Tag Archives: coronary heart disease

The MESA App-Estimating Your Risk of Cardiovascular Disease With And Without Coronary Calcium Score

Yesterday, I laid out the case for utilizing coronary artery calcium score (CACS) to further refine the assessment of youngish patients risk of developing cardiovascular disease (ASCVD). I referenced the ACC/AHA ASCVD risk estimator tool (app available here) as the starting point but if I have information on my patient’s CACS I use a new and improved tool called the MESA risk score calculator.

It is available online and through an app for Apple and Android (search in the app store on “MESA Risk Score” for the (free) download.)

The MESA tool allows you to easily calculate how the CACS effects you or your patient’s 10 year risk of ASCVD.

The Multi-Ethnic Study of Atherosclerosis (MESA) is a study of the characteristics of subclinical cardiovascular disease (disease detected non-invasively before it has produced clinical signs and symptoms) and the risk factors that predict progression to clinically overt cardiovascular disease or progression of the subclinical disease. MESA researchers study a diverse, population-based sample of 6,814 asymptomatic men and women aged 45-84. Approximately 38 percent of the recruited participants are white, 28 percent African-American, 22 percent Hispanic, and 12 percent Asian, predominantly of Chinese descent.

To use the score you will need information on the following risk factors:

age, gender, race/ethnicity, diabetes (yes/no), current smoker (yes/no), total and HDL cholesterol, use of lipid lowering medication (yes/no), systolic blood pressure (mmHg), use of anti-hypertensive medication (yes/no), any family history of heart attack in first degree relative (parent/sibling/child) (yes/no), and a coronary artery calcium score (Agatston units).

In many cases the CACS dramatically lowers or increases the risk estimate.

In this example a 64 year old man with no discernible risk factors has a CACS of 175
The 10 year risk of a CHD event almost doubles from 4.7% to 7.6% when the CACS is added to the standard risk factors and moves into a range where we need much more aggressive risk factor modification.

On the other hand if we enter in zero for this same patient the risk drops to a very low 1.9%.

It’s also instructive to adjust different variables. For example, if we change the family history of heart attack (parents, siblings, or children) from no to yes, this same patient’s risk jumps to 7.2% (2.6% with zero calcium score and to 10.4% with CACS 175.)

It can also be used to help modify risk-enhancing behaviors. For example if you click smoker instead of non-smoker the risk goes from 4.7% to 7.5%. Thus, you can tell your smoking patient that his risk is halved if he stops.

Discussions on the value of tighter BP control can also be informed by the calculator. For example, if  our 64 year old’s systolic blood pressure was 160 his risk has increased to 6.8%.

How Does Your CACS Compare To Your Peers?

A separate calculator let’s you see exactly where your score stands in comparison individuals with your same age, gender, and ethnicity

The Coronary Artery Calcium (CAC) Score Reference Values web tool will provide the estimated probability of non-zero calcium, and the 25th, 50th, 75th, and 90th percentiles of the calcium score distribution for a particular age, gender and race. Additionally, if an observed calcium score is entered the program will provide the estimated percentile for this particular score. These reference values are based on participants in the MESA study who were free of clinical cardiovascular disease and treated diabetes at baseline. These participants were between 45-84 years of age, and identified themselves as White, African-American, Hispanic, or Chinese. The current tool is thus applicable only for these four race/ethnicity categories and within this age range.

The calculator tells us that 75% of 64 year old white males have a zero CACS and that the average CACS is 61.

Unlike SAT scores or Echo Board scores you don’t want your CACS percentile status to be high. Scores >75th percentile typically move you to a higher risk category, whereas scores <25th percentile move you to a lower risk category, often with significant therapeutic implications.

Scores between the 25th and 75th percentile typically don’t significantly change the risk calculation.

Exploring Gender Differences In CACS

If we change the gender from male to female on our 64 year old the risk drops considerably from 4.7% down to 3.3%. This graph demonstrates that over 20% of women between the ages of 75 and 84 years will have zero calcium scores.

The graph for men in that same range shows that only around 10% will have a zero CACS.

I’ve been asked what the upper limit is for CACS but I don’t think there is one. I’ve seen numerous patients with scores in the high two thousands and these graphs show individuals in the lowest age decile having scores over 2981.

If you want to be proactive about the cardiovascular health of yourself or a loved one, download the MESA app and evaluate your risk. Ask your doctor if a CACS will help refine that risk further.

Antiatherosclerotically Yours,

-ACP

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

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

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

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

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

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

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

Total Cholesterol          223

LDL Cholesterol            143

HDL Cholesterol              67

Systolic Blood Pressure 122

Never Smoked Cigarettes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Nonalarmingly Yours,

-ACP

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

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

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

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

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

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

More Evidence That Dairy Fat Is Associated With A Lower Risk of Heart Disease

Although most nutritional authorities are now admitting that reducing saturated fat consumption by substituting carbohydrates was really bad advice, they, for the most part, are still sticking to the overall concept of limiting all saturated fats to <10% of daily calories and substituting “healthy” polyunsaturated fats for “unhealthy” saturated fats whenever possible.

