Tag Archives: heart attacks

Why Are The Dutch So Heart Healthy and Happy (And Tall)? Part I: Is It Their Diet?

The Skeptical Cardiologist and his  eternal fiancee’ recently spent 5 days in the Netherlands trying to understand why the Dutch are so happy and heart healthy.

We were driven by Geo (former statin fence-sitter) from Bruges to Haarlem, a city of 150,000, which lies about 15 km west of Amsterdam and about 5 km east of the North Sea.

 

Haarlem is one of the most delightful towns I’ve ever stayed in.

 

 

I was struck by  the beauty of its architecture, its canals and the happiness, height and friendliness of its inhabitants.

I was lucky enough to have a bike at my disposal. One day I set off randomly, and after 20 minutes of riding on delightfully demarcated bike lanes, I scrambled up a sand dune and looked out at the North Sea.

Just down the road was the  beach resort of Zandvoort, where one can enjoy sunbathing, surfing or a fine meal while gazing at a glorious sunset.

 

 

 

 

Like Amsterdam, which is a 15 minute train ride away, bikes and biking abound in Haarlem, but unlike Amsterdamers, the Haarlemers were universally engaging, polite and friendly. Everything and everyone seemed clean, well-organized, relaxed and pretty…and, well, …happy.

The Dutch High Happiness Rating

The World Happiness Report 2017, which ranks 155 countries by their happiness levels, was released in March of this year at the United Nations at an event celebrating The International Day of Happiness.

The report notes that:

Increasingly, happiness is considered to be the proper measure of social progress and the goal of public policy

Norway was at the top of the happiness list but

All of the other countries in the top ten also have high values in all six of the key variables used to explain happiness differences among countries and through time – income, healthy life expectancy, having someone to count on in times of trouble, generosity, freedom and trust, with the latter measured by the absence of corruption in business and government.

The top 4 were closely bunched with Finland in 5th place, followed by the Netherlands, Canada, New Zealand, and Australia and Sweden all tied for the 9th position.

Despite the immense wealth of Americans, the report notes:

The USA is a story of reduced happiness. In 2007 the USA ranked 3rd among the OECD countries; in 2016 it came 19th. The reasons are declining social support and increased corruption  and it is these same factors that explain why the Nordic countries do so much better.

Dutch children seem to be especially happy.

A UNICEF report from 2013 found that Dutch children were the happiest of the world’s 29 richest industrialized countries.  America ranked 26th, barely beating out Lithuania and Latvia.

Cardiovascular Disease in The Netherlands

Ischemic heart disease (IHD) deaths are due to blockages in the coronary arteries. Typically, this comes from the build up of atherosclerotic plaques in the arterial system and in most countries heart attacks from this process are the major cause of death.

The Netherlands has the third lowest rate of IHD deaths in developed countries, only slightly higher than France and less than half the rate of the USA.Screen Shot 2017-07-26 at 10.53.26 AM

In all developed countries over the last thirty years we have seen a marked drop in deaths due to IHD. In The Netherlands it has dropped 70% and the rate in 2013 was nearly as low as France’s rate.

In addition, the Netherlands has a very low rate of deaths from  hypertensive heart disease. This table from 2008 shows that they are second only to Japan and their mortality rate is a third of that in the US.

A recent update noted

The current Dutch age-standardised mortality from circulatory disease is 147 per 100,000, and only Spain and France have lower cardiovascular mortality rates (143 and 126 per 100,000, respectively). In all other European countries, including for instance Switzerland and Greece, cardiovascular mortality is higher [26].

What factors could be causing all this happiness and heart healthiness?

The Seemingly Horrid Dutch Diet

We have been programmed to believe that heart attack rates are related to saturated fat in our diets.

The fact that the French consume lots of saturated fat and rank so low in IHD deaths has been called the French Paradox as it seems to contradict the expected association.

One thing is clear-the Dutch are not following a whole foods, plant-based diet. They are among the world leaders in consumption of both fat and sugar as the graph below indicates.

While in The Netherlands I sought out raw herring,  a dish which Rick Steves and others indicate is a Dutch obsession.

Since there is evidence that fish consumption, especially fatty ones like herring and mackerel, is associated with a lower risk of coronary heart disease, perhaps this was protecting the Dutch.

I didn’t see much herring consumption in Haarlem (a native Haarlemer informs me that the Dutch raw herring consumption might be confined to older generations or tourists).

It turns out that the Dutch aren’t meeting their own nutritional guidelines for healthy food .

The recommendation to eat fish at least twice a week, of which at least once fatty fish such as salmon, herring or mackerel, is followed by a mere 14 percent of the population. Less than 25% of them meet the recommended daily amount of fish, fruit, and vegetable consumption.

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purple bar=women yellow bar=men orange bar= total

They do catch and export a lot of fish and shellfish and are in the top 10 of seafood exporting countries (99% of all those mussels consumed in Belgium come from The Netherlands).

And, to my great surprise, they eat lots of French, or as I have started calling them, Flanders fries.

 

I personally witnessed  massive amounts of cheese and butter consumption.

In fact, the Dutch average 15% of calories from saturated fat, which is far above the 10% recommended by the Dietary Guidelines for Americans.

A recent analysis of Dutch fat consumption found:

The mean baseline intake of total saturated fatty acids (SFAs)  in the population was 15.0% of energy. More than 97% of the population exceeded the upper intake limit of 10% of energy/d as recommended by the Health Council of the Netherlands.

The Dutch weren’t eating so-called healthy fats as “The main food sources of SFAs were cheese (17.4%), milk and milk products (16.6%), meat (17.5%), hard and solid fats (8.6%), and butter (7.3%).”

Surprisingly, the more saturated fat the Dutch consumed, the LOWER their risk of death from IHD:

After multivariable adjustment for lifestyle and dietary factors (model 4), a higher intake of energy from SFAs was significantly associated with a 17% lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93)

The Dutch Paradox

Data shows that  the Dutch are eating lots of saturated fat from dairy and meat, but it appears to be lowering their risk for heart attacks

Yes, despite 40 years of high saturated fat consumption, the Dutch have seen a 70% drop in mortality from heart attacks. Their rate of dying from ischemic heart disease is lower than the US and only slightly higher than the French.

Thus, rather than talk about a French paradox, we should be talking about the Dutch paradox.

For the French paradox many theories, both fanciful and serious,  have been proposed

The one most laypeople remember (due to a 60 Minutes episode in 1991) is that the French are protected by their high red wine consumption. Although this theory proved a great boon to the red wine industry (sales rose 40% the year after Morley Safer made his presentation on 60 Minutes), it has never had any serious scientific credibility.  Current thinking is that all forms of alcohol in moderation are equally protective.

Others have proposed garlic or onion or faux gras consumption. My own theory for the French is that it is fine cheese and chocolate consumption that protects them.

In subsequent posts I’ll lay out the evidence for my startling new theory to explain the Dutch paradox.

