all school children to drink low fat or skim milk has resulted in less children drinking milk.

And the government’s solution to making unpalatable skim milk tastier to children is to add sugar, something we have learned in the last decade we should not be doing to our food.

As Ludwig and Willet noted:

Consumption of sugar-sweetened, flavored (eg, chocolate) milk warrants special attention. While limit ing whole milk, some healthy beverage guidelines con done, and many schools provide, sugar-sweetened milk, with the aim of achieving recommended levels of total milk consumption in children. Not surprisingly, children prefer sweetened to unsweetened milk when given the choice, leading to a marked increase in the proportion of sweetened milk consumption in recent years. This trend may reflect, to some degree, compensation for the lower palatability and satiety value of fat-reduced milk. However, the substitution of sweetened reduced-fat milk for unsweetened whole milk—which lowers saturated fat by 3 g but increases sugar by 13 g per cup—clearly undermines diet quality, especially in a population with excessive sugar consumption.

The bulk of the dairy industry actually prefers you and your children drink skim milk (see here) and they are happy to adulterate the tasteless, nutritionless beverage with anything that makes it more palatable.

Witness this quote from AgWeb:

This is great news, not only for dairy farmers and processors, but also for schoolkids across the U.S.,” says John Rettler, president of FarmFirst Dairy Cooperative. “This is a step in the right direction in ensuring that school cafeterias are able to provide valuable nutrition in options that appeal to growing children’s taste buds. Their good habits now have the potential to make them lifelong milk-drinkers.”

Adding sugar to mandated unpalatable low fat milk might increase consumption of the beverage but it is definitely not a  step forward for our kid’s health.

This unethical, unscientific experiment might be contributing already  to higher rates of childhood obesity and diabetes.

Making Skepticism Great Again,

-ACP

N.B. To help understand how skim milk despite having less calories than whole milk could actually worsen obesity Ludwig and Willet provide the following instructive  paragraph:

Suppose a child, who habitually consumes a cup of whole milk and two 60-kcal cookies for a snack, instead had nonfat milk. Energy intake with that snack would not decrease if that child felt less satiated and consequently ate just  extra cookie. Rather than weight loss, this substitution of refined starch and sugar (ie, high glycemic index carbohydrate) for fat might actually cause weight gain. Consumption of a low-fat, high glycemic index diet may not only increase hunger, but also adversely affect energy expenditure compared with diets with a higher proportion of fat. In an analysis of 3 major cohorts, high glycemic index carbohydrates, such as refined grains, sugary beverages, and sweet desserts, were positively associated with weight gain, whereas whole milk was not. Of particular relevance, prospective studies in young children, adolescents, and adults observed the same or greater rates of weight gain with consumption of reduced-fat compared with whole milk, suggesting that people compensate or overcompensate for the lower calorie content of reduced-fat milk by eating more of other foods.

full text available here.

The Pearson Potato Theory of Obesity

The skeptical cardiologist developed “Pearson’s Potato Hypothesis” aka the potato theory of obesity a few years ago but became bogged down in frying oil and never published it.

Now I’m really glad I never got around to finishing my post on the theory-it appears that defenders of the potato are legion and vocal. ConscienHealth points out that a NY Times piece on the dangers of french fries quoted a Harvard epidemiologist  (Eric Rimm) as calling potatoes “starch bombs” and weapons of “dietary destruction.”

Potatoes rank near the bottom of healthful vegetables and lack the compounds and nutrients found in green leafy vegetables, he said. If you take a potato, remove its skin (where at least some nutrients are found), cut it, deep fry the pieces in oil and top it all off with salt, cheese, chili or gravy, that starch bomb can be turned into a weapon of dietary destruction.

The article goes on to recommend portion size control when dealing with French fries and further quoted Rimm:

“There aren’t a lot of people who are sending back three-quarters of an order of French fries. I think it would be nice if your meal came with a side salad and six French fries.”