The recently published (and highly criticized) Dietary Guidelines For Americans state:

The recommendation to limit intake of calories from saturated fats to less than 10 percent per day is a target based on evidence that replacing saturated fats with unsaturated fats is associated with reduced risk of cardiovascular disease. The limit on calories from saturated fats is not a UL set by the IOM. For most calorie levels, there are not enough calories available after meeting food group needs to consume 10 percent of calories from added sugars and 10 percent of calories from saturated fats and still stay within calorie limits.

Recommendations to limit saturated fatty acids (SFAs) to <10% of calories persist, despite a spate of recent meta-analyses showing no relationship between saturated fat consumption and coronary heart disease (CHD, also known as ischemic heart disease (IHD)).

In addition, it should be abundantly clear by now that not all SFAs behave the same with respect to our lipids or our IHD risk.

Wide Variety Of Saturated Fats

Most SFAs come from animal origins, including meat and dairy products. The types of SFAs differ markedly between meat and dairy products; the associated nutrients and their interaction with SFAs also differs widely and all of this is likely to affect the risk of IHD.

There is quite a bit of evidence that dairy fat actually lowers the risk of IHD.

For example, in the MESA  (Multi-Ethnic Study of Atherosclerosis) study, each 5-g/d intake of dairy SFAs was associated with a 16% lower risk of IHD, whereas each 5-g/d intake of meat SFAs was related to a 29% higher risk of IHD.

Despite this, current guidelines continue to repeat the unsubstantiated recommendation to consume low fat dairy over full fat dairy.

Lower Risk Of Heart Disease With Dairy Saturated Fats

Hopefully, a paper just published in the American Journal of Nutrition, will provide the nail in the coffin of the concept that all saturated fats are similar in their affects on blood lipids and cardiovascular risk and should be restricted.

This study found that higher intakes of SFA in 35,597 Dutch men and women were associated with lower risks of ischemic heart disease (IHD).

In other words, the more SFA the Dutch eat, the less their chance of having a heart attack.

And, the association “did not depend on the substituting macronutrient.” Those who ate less saturated fats and more “healthy” polyunsaturated fats did no better than those who substituted carbohydrates.

The association was dependent “on the chain length and food source of SFAs.”

The authors noted that the lower risk of IHD was driven by consumption of:

short-to-medium chain SFAs (myristic acid, the sum of pentadeclyic and margaric acids, and SFAs from dairy sources including butter, cheese, and milk and milk products.

Skeptics amongst my readers might think that this study was funded by the dairy industry, but as Marion Nestle pointed out on her Food Politics blog, support came from Unilever, who would have a vested interest in promoting their low saturated fat/high polyunsaturated fat margarines as substitutes for butter fat. This is only one of 11 industry-funded studies with findings different from what the sponsors would have liked, versus 105 studies with findings supporting products of the sponsors (since Marion has been tracking such studies).

It’s likely that some saturated fats, especially when eaten immoderately, without an otherwise balanced and diverse diet, can increase your risk of heart disease.

However, the saturated fats that come from dairy products are clearly not contributing to heart disease risk or obesity and our nutritional guidelines should recommend full fat dairy, not low fat or non fat products that require addition of added sugar to maintain palatability.

-Kind Regards

-ACP

 

 

Saturated Fat: Traditionalists versus Progressives

Why is death from coronary heart disease declining in the US at the same time that obesity and diabetes rates are climbing?

Two editorials recently published in The Lancet show the widely varying opinions on the optimal diet for controlling obesity , diabetes and coronary heart disease that experts on nutrition, diabetes and heart disease hold.

fats
Typical innocent and usual suspects rounded up in the war on fat: Cheese-data show it lower heart disease risk Full fat yogurt (Trader’s Point Creamery)-data show it is associated with lower heart disease risk Butter-Delicious. Used in moderation not a culprit.

The first paper contains what I would  consider the saturated fat “traditionalist” viewpoint. This is a modification of the misguided concept that was foisted on the American public in the 1980s and resulted in the widespread consumption of industrially produced trans-fats and high sugar junk food that was considered heart healthy.

The traditionalists have shifted from condemning all fats to vilifying only saturated and trans fats. They would like to explain at least part of the reduction in coronary heart mortality as due to lower saturated fat consumption and the accompanying lowering of LDL (“bad”) cholesterol.

The SFA traditionalists fortunately are in decline and more and more in the last five years, prominent thinkers, researchers and scientists working on the connection between diet and the heart believe saturated fats are neutral but sugar and refined carbohydrates are harmful in the diet.

Darius Mozzafarian, a highly respected cardiologist and epidemiologist, who is dean of the School of Nutrition Science and Policy at Tufts, wrote the second editorial and is what I would term a saturated fatty acid (SFA) progressive.