 

 

The Widowmaker Documentary: A Need For Heroes and Villains Detracts From The Truth

The documentary, The Widowmaker (available on Netflix streaming)  should definitely be watched by everyone.

It presents some great information on dying suddenly from heart attacks in an entertaining way.

It makes two important points: coronary stents don’t prevent heart attacks and coronary scans can identify advanced coronary artery disease before heart attacks happen.

I am in total agreement with these two points and have made them several times in previous posts (here and here).

The film is a work of advocacy, however, and twists the truth to prove its underlying theory: that greedy doctors and hospitals are choosing to “push” expensive coronary stents that do no good until you are having a heart attack. Also, that doctors and hospitals are also somehow suppressing the use of coronary calcium scans, which could prevent millions of heart attacks and deaths.

Creating black and white heroes and villains in documentaries makes for riveting entertainment, but often at the cost of sacrificing the truth.

Let’s look at the  villains that The Widowmaker presents.

First up is Julio Palmatz. Dr. Palmatz is a vascular radiologist who invented, along with Dr. Shatz, one of the three primary stents that ultimately gained widespread clinical usage. The Widowmaker implies that Palmatz was THE stent developer, and follows Julio as he revisits the garage in Texas where he developed prototypes for the slotted tube stent.

At this point in the movie, it would be understandable if you thought Julio was going to be one of the heroes. He seems very personable as he describes the inspiration for his stent design and points out the area in the garage where his work bench stood.

However, the documentary wants, ultimately, to portray Palmatz as greedy, unconcerned about patient welfare, and in the pocket of wealthy investors.

He has done well financially because the patent on his coronary stent was eventually sold to Johnson and Johnson for millions (and he is interviewed on the grounds of his Napa Valley vineyard).

A recent scholarly analysis of the process of the development of stents differs with this portrayal of Palmatz:

“We found that the first coronary artery stents emerged from three teams: Julio Palmaz and Richard Schatz, Cesare Gianturco and Gary Roubin, and Ulrich Sigwart. First, these individual physician-inventors saw the need for coronary artery stents in their clinical practice. In response, they developed prototypes with the support of academic medical centers leading to early validation studies. Larger companies entered afterwards with engineering support. Patents became paramount once the technology diffused. The case of coronary stents suggests that innovation policy should focus on supporting early physician-inventors at academic centers.”

Although stents ultimately have become over-utilized, they represent a tremendous invention and contribution to cardiac care.

In the setting of acute heart attacks, stents are clearly life saving and thousands of patients have had their clinical angina or claudication greatly relieved when stents are utilized appropriately for blocked coronary and peripheral arteries.

Consequently, Palmatz and many of the other interventional cardiologists who developed and performed early studies on coronary stents are widely considered heroes by the vast majority of knowledgeable cardiologists.

There is no evidence that they have colluded with industry to inappropriately promote stents or to suppress utilization of methods for early diagnosis and prevention of coronary artery disease.

The documentary then switches to characterizing the world of cardiology after stents were approved by the FDA in the early 90s.

There clearly was (and is) an irrational exuberance about stents and some of this sprang from excellent reimbursement for doing the procedures.

The focus moves to Mt. Sinai Hospital in Manhattan, and arguably the busiest interventional cardiologist in the world, Samir Sharmin.

The movie implies that Mt. Sinai was going broke until it began performing lots of catheterization and stent procedures. Sharmin who does over 1500 interventions per year and apparently earns over 3 million dollars per year is interviewed and filmed performing a stent procedure.

The average viewer likely gathers from the context of the interview with Sharmin, that he is only doing these procedures to make money.

At various points during the movie, Dr. Steven Nissen, past president of the American College of Cardiology, is interviewed and referred to as “America’s top cardiologist.”

In my opinion, Nissen has been an outstanding, independent voice of reason in the world of cardiology. During the interview, he makes the very valid points that coronary calcium scans have not been embraced for routine usage because there are no outcomes data.

At one point he says, “I don’t like medical cults” in reference to those who support more widespread coronary calcium scans.

The movie leaves the uninformed viewer thinking that Nissen is part of a cabal blocking coronary calcium scans, perhaps due to his connections with industry or an inappropriate resentment of the “calcium club” pushing the scans.

Nothing could be further from the truth. I think Nissen is one of the few prominent cardiologists who are not subject to major bias of one type or another and I strongly respect his opinions.

The movie also attempts to portray the editor of Circulation, a major cardiology journal supported by the American Heart Association as inappropriately withdrawing a paper that would have endorsed coronary calcium scanning. It’s not possible to really tell what the truth is about this withdrawal, but this is a very minor episode in the history of coronary calcium scanning.

Ultimately, The Widowmaker fails its audience in presenting the truth because it desperately wants to convince us that there is a connection between the promotion of coronary stents and the failure of coronary calcium scans to be accepted by guidelines and covered by insurance.

There is no such connection. Many interventional cardiologists are enthusiastic promoters of prevention and aggressive use of coronary calcium scans. I have seen no evidence of greedy interventionists trying to  suppress coronary scans.

In Part II of this analysis, I will take a look at the “heroes” of The Widowmaker, the inventors and promoters of coronary calcium scans, and we will see if they are truly heroic.

 

 

The Incredibly Bad Science Behind Dr. Esselstyn’s Plant-based Diet

txorito pamplona
Txorizo Pamplona. This delightful sausage of Navarra in the basque region of Spain is right out in Esselsystn’s plant-based diets.

The skeptical cardiologist has heard a few cardiologist colleagues rave about the movie “Forks Over Knives” and promote the so-called “whole-foods, plant based diet.”

One of the two major physician figures in the movie is Dr. Caldwell Esselstyn, a former surgeon and now a vegan evangelist.

salad
You’ll be eating a lot of this on the Esselstyn diet but do not, under any circumstances add a salad dressing containing any oil of any kind to attempt to make it palatable or satiating.

Esselstyn, along with T. Colin Campbell (of the completely discredited “China Study” (see here for a summary of critical analyses of that data), Dean Ornish, and Nathan Pritikin, are the leading lights of a dying effort to indict any and all fat as promoting heart disease and all the chronic diseases of western civilization.

Esselstyn, in his book, “Preventing and Reversing Heart Disease” lists the following rules:

  • you may not eat anything with a mother or a face (no meat, poultry, or fish)
  • you cannot eat dairy products
  • you must not consume oil of any kind
  • generally you cannot eat nuts or avocados

What? No Fish or Olive Oil? You Cannot Be Serious!

oil
Whatever oil this might be (?sunflower) is right out even though it comes from a plant. According to Esselstyn, using his brilliant ‘logic and intuition” all fats, whether saturated or unsaturated are going to damage the lining of your arteries.

The best randomized controlled trials we have for diet to prevent coronary artery disease (CAD, the cause of heart attacks) have shown that supplementing diet with olive oil and nuts substantially lowers CAD.

Every observational study in nutrition has demonstrated that fish consumption is associated with lower cardiovascular disease.