Apparently the notion of limiting one’s French fries is abhorrent to many and Rimm has been attacked by thousands in the twitter-sphere.

I happen to think he’s right so I’ll go out on a limb here and post the essence of my theory without all the backing references and statistics with which I had hoped to buttress it.


Pearson Potato Theory of Obesity:

Because potatoes are cheap,  restaurants add lots of them to dishes to make the dishes seem larger and (to some) better and more satiating. Because the potatoes are so gosh darn tasty when sliced up thinly and fried and salted patrons can’t resist eating them even when they are not hungry. Eating any food when you are full is a recipe for….obesity.


To illustrate this issue I’ve started noting what restaurants serve along with the main dish that I’m interested in.

The vast majority of time breakfast orders come with fried potatoes like those below that came with the egg dish that I ordered.potato egg

I was sorely tempted to eat all these fried potatoes although full from my egg dish because when cooked properly the combination of the crispy fat, salt and warm fluffy potato interior is irresistible. Instead I ate just a few and put the rest in a to-go box, took them home, weighed them on a scale and took this picture.

IMG_8758

Interestingly, the weight of the potatoes that I had not consumed was 150 grams which is roughly equivalent to a large order of fries at McDonald’s. A large order of McDonald’s fries gives you 500 calories with 66 grams of carbohydrates,.

Thus, if I had not been disciplined that morning I likely would have ended up consuming more calories in fried potatoes than the main dish and over half of the calories I consume in a typical full day.

French fries (and their (equally addictive to me) cousin the potato chip) are the side for almost all hamburgers and sandwiches served in the US thus the possibility of unintended excess starch bomb consumption extends from breakfast to lunch to dinner in meals consumed outside the home.

Sweet Potatoes Versus Potatoes

In 2015 I pointed out that sweet potatoes which are embraced by nutrition experts are very similar nutritionally to potatoes.

A serving of either one provides 37 grams of carbohydrates and 4 grams of protein. Sweet potatoes have more fiber ( 6 grams vxs 4 grams) but more sugars (12 grams vs 2 grams.)

The Harvard School of Public health has decided potatoes are not a vegetable:

“However, potatoes don’t count as a vegetable on Harvard’s Healthy Eating Plate because they are high in carbohydrate – and in particular, the kind of carbohydrate that the body digests rapidly, causing blood sugar and insulin to surge and then dip (in scientific terms, they have a high glycemic load).”

but gives sweet potatoes a pass.

If sweet potatoes were as ubiquitous as potatoes and became a staple of fast food restaurants and a side for any and all dishes (and if they were separated out from the rest of the vegetable world), I suspect they would also be associated with weight gain.

If, on the other hand, potatoes were not markers of fast, tasty, and easily prepared and consumed food and were only eaten at trendy locavore restaurants or prepared at home, I think they would no longer be associated with obesity.

So, yes it does make sense to ask for a side salad and limit your fries to six (or perhaps seven on days of debauchery) in place of the typical mountain of potato if you are seeking weight loss.

Spudlimitingly Yours,

-ACP

Life’s Simple 7 And The Prevention Of Atrial Fibrillation

In 2010 the AHA came up with “Life’s Simple 7”-seven modifiable health behaviors and biological factors- as part of its 2020 impact goal to improve the cardiovascular health of all Americans by 20% while reducing deaths from cardiovascular disease (CVD) and stroke by 20%.

The seven factors (LS7) were smoking, body mass index [BMI], physical activity, diet, total cholesterol, blood pressure, and fasting blood glucose, Attainment of optimal LS7 status has been associated with a reduced incidence of coronary heart disease, stroke, and heart failure (HF).