Esselsstyn’s Really Bad Science

While working at the Cleveland Clinic, Esselstyn developed an interest in using a plant-based diet to treat patients with advanced CAD. He says he had an epiphany one rainy, depressing day when he was served a slab of bloody roast beef.

In his own words:

“my original intent was to have one group of patients eating a very-low fat diet and another receiving standard cardiac care and then compare how the two groups had fared after three years.”

If he had followed his original intent, and randomized patients entering the study, he could claim that he had performed a legitimate, important scientific study. Twelve of the 24 would be allocated by lottery to the Esselstyn diet and 12 to whatever was the standard recommended CAD diet at the time. Unfortunately this approach, due to a “lack of funding, was not practical.”

So instead, 24 patients were sent to him, “all suffering from advanced CAD” and began the horrifically strict dietary program he had developed based on his “logic and intuition.”

Interestingly, patients not only were put on Esselstyn’s incredibly low fat diet, but they were also given cholesterol lowering medications and were “switched to statin as soon as these became available in 1987.”

In addition, 9 of the 18 patients who stuck with the program had previously undergone coronary bypass surgery and two had undergone angioplasty of a coronary artery.

6 of the 24 original patients “could not comply with the program” and were sent back to their regular cardiologists. This gives you an idea of how difficult it was to follow this diet.

Esselsstyn’s “data” then consists of following 18 patients, 9 of whom had already undergone coronary bypass surgery, all of whom were taking statin drugs with his diet without any comparison group.

This group of 18 did well from a heart standpoint, of course. It is impossible to know if the diet had anything to with their outcome.  Most of them had already undergone the “knife” or had had angioplasties that took care of their most worrisome coronary blockages. They were all taking statin drugs . They were all nonsmokers and they were all highly motivated to take good care of themselves in all lifestyle choices.

Any patients who were not intensely motivated to radically change their diet would have avoided this crazy “study” like the plague.

This “study” is merely a collection of 18 anecdotes, none of which would be worthy of publication in any current legitimate medical journal.

Three of the 18 patients have died, one from pulmonary fibrosis, one presumably from a GI bleed, and one from depression. Could these deaths be related to the diet in some way? We can’t know because there is no comparison group.

Should Anyone Eat Ultra-low Fat Diets?

It is possible that the type of vegan/ultra-low fat diets espoused by Esselstyn and his ilk have some beneficial effects on preventing CAD, but there is nothing in the scientific literature which proves it.

Scientific reviews of the effect of diet on CAD in the last 5 years have concluded that the evidence is best for the Mediterranean diet, which emphasizes fish consumption, olive oil and nuts. These reviews dismiss ultra-low fat diets because of a lack of evidence supporting them, and an inability to get people to follow them.

If you have ethical or philosophic reasons for only eating things with no mother or face, then by all means follow your conscience.

Too often, however, I find that those who choose veganism for philosophic reasons want to find health reasons to support their diet and mix the bad science and philosophy into a bland evangelical stew they recommend for all.

I remain, therefore, in favor of cioppino, paella, butter and all the glories of the omnivore that make life so rich.

Omnivorously yours,

-ACP

I have updated this post with comments from readers and my response along with analysis of the latest “data” from Dr. Esseslstyn’s “study” at my post entitle

more-incredibly-bad-science-from-dr-esselstyns-plant-based-vegan-diet-study

For an amazingly complete (and surprisingly entertaining) dissection of the scientific inaccuracies of “Forks Over Knives” with humorous overtones, I recommend Denise Minger’s post “Forks Over Knives: Is the Science Legit? (A Review and Critique). Be prepared for lots of graphs!

Low T and Me: Does Testosterone Therapy Increase Cardiovascular Risk?

In the last year, several of my patients have asked me whether it is safe for them to take testosterone for “low T.” They were responding to media reports suggesting that testosterone therapy raised heart attack risk by one-third.

I must admit, I had been skeptical of the legitimacy of the “low T” diagnosis.  Many of the symptoms attributed to testosterone (T) deficiency, it seemed, were just part of normal male aging: decreased libido, fatigue, weight gain, and loss of muscle mass.

Perhaps, I thought, men should just be more willing to exercise regularly and lose weight and accept the indignities of aging that result despite our best efforts.

On the other hand, in the back of mind was the idea that perhaps I, as a sixty-something male with declining strength and endurance, could somehow forestall the ravages of aging by taking T.

I googled “low T” and immediately found some sponsored sites, including “is it low T.com,” which appears to be an educational site for patients. However, the one treatment option that they provide links to is made by Abbvie, the somewhat hidden host of the site. Abbvie is a pharmaceutical company that makes Androgel, the most widely prescribed testosterone cream.

lowTquiz

I answered yes to the 3 questions I thought were just uniform consequences of aging:

1. Reduction in strength and/or endurance.

2. Loss of height.

3. Deterioration in your ability to play sports.

After taking the quiz, I was told that answering yes to 3 of the 10 questions strongly suggests you have low T.

In addition, according to the site, if you answered yes to question 1 (decreased libido) or 7 (less strong erections) you have low T.

Based on this quiz, I and 99% of men my age must have low T!!

In the last 10 years, the use of testosterone therapy has quadrupled, driven by better formulations for testosterone delivery and by direct-to-consumer marketing campaigns that suggest that treating low T will reverse these normal consequences of aging.

As a result, in 2013, 2.3 million American men received testosterone therapy and 25% of these men had no baseline testosterone levels tested.

A year ago, the New York Times editorial board opined on the dangers of overprescribing testosterone and the influence of pharmaceutical companies in over-promoting the drug, in a piece entitled “Overprescribing testosterone, dangerously.”  Articles like this are what have raised patients’ concerns about T therapy and increased risk of heart attack.

Testosterone and Mortality

There is a large body of evidence that shows an association between lower T levels and increased mortality and coronary artery disease. Lower T levels are also associated with higher risk of diabetes and the metabolic syndrome.  Studies also show that T therapy in T-deficient men increase lean mass and reduce fat mass and are associated with a reduction in mortality. A recent review article by Morgenthaler, et al in Mayo Clinic Proceedings, provides a detailed and meticulous summary of these studies and data.

Two recent studies contradict this large body of evidence and gained enormous media attention. The first, by Vigen et al in JAMA 2013, was a retrospective analysis of VA patients which has received extensive criticism for its statistical technique and has been corrected twice. The second study was by Finical, et al in PLoS One 2014, suggesting increased mortality in patients for 90 days after receiving their prescription for T. This study also contains methodologic issues and is hardly conclusive.

Is it Safe to Take T for low T

My recommendation to patients who want to take T after looking at all the data is as follows:

-Make sure that you really have low T.  Your total T levels should be less than 300 ng/dL done in a reliable, certified lab.

-At this time, I don’t see solid evidence that taking T, if you definitely have T deficiency, increases the risk of cardiovascular complications or death.

As with all medications, the shortest duration and smallest effective amount is what you should take. All medications have side effects, some that we know and some that we don’t know. Most of the studies that have been published were on small numbers of patients for short periods of time.

-If you are overweight and/or sedentary, there is good evidence that losing weight and exercising will improve many of the symptoms ascribed to low T.  These will also improve your life expectancy and lower your risk of heart attack.

…And you won’t have to worry about any side effects!

Do I have low T? Like all sixty-somethings my T levels are lower than when I was 30. My endurance is less. I’m losing height. Fat wants to build up in my abdomen, despite my best efforts.

It’s only going to get worse, but I’m willing to accept these as normal consequences of the aging process, rather than introduce external T into my system with its unknown consequences.

I will not go gentle into that good night but will continue to rage against the dying of the light without the wonders of pharmaceutical grade T.

Yours in aging,

-ACP

 

 

 

 

 

Nuts, Legumes, Drupes and Mortality

When I was a child in small town Oklahoma, I collapsed walking home from school one day after eating pecans. Apparently I had never encountered pecans in England where I grew up and I had a very severe, life-threatening  allergic reaction (anaphylaxis.)

My pediatrician was promptly called, drove over, picked me out of the street and (legend has it) with one hand on the steering wheel and the other jabbing me with epinephrine drove me to the local hospital (apparently ambulances were not invented at this time). There I spent several days in an oxygen tent recuperating.

Since then I had, until recently,  concluded (based on my own multiple food reactions and research) that I was allergic to “tree nuts.”

I would patiently explain to the uninitiated that I could eat almonds because they are in the peach family and I could eat peanuts because they are in the legume family: neither one of these, therefore, were true “tree nuts.”

To all whom I gave this seemingly erudite explanation I owe an apology for I have learned the earth-shattering truth that pecans are drupes! They are no more a nut than an almond is!

In fact, even walnuts are not nuts as hard as that is to believe.

Pecans, walnuts and almonds are all drupes.

Why, you may wonder, is any of this botanical folderol of any relevance to cardiology?

Nuts and Cardiovascular Death

For those paying attention to media reports on the latest food that will either kill you or make you live for ever you may already know the answer. This paper published in JAMA made big headlines.

Jane Brody of the New York Times wrote a piece extolling the virtues of nuts entitled “Nuts are a Nutritional Powerhouse”. Medical New Today wrote “Eating Nuts Linked to 20% Cut in Death Rates”.

It turns out, however, that most of what the 136,000 Chinese were eating and half of  the “nuts” the 85,000 low income Americans were eating in that JAMA study  were legumes: peanuts or peanut butter. The authors wrote:

“Our findings … raise the possibility that a diet including peanuts may offer some CVD (cardiovascular)  protection. We cannot, however, make etiologic inferences from these observational data, especially with the lack of a clear dose-response trend in many of the analyses. Nevertheless, the findings highlight a substantive public health impact of nut/peanut consumption in lowering CVD mortality, given the affordability of peanuts to individuals from all [socioeconomic status] backgrounds.”

These findings follow another large observational study published in 2013 which also found (in American doctors and nurses) an inverse relationship between nut consumption and mortality.

“compared with participants who did not eat nuts, those who consumed nuts seven or more times per week had a 20% lower death rate. Inverse associations were observed for most major causes of death, including heart disease, cancer, and respiratory diseases. Results were similar for peanuts and tree nuts, and the inverse association persisted across all subgroups.”

We also have a very good randomized trial (the PREDIMED study) that showed that  the Mediterranean diet plus supplementation with extra-virgin olive oil or mixed nuts performed much better than a control diet in reducing cardiovascular events.

Participants in the two Mediterranean-diet groups received either extra-virgin olive oil (approximately 1 liter per week) or 30 g of mixed nuts per day (15 g of walnuts, 7.5 g of hazelnuts, and 7.5 g of almonds) at no cost, and those in the control group received small nonfood gifts (I wonder what these were?)

After 5 years, those on the Med diet had about a 30% lower rate of heart attack, stroke or cardiovascular death.

Nuts versus Drupes versus Legumes

The evidence supporting “nut” consumption as a major part of a heart healthy diet is pretty overwhelming. But what is a nut and which nuts or nut-like foods qualify?

Let’s lay out the basic definitions:

Nut-Generally has a hard outer shell that stays tightly shut until cracked open revealing a single fruit inside. Examples are hazelnuts and acorns.

Drupe-Has a soft, fleshy exterior surrounding a hard nut. Classic drupes are peaches and plums with interior nuts so hard we won’t eat them. Examples are pecans, almonds, walnuts and coconuts.

Legume-generally has a pod with multiple fruit which splits open when ready. Examples are peas, carob, peanuts, soybeans and beans.

What Nuts Were Consumed in Studies Showing Benefits of Nuts?

Initially participants were given a questionnaire and asked

” how often they had consumed a serving of nuts (serving size, 28 g [1 oz]) during the preceding year: never or almost never, one to three times a month, once a week, two to four times a week, five or six times a week, once a day, two or three times a day, four to six times a day, or more than six times a day.”

After initial surveys, the questionnaires split out peanut consumption from “tree nut” consumption and whether you ate peanuts or nuts the benefits were similar.

Thus, for the most part, participants were left to their own devices to define what a nut is.  Since most people don’t know what a true nut is, they could have been eating anything from almonds (drupe related to peaches) to hazelnuts (true nut) to a pistachio “nut” (drupe) to a pine “nut” (nutlike gymnosperm seed).

Nutrient Content of Nuts

The nutrient components of these nuts varies widely but one consistency is a very high fat content. For this reason, in the dark days when fat was considered harmful, nuts were shunned.

However, in our more enlightened era we now know that fat does not cause heart disease or make you fat.

Please repeat after me “Fat does not cause heart disease or make you fat.”

A one ounce portion of pecans contains 20.4 grams of fat (11.6 arms monounsaturated and 6.1 polyunsaturated) so that 90% of its 204 calories come from fat.

Nuts, of course, also contain numerous other biologically active compounds that all interact and participate in the overall  beneficial effects that they have on cardiovascular disease and mortality.

They are a whole, real food which can be eaten intact without processing and these are the foods we now recognize provide the best choices in our diets, irrespective of fat or carbohydrate content.

They are also convenient, as they are easy to store and carry with you, providing a perfect snack.

If You Think It’s A Nut, It’s A Nut

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Hazelnut Death Experiment (Don’t try this at home!) A single hazelnut was partitioned into halves, quarters, slivers and little tiny bits. Progressively larger portions were consumed at 5 minute intervals. An Epipen (right) was available in case of anaphylaxis.

It turns out, that my attempts to put pecans and walnuts in to a specific family of nuts that increased my risk of dying if I consumed them were misguided.

I’m allergic to drupes.

In fact, I did an experiment recently and consumed a true nut (a hazelnut) and found I had no reaction.

I’m not allergic to nuts!!!

In the world of allergic reactions, thus,  there is no particular value to partitioning nuts from drupes from legumes.

Similarly, for heart healthy diets, it doesn’t matter if you are consuming a true nut or a drupe as long as you think of it as a nut.