A recent observationsl study found that high LS7 scores was associated with a lower risk of developing atrial fibrillation

Each individual component was categorized as poor, intermediate, or ideal according to the American Heart Association’s LS7 criteria.1 Ideal levels of health factors were: nonsmoker or quit >1 year ago; body mass index <25 kg/m2; blood pressure <120/80 mm Hg; total cholesterol <200 mg/dL; fasting blood glucose <100 mg/dL; ≥150 min/week of physical activity; and a healthy diet score (≥4 components). Study participants who were treated to target levels for hypercholesterolemia, hypertension, or diabetes mellitus were classified as intermediate for the respective health factor. An overall LS7 score ranging from 0 to 14 was calculated as the sum of the LS7 component scores (2 points for ideal, 1 point for intermediate, and 0 for poor). This score was classified as inadequate (0‐4), average (5‐9), or optimum (10‐14) cardiovascular health.

I found this figure from the paper particularly interesting

 

Notice that there is a substantially lower risk of AF with lower BMI , blood sugar and blood pressure  but no relationship between the diet score and AF risk.

Clearly if you can get and keep your body weight down (which improves  blood pressure and diabetes risk) you will be in a lower risk category for atrial fibrillation.

On the other hand, having a total cholesterol <200 mg/dl is not associated with lower  risk of AF and in fact having an ideal score on this parameter is associated with higher risk. A total cholesterol is really not something that is a good marker for CV health and should be eliminated from the Life’s Simple 7 goals.

Even more enlightening is the total lack of any association between “healthy” diet and atrial fibrillation.

The healthy diet score was calculated as the sum of the scores for each of 5 individual components: fruits and vegetables (≥4.5 cups per day), fish (≥2 3.5‐oz servings per week), fiber‐rich whole grains (≥3 1‐oz‐equivalent serving per day), sodium (<1500 mg/day), sugar‐sweetened beverages (≤450 kcal/week). The range is from 0 to 5, with a lower score being unhealthy.

Taken in conjunction with studies showing reduced AF recurrence after weight loss it seems very clear that the single best thing obese afib patients can do to prevent recurrence is lose weight.  And it doesn’t matter what diet they utilize to accomplish the weight loss.

Skeptically Yours,

-ACP

A Heart Healthy Egg Nog Holiday Toast From Dr. and Mrs. Skeptical Cardiologist!

The skeptical cardiologist wrote a post extolling the virtues of egg nog back in 2013.

Today I’m reposting it and wishing all my readers and patients a great Christmas and a fantastic 2019.

IMG_2051-1



It’s Christmas Eve and you are starting to make merry. Time to break out the egg nog? Or should you eschew this fascinating combination of eggs, dairy and (often) alcohol due to concerns about heart disease?

egg

    • Cardiac deaths

increase in frequency

    • in the days around Christmas.

Could this be related to excessive consumption of egg nog?

Egg nog is composed of eggs, cream, milk and booze. All of these ingredients have become associated with increased risk of heart disease in the mind of the public.
Nutritional guidelines advise us to limit egg consumption, especially the yolk, and use low-fat dairy to reduce our risk of heart disease

A close look at the science, however, suggests that egg nog may actually lower your risk of heart disease.

Eggs are high in cholesterol but as I’ve discussed in a previous post, cholesterol in the diet is not a major determinant of cholesterol in the blood and eggs have not been shown to increase heart disease risk.

Full fat dairy contains saturated fat, the fat that nutritional guidelines tell us increases bad cholesterol in the blood and increases risk of heart attacks. But some saturated fats improve your cholesterol profile and organic (grass-fed, see my previous post) milk contains significant amounts of omega-3 fatty acids which are felt to be protective from heart disease.
Milk and dairy products are associated with a lower risk of vascular disease!

Whether you mix rum, brandy, or whisky into your egg nog or you drink a glass of wine on the side you are probably lowering your chances of a heart attack compared to your abstemious relatives. Moderate alcohol consumption of any kind is associated with a lower risk of dying from cardiovascular disease compared to no alcohol consumption.

So, drink your egg nog without guilt this Holiday Season!
You’re actually engaging in heart healthy behavior.

Eggnoggingly Yours,

-ACP