Consume them without concern about the fat content and consume them daily and as along you are not allergic to them they will prolong your life.

Skeptically Yours,
-ACP

 

 

 

Should All Men Over Sixty Take a Statin Drug?

The updated AHA/ACC Cardiovascular Prevention Guidelines (CPG) which include the   excessively wordy “The Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults Risk” were published late last year and immediately were the center of controversy.

After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.

As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.

Should we be starting all elderly Americans on statin drugs?

My simple answer is no. It doesn’t make sense to do this, because clearly not all elderly individuals have atherosclerosis or will ever develop its consequences of heart attack and stroke. Many have inherited the genes that allowed their parents to live free of heart disease into their 90s and will not benefit at all from long term statin therapy; they may actually suffer the expense and side effects instead.

How can we better decide who among the elderly will benefit from statin therapy?

If you have read my previous posts on searching for subclinical atherosclerosis here and here you probably know the answer. Let’s look at a specific case and apply those principles.

Robert is 69 years old. I see him because, in 2010, the posterior leaflet of his mitral valve ruptured, resulting in the mitral valve becoming severely incompetent at its job of preventing back flow from the left ventricle into the left atrium. I sent him to a cardiac surgeon who repaired the ruptured leaflet. Although he has a form of “heart disease,” this is a form that has nothing to do with cholesterol, hypertension or diabetes and is not associated with ASCVD.

However, it is my job to assess in him, like all individuals, the risk of developing coronary heart disease or ASCVD.

He has no family history of ASCVD and he feels great since the surgery, exercising aerobically 4-5 times per week.

His BMI is 23.87 which is in the normal range. His BP runs 116/80.

His total cholesterol is 210 and LDL or bad cholesterol is 142. Good or HDL cholesterol is 56 and triglycerides 59. The total and LDL cholesterol levels are considered “high,” but they could be perfectly acceptable for this man.

When I ran his 10 year ASCVD risk (risk of developing a heart attack or stroke over the next 10 years), it came back as 14%. The new guidelines would suggest having a conversation with him about starting a statin if his risk is over 7.5%. His risk is double this and statins are definitely recommended in this intermediate risk range. Interestingly, I cannot enter a cholesterol level or blood pressure for a man of this age that yields a risk less than 7.5%.

When I had my discussion with him about his risk for ASCVD, I plugged his numbers into my iPhone and showed him the results and gave him the guideline recommendation.

Lifestyle Changes to Lower Cholesterol

The new Cardiovascular Prevention Guidelines have a section devoted to Lifestyle Management to Reduce Cardiovascular Risk. Unfortunately, none of the lifestyle changes they recommend have been shown to reduce ASCVD risk in an individual like Robert. He already exercises the recommended amount, is at his ideal body weight and eats a healthy diet. If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD and the calculated 10 year ASCVD risk would still be in the range where statins are recommended.

Therefore, I am not going to tell Robert that he should reduce his saturated fat consumption (he already has incorporated that into his diet since he’s been bombarded with the low fat mantra for 30 years).

Searching for Subclinical Atherosclerosis

I’m going to tell Robert that we need to know if he has atherosclerosis, the disease that we are attempting to modify.

We started with an ultrasound to look at the lining of the large arteries in his neck that supply blood to the brain, the carotid arteries (a process I describe in more detail here). Although severe atherosclerotic blockages in these arteries put one at risk of a stroke, I was much more interested in the subtle changes in the arteries that precede symptoms and are an early harbinger of atherosclerosis.

Careful ultrasound recording and measurement of the main common carotid arteries from both the left and right side showed that the IMT or thickness was lower than average for his age, gender and ethnicity. His carotid IMT was at the average for a 60 year old, therefore, his so-called vascular age was 60 years, younger than his chronological age. If I plug that age into the ASCVD risk estimator, I get an 8.2% 10 year risk, just barely above the statin treatment cut-off.

Careful scrutiny with ultrasound of the entire visible carotid system in the neck on both sides did not reveal any early fatty plaques or calcium in the lining of the carotid arteries. He had no evidence for atherosclerosis, even very subtle early forms, in this large artery, a finding which is usually predictive of what is going on in the other large arteries in the body, including the coronary arteries, which supply blood to the heart.

At this point, I think, we could have stopped the search for subclinical atherosclerosis and agreed that no statin therapy was warranted. However, Robert wanted further reassurance that his coronary arteries were OK, therefore we set him up with a coronary calcium study (see my full description of this test here).

Searching for Subclinical Atherosclerosis: The Calcium Score

Robert’s coronary calcium score came back at 21 (all in the LAD coronary artery) , which put him at the 26th percentile compared to normal men of his age and gender. A score of 21 is average for a 59 year old man and 82% of men aged 69 have a score greater than zero. Robert had much less calcium in his coronaries than men his age, another factor putting him in a low risk category.

Given the low risk findings from both the vascular screening and the coronary calcium, I felt comfortable recommending no statin therapy and going against the guidelines.

Statins: Better Targets for The Two-edged Sword

This is not an unusual scenario; many of my older patients without heart attacks, strokes or diabetes fall into the risk category that would warrant statin therapy and if they have no clinical or subclinical evidence of atherosclerosis, I don’t advise statin therapy. My patients are free to follow the guidelines and take statin drugs after this advice, but most are very grateful that another pill (which they likely have heard bad things about on the internet or from friends with adverse experiences) can be avoided.

Statins are wonderful drugs when utilized in the right population, but they also carry a  9% increased risk of diabetes and about a 10% real world risk of developing muscle aches and weakness (myalgia).

I think it is essential to aim these two-edged swords at the right targets if we are to maximize the overall health benefits.

Salt Consumption: Less Is Not Always Better

After a week of trying to track my salt consumption I have learned two things

1. Tracking salt consumption (unless you make  all your meals at home from scratch or buy from fast food restaurants) is very tedious.

2. My salt consumption is low: less than the 1.5 grams per day recommended by the American Heart Association (AHA) every day (unless I attend a Cardinals game)

After reviewing the latest scientific publications on salt, however, I have to think that for most people, it is not worth the effort to  track daily salt consumption.

Yes , this is nutritional heresy and goes against what my patients have been reading from authoritative nutritional sources for decades.

The AHA 1.5 gram/day limit for all Americans comes from a small, short term (4 weeks) study (Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med2001;344:3-10.)

The findings are not applicable to all Americans because more than 50% of participants in the DASH study had hypertension or prehypertension, more than 50% of participants were of African ancestry, potassium intake was markedly lower than in the general U.S. population, the trial involved only 412 persons, and a limited range of sodium intake was studied (1.5 to 3.3 g per day).

I asked most  of my patients this week about their salt consumption. None of them could tell me what their average daily salt consumption was. However, almost to a man (or woman) they told me they had been consciously limiting their consumption of salt because they knew that this was healthy.

Thus, the 35 year old white woman with a blood pressure of 110/50 , palpitations and periodic dizzy spells is following the same recommendations to limit salt consumption as the 70 year old African-American with poorly controlled hypertension.

In the last few years this focus on lower salt consumption has been questioned after close analysis by the Institute of Medicine and the Cochrane Analysis.

Two articles in the prestigious New England journal of Medicine published a few weeks ago have convinced me that most individuals who are following a Mediterranean diet do not need to be concerned about their salt consumption.

Salt and Blood Pressure

In the first PURE study paper,(a prospective cohort study that included 101,945 people from five continents)

very few participants had an estimated sodium intake of less than 2.3 g per day, and almost none had an intake of less than 1.5 g per day. This suggests that, at present, human consumption of extremely low amounts of sodium for prolonged periods is rare.

The PURE Study looked at sodium excretion versus blood pressure and

 found a steep slope for this association among study participants with sodium excretion of more than 5 g per day, a modest association among those with sodium excretion of 3 to 5 g per day, and no significant association among those with sodium excretion of less than 3 g per day.

Salt and Death

The second PURE study paper examined the relationship between sodium excretion (a measure of sodium consumption) and death and cardiovascular events

 

saltvsdeath
As Eric Topol has opined at the heart.org ” In other words, consumption of too little sodium is as harmful as consumption of too much sodium. In fact, the AHA guideline would lead — at least according to this latest research — to about a twofold risk for major adverse events.”

This graph of data from the PURE study  shows that lower levels of sodium excretion , below about 3 grams per day were associated with a higher risk of death.

Starting above about 5 grams per day  the risk of death increased with increasing amounts of sodium excretion.

 

This is quite a shocker for those of us who have assumed for the last 20  years that the less salt we consumed the longer we would live.

 

Potassium Consumption

Drawing less controversy were the findings from these two studies on potassium consumption. Higher levels of potassium consumption were associated with lower blood pressures and lower risk of death. The authors point out that high potassium intake may simply be a marker of healthy dietary patterns that are rich in potassium (e.g., high consumption of fruit and vegetables).

You can read more about these papers, including critical and positive comments at the heart.org here.

My Recommendations on Salt Consumption

Here is what I will be telling my patients about salt after a week of tracking my consumption and reading the relevant scientific literature.

  • Spend a day or two accurately tracking your consumption of salt to educate yourself. I found this app to be really helpful. I’ll expand on this in a future post.
  • Recognize that not everybody needs to follow a low salt diet. If your blood pressure is not elevated and you have no heart failure you don’t need to change your salt consumption.
  • If your blood pressure is on the low side and especially if you get periodic dizzy spells, often associated with standing quickly liberalize your salt intake, you will feel better.
  • If you have high blood pressure, you are the best judge of how salt effects your blood pressure. In the example I gave in a previous post, my patient realized that all the salt he was sprinkling on his tomatoes was the major factor causing his blood pressure to spike.
  • The kidneys do a great job of balancing sodium intake and sodium excretion if they are working normally. If you have kidney dysfunction you will  be more sensitive to the effects of salt consumption on your blood pressure and fluid retention.
  • If you are following a Mediterranean diet with plenty of fresh fruits and vegetables you are going to be in the ideal range for both potassium and sodium consumption.

Public health experts are always seeking a “one size fits all” message to give the public. In the case of salt consumption, however, the message of less is better does not apply to all.

 

 

Cheerios, Soluble Fiber and Your Heart

IMG_3239The skeptical cardiologist usually eschews the breakfast offerings in the Doctor’s lounge. I’m not really interested in consuming donuts, muffins, or bagels with their high carbohydrate load. As I’ve ranted out about previously, the only yogurt available is Yoplait low fat , highly sugared-up yogurt which is arguably worse than starting the day with a candy bar.

A selection of breakfast cereals is available including Cheerios, Raisin Bran, and Frosted Flakes. Occasionally, when I have neglected to bring in my own yogurt, granola and/or fruit I will open up one of the Cheerios containers and consume a bowl mixed with 2% milk (full-fat, organic milk which I passionately advocate here and here is not available)

Pondering the Cheerios packaging and the cute little O’s made me wonder whether this highly processed and packaged food with a seemingly endless shelf life was truly a healthy choice.

The “ready-to-eat”  and allegedly heart-healthy cereal

Cheerios and Honey-nut cheerios were  the #4 and #1 breakfast cereals in the US in 2013, generating almost a billion dollars in sales. Both of these GM blockbusters undoubtedly have reached their popularity by heavily promoting the concept that they are heart healthy.

The Cheerios label is all about the heart. The little O’s sit in a heart-shaped bowl. A prominent red heart with a check inside it attests to the AHA having certified Cheerios as part of its checkmark.heart.org program. Additional text states “low  in Saturated fat and cholesterol” and “diets low in saturated fat and cholesterol may reduce the risk of heart disease.”

For those concerned about GMO  the package also states “not made with genetically modified ingredients”

Is the Fiber in Cheerios “heart-healthy” ?

Beta-glucan is a soluble fiber primarily located in the endosperm cell wall of oats. Early studies showed that oats and beta-glucan soluble fiber could reduce total and LDL (bad cholesterol) levels. The mechanism isn’t really known. (see the end of post for possible mechanisms). The Quaker oats web site oversimplifies the mechanism thusly :

“In your digestive tract, it acts as a sponge, soaking up cholesterol and carrying it out of the body”

This narrative fits with the oversimplified and now discredited descriptions of atherosclerosis which attribute it directly to consumption of cholesterol and fatty acids. See here if you’d like to appreciate how complex the process truly is.

The FDA sanctions oats as heart healthy

In 1997, the FDA reviewed 33 studies (21 showing benefit and 12 not) and decided to allow a health claim for foods that contain oats and soluble fiber. A minimum dose of 3 grams/day of oat beta-glucan was suggested for a beneficial reduction in blood cholesterol and (presumably, although never documented) a subsequent decline in coronary heart disease.

In 1998 Johnson, et al, published the results of a study funded by a grant from General Mills that showed that  inclusion of whole grain oat ready to eat cereal providing 3 grams of beta-glucan as part of a low fat diet reduced  LDL cholesterol by 4% after 6 weeks. HDL was unchanged. Patients in this study consumed 45 grams (1.5 oz) of cheerios at breakfast and then again in the evening. There was a total of 3 grams of soluble fibre in this amount of Cheerios. A control group consumed corn flakes in a similar fashion without change in LDL.

General Mills took this weak data and ran with it and began posting on Cheerios the following statements

 “Did you know that in just 6 weeks Cheerios can reduce bad cholesterol by an average of 4 percent? Cheerios is … clinically proven to lower cholesterol. A clinical study showed that eating two 1 1/2 cup servings daily of Cheerios cereal reduced bad cholesterol when eaten as part of a diet low in saturated fat and cholesterol.”

Although the FDA had approved verbiage indicating oats may reduce heart disease “when eaten as part of a diet low in saturated fat and cholesterol” the agency objected to General Mills claiming that Cheerios lowers cholesterol “when eaten as part of a diet low in saturated fat and cholesterol”.

The FDA  issued a warning letter to General Mills in 2009 in which the agency alleged “serious violations” of the FDC Act in the label and labeling of Cheerios cereal.

Based on claims made on your product’s label, we have determined that your Cheerios® Toasted Whole Grain Oat Cereal is promoted for conditions that cause it to be a drug because the product is intended for use in the prevention, mitigation, and treatment of disease.

Should We Be Treating High Cholesterol or Preventing Heart Disease?

The FDA was telling General Mills that it was OK to say that Cheerios may reduce heart disease but not that it can reduce cholesterol because that made it a drug. It makes no sense.

The only thing that had been demonstrated for oat soluble fiber and Cheerios in particular was a reduction in cholesterol. There has never been a study with oats showing a reduction in heart disease..

It’s the heart disease, the atherosclerosis clogging our arteries and causing heart attacks and strokes that we want to prevent. We could care less about lowering cholesterol if it doesn’t prevent atherosclerosis.

A recent review of studies since the FDA ruling shows that 70% of studies show some reduction in LDL with beta-glucan. Interstingly, the studies which added beta-glucan to liquids were generally positive whereas addition to solids such as muffins usually did not show benefit.

I’m going to accept as evidence-based the claim that whole oats can lower your LDL about 7% if you consume a very large amount of them on a daily basis.

However, the critical question for any drug or dietary intervention is does it prevent atherosclerosis, the root cause of heart attacks and strokes. There has been in the past an assumption that lowering cholesterol by any means would result in lowering of atherosclerosis. This theory has been disproven by recent studies showing that ezetimibe and niacin which significantly lower LDL do not reduce surrogate markers of atherosclerosis or cardiovascular events any more than placebo when added on to statin drugs. The recently revised cholesterol guidelines endorse the concept of treating risk of atherosclerosis rather than cholesterol levels.

Eat Real Foods, Mostly Plants, Not Too Much

If you follow Michael Pollan’s simple dictum you will get plenty of fiber, soluble or otherwise and you will avoid the necessity to obsess over the macronutrients in your diet, fiber or otherwise. Throw in some cheerios and oatmeal every once in a while if you like them, in their unadulterated state they are a healthy food choice.

To quote David Katz

Wholesome foods in sensible combinations, as prevail in the world’s Blue Zones, seemingly take care of all nutrients, by focusing on none. Such dietary patterns can be low in fat, as vegan and traditional Asian diets tend to be; or high in fat, as Mediterranean diets tend to be. Variations on a common theme nicely accommodate personal preference, allowing us all to find a dietary pattern to love that loves our health back.

Addendum

As promised, for those with inquiring minds and oatmeal-induced fortitude, I present from a recent review of fiber some discussion of proposed mechanisms of cholesterol lowering

The mechanism by which fiber lowers blood cholesterol remains undefined. Evidence suggests that some soluble fibers bind bile acids or cholesterol during the intraluminal formation of micelles. The resulting reduction in the cholesterol content of liver cells leads to an up-regulation of the LDL receptors and thus increased clearance of LDL cholesterol. However, increased bile acid excretion may not be sufficient to account for the observed cholesterol reduction. Other suggested mechanisms include inhibition of hepatic fatty acid synthesis by products of fermentation (production of short-chain fatty acids such as acetate, butyrate, propionate) ; changes in intestinal motility; fibers with high viscosity causing slowed absorption of macronutrients, leading to increased insulin sensitivity; and increased satiety, leading to lower overall energy intake.

and their take on soluble fibers overall importance

The modest reductions in cholesterol expected from intakes of soluble fiber within practical ranges may exert only a small effect on the risk of heart disease. For example, daily intake of 3 g soluble fiber from either 3 apples or 3 bowls (28-g servings) of oatmeal can decrease total cholesterol by ≈0.129 mmol/L (5 mg/dL), a ≈2% reduction. On the basis of estimates from clinical studies of cholesterol treatment,, this could lower the incidence of coronary artery disease by ≈4%.

and a comment on publication bias: the finding that studies that do not show a positive effect of the intervention tend not to get published.

Publication bias toward studies that showed positive results is always a potential issue in meta-analyses and could be operating in this study. If this were true, then the small effect estimates associated with intake of dietary soluble fiber would be further attenuated, further highlighting the need for conservative public health claims. The major benefit from eating fiber-rich foods may be a change in dietary pattern, resulting in a diet that is lower in saturated and trans-unsaturated fats and cholesterol and higher in protective nutrients such as unsaturated fatty acids, minerals, folate, and antioxidant vitamins.

 

Tofu: Heart Healthy SuperFood or Environmental Nightmare?

Most of my patients think tofu and soy protein are particularly heart healthy food choices. Since tofu contains significant calcium and protein, it is often viewed as a healthier alternative to dairy (which has inappropriately been labeled as heart unhealthy).

A huge growth in the use of soy protein occurred between 1996 and 2009 with annual sales of foods containing soy expanding from $1 billion to $4.5 billion. This appears to have been driven by a perception that soy is more healthful than other sources of protein (especially animal protein).

Much of the success of soy foods followed a 1999 decision by the FDA which approved a food-labeling health claim for soy protein for the prevention of coronary heart disease (CHD):

25 grams of soy protein a day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease.

 Does soy deserve this designation? Should we be purposefully trying to consume more soy to lower our risk of heart disease?

Early studies, which compared consumption of 25 grams of soy protein versus control protein consumption, suggested a slight reduction in total and bad cholesterol levels. The problem with these studies is that a flawed surrogate marker (cholesterol or bad cholesterol) is being studied in place of the real disease (atherosclerosis and its associated complications, including heart attack and stroke). We now know that dietary interventions or drug therapies that lower cholesterol don’t necessarily reduce heart attacks or prolong life.

In 2000, the AHA published a document supporting the concept that 50 grams of soy protein per day would reduce heart disease risk .

However the AHA reversed this recommendation in a 2006 publication finding that

 In the majority of 22 randomized trials, isolated soy protein with isoflavones, as compared with milk or other proteins, decreased LDL cholesterol concentrations; the average effect was approximately 3%. This reduction is very small relative to the large amount of soy protein tested in these studies, averaging 50 g, about half the usual total daily protein intake. No significant effects on HDL cholesterol, triglycerides, lipoprotein(a), or blood pressure were evident. Among 19 studies of soy isoflavones, the average effect on LDL cholesterol and other lipid risk factors was nil. Soy protein and isoflavones have not been shown to lessen vasomotor symptoms of menopause, and results are mixed with regard to soy’s ability to slow postmenopausal bone loss. The efficacy and safety of soy isoflavones for preventing or treating cancer of the breast, endometrium, and prostate are not established; evidence from clinical trials is meager and cautionary with regard to a possible adverse effect. For this reason, use of isoflavone supplements in food or pills is not recommended. Thus, earlier research indicating that soy protein has clinically important favorable effects as compared with other proteins has not been confirmed. 

There is no scientific evidence that consuming soy protein lowers your risk of heart disease. There is no evidence that substituting soy protein for animal protein lowers your risk of heart disease. Certainly, if you like tofu (does anyone really like tofu?) and/or you have a philosophical desire to avoid meat and dairy consumption, tofu can provide a lot of the protein and calcium that you cannot get from eating only vegetables.

What does the searching the Internet tell us about tofu?

A Google search on the health benefits of tofu reveals stridently negative and positive (allegedly  evidence-based) articles (as is typical for everything in the world of nutrition). Medical News Today (“a leading health care internet publishing company,” which gets 9,000,00 views a month for unknown reasons), for example, has an overwhelmingly positive article written by a dietician which claims:

Countless studies have suggested that increasing consumption of plant-based foods like tofu, decreases the risk of obesity and overall mortality, diabetes, and heart disease and promotes a healthy complexion and hair, increased energy, and overall lower weight

The “Foundation for Integrative Medicine” (when you see the word “integrative” before the word “medicine,” substitute “unproven” and move to another website. This is a marker for quackery) cites similar claims, adding that regular tofu consumption reduces breast and lung cancer and osteoporosis.

None of these claims are supported in the medical literature.

On the anti-tofu side, we have this blog post from a chiropractor (chiropractors are usually big advocates of “integrative” medicine) who finds unfermented soy consumption to be the cause of myriad health problems including:

  • Breast Cancer
  • Brain damage
  • Infant abnormalities
  • Thyroid disorders
  • Kidney stones
  • Immune system impairment
  • Severe, and potentially fatal food allergies
  • Impaired fertility
  • Danger during pregnancy and nursing

None of these claims are supported by the medical literature

You can also read about why soy “May be a health risk and environmental Nightmare” here. The majority of soy grown in the US comes from genetically modified plants from Monsanto which have had a gene inserted that allows them to resist Roundup. Consequently, farmers can spray all the Roundup they want on the plants.

Nobody knows if this is a health risk or not. Monsanto likes to make the case that the overall effects of RoundupReady soy, as they like to call it, are positive, whereas Mother Jones writes that soy is “Scarier Than You Think”.

My bottom line recommendation on soy is that, like all other foods, we should try to consume it in its least industrially processed form as part of a balanced diet of real foods.

There is no scientifically proven reason to  avoid it or seek it out.

 

 

Statin Drugs Have Benefits Beyond Cholesterol Lowering

For most of the last 25 years I have told patients when I recommend  a statin drug to them that they should take it in order to lower their bad cholesterol (and raise the good cholesterol) thereby lowering their risk of future heart attacks.

I based this statement on my understanding of large statin trials which demonstrated reduction in heart attacks seemingly closely tied to drops in the bad cholesterol level.

Although I was aware of the so-called “pleiotropic” (meaning effecting multiple pathways leading to atherosclerosis) of statins it was easier to point to the cholesterol lowering effects and unify that message with the recommendation to reduce fat and cholesterol in the diet , thereby lowering cholesterol in the blood and arteries and cut heart attack risks.

Thus emerged a very simple (and likely false) paradigm: Fat in the diet causes fat in the blood which causes fat in the arteries which causes fatty plaques in the coronary arteries which causes heart attacks when they get too big and block off the blood flow.

I, like most cardiologists and lay people  mistakenly assumed that since lower bad cholesterol levels associated with taking a statin drug were associated with lower heart attack risks then dietary changes aimed at lowering bad cholesterol levels would also lower heart attack risk.

It turns out that we don’t really know how the statins reduce heart attacks . As a recent review points out:

 some of the cholesterol-independent or “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone. Many of these pleiotropic effects are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signaling molecules. In particular, inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the pleiotropic effects of statins.

Supporting the non cholesterol lowering effects of statins on reducing CVD are the following observations

-Most heart attack victims don’t have elevated bad cholesterol levels and dietary reduction of bad cholesterol doesn’t seem very effective at preventing heart attacks.

-Drugs, like Zetia or ezetimibe which lower cholesterol level by other mechanisms don’t seem to prevent atherosclerosis even though they substantially lower bad cholesterol levels.

-Statin drugs reduce heart attacks in patients who have normal or low bad cholesterol levels

What Causes Atherosclerosis?

An article (Innate and adaptive inflammation as a Therapeutic Target in Vascular Disease) published in JACC recently by Tousoulis,et al. summarizes the current understanding of how atherosclerosis develops and the multiple ways that statins may affect that process. They write

Atherosclerosis, once thought to be a lipid storage disease, is now considered a chronic low-grade inflammatory condition that affects the vascular wall. It is characterized by the deposition of cholesterol and lipids followed by infiltration of T cells and macrophages, all as a result of an endothelial injury response.

I’m including this figure from the article to give you some idea of how incredibly complicated the process is.

atherosclerosis
Overview of Mechanisms Involved in Atherosclerosis Low-density lipoprotein (LDL) is oxidized in the presence of reactive oxygen species (ROS) and binds to proteoglycans (heparin sulfate) while simultaneously stimulating the endothelium, leading to adhesion molecule overexpression and increasing its permeability. Apart from this action, oxidized low-density lipoprotein (ox-LDL) inhibits nitric oxide (NO) production, prohibiting vasodilation. Furthermore, cytokines and other chemoattractant molecules, such as MCP-1, are secreted, favoring leukocyte adhesion. Leukocytes come into random contact with the activated endothelium and, due to interactions with adhesion molecules, roll and tether and are subsequently firmly arrested. In addition, leukocytes transmigrate into the subendothelial space, where they differentiate into macrophages, which in turn take up ox-LDL, forming foam cells. Ox-LDL antigens are presented by macrophage major histocompatibility complex class II (MHC-II) proteins and are recognized by CD4+ T cells. These preferentially differentiate into Th-1 cells, pro-inflammatory cytokine production. Finally, smooth muscle cell (SMC) proliferation and migration are induced as a result of cytokine and growth factor secretion.

Can you imagine trying to explain this to the average patient?

My eyes glazed over once I reached MCP-1.

Thus, doctors end up giving the simple, accepted conventional wisdom that we are “treating” high cholesterol by giving statin drugs. What we are really treating is atherosclerosis. And statins are the only effective drug treatment we have identified for this ubiqitous  and complex process.

It is entirely possible that the lower LDL cholesterol caused by statin drugs is totally unrelated to their ability to forestall atherosclerosis. The new cholesterol guidelines reflect this concept as they don’t recommend treating to an LDL target level.

I end with the closing comments from the article by Tousoulis, et al.

Given the fact that atherosclerosis is a multivariable disease, with several molecules involved in each stage, it is vey difficult to find an effective treatment. However, statins prove to be the most effective treatment so far because they interfere with most of the critical components of the atherosclerotic process and have been proven to have beneficial effects. Further to their well-established impact on nonspecific low-grade inflammation, statins also appear to have significant effects on innate and adaptive immunity that have been underestimated so far.