He makes the following points which are extremely important to understand and which I have covered in previous posts. I’ve included his supporting references which can be accessed here.

Fat Doesn’t Make You Fat, Refined Starches And Sugar Do

"Foods rich in refined starches and sugars—not fats—seem to be the primary culprits for weight gain and, in turn, risk of type 2 diabetes. To blame dietary fats, or even all   calories, is incorrect
Although any calorie is energetically equivalent for short-term weight loss, a food's long-term obesogenicity is modified by its complex effects on satiety, glucose–insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure Thus, foods rich in rapidly digestible, low-fibre carbohydrates promote long-term weight gain, whereas fruits, non-starchy vegetables, nuts, yoghurt, fish, and whole grains reduce       long-term weight gain.123
Overall, increases in refined starches, sugars, and other ultraprocessed foods; advances in food industry marketing; decreasing physical activity and increasing urbanisation in developing nations; and possibly maternal–fetal influences and reduced sleep may be the main drivers of obesity and diabetes worldwide".

There Are Many Different Kinds of Saturated Fats With Markedly Different Health Effects: It Makes No Sense to Lump Them All Together 

"SFAs are heterogeneous, ranging from six to 24 carbon atoms and having dissimilar biology. For example, palmitic acid (16:0) exhibits in vitro adverse metabolic effects, whereas medium-chain (6:0–12:0), odd-chain (15:0, 17:0), and very-long-chain (20:0–24:0) SFAs might have metabolic benefits.4 This biological and metabolic diversity belies the wisdom of grouping of SFAs based on a single common chemical characteristic—the absence of double bonds. Even for any single SFA, physiological effects are complex: eg, compared with carbohydrate, 16:0 raises blood LDL cholesterol, while simultaneously raising HDL cholesterol, reducing triglyceride-rich lipoproteins and remnants, and having no appreciable effect on apolipoprotein B,  5 the most salient LDL-related characteristic. Based on triglyceride-lowering effects, 16:0 could also reduce apolipoprotein CIII, an important modifier of cardiovascular effects of LDL and HDL cholesterol. SFAs also reduce concentrations of lipoprotein(a) ,6 an independent risk factor for coronary heart disease."

The Effects of Dietary Saturated Fats Depend on Complex Interactions With The Other Ingredients in Food

"Dietary SFAs are also obtained from diverse foods, including cheese, grain-based desserts, dairy desserts, chicken, processed meats, unprocessed red meat, milk, yoghurt, butter, vegetable oils, and nuts. Each food has, in addition to SFAs, many other ingredients and characteristics that modify the health effects of that food and perhaps even its fats. Judging the long-term health effects of foods or diets based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations. Endogenous metabolism of SFAs provide further caution against oversimplified inference: for example, 14:0 and 16:0 in blood and tissues, where they are most relevant, are often synthesised endogenously from dietary carbohydrate and correlate more with intake of dietary starches and sugars than with intake of meats and dairy.4"

Dietary Saturated Fat Should Not Be a Target for Health Promotion

"These complexities clarify why total dietary SFA intake has little health effect or relevance as a target. Judging a food or an individual's diet as harmful because it contains more SFAs, or beneficial because it contains less, is intrinsically flawed. A wealth of high-quality cohort data show largely neutral cardiovascular and metabolic effects of overall SFA intake.7 Among meats, those highest in processing and sodium, rather than SFAs, are most strongly linked to coronary heart disease.7Conversely, higher intake of all red meats, irrespective of SFA content, increases risk of weight gain and type 2 diabetes; the risk of the latter may be linked to the iron content of meats.28 Cheese, a leading source of SFAs, is actually linked to no difference in or reduced risk of coronary heart disease and type 2 diabetes.910 Notably, based on correlations of SFA-rich food with other unhealthy lifestyle factors, residual confounding in these cohorts would lead to upward bias, causing overestimation of harms, not neutral effects or benefits. To summarise, these lines of evidence—no influence on apolipoprotein B, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources—provide powerful and consistent evidence for absence of appreciable harms of SFAs."

Dietary Saturated Fats May Raise LDL cholesterol But This Is Not Important: Overall Effects On Obesity and Atherosclerosis Are What Matters

"a common mistake made by SFA traditionalists is to consider only slices of data—for example, effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trends; and expedient nutrient contrasts. Reductions in blood cholesterol concentrations in Western countries are invoked, yet without systematic quantification of whether such declines are explained by changes in dietary SFAs. For example, whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France.11Changes in dietary fats11 simply cannot explain most of the reductions in blood cholesterol in Western countries—even less so in view of the increasing prevalence of obesity. Medication use also can explain only a small part of the observed global trends in blood cholesterol and blood pressure. Whether decreases in these parameters are caused by changes in fetal nutrition, the microbiome, or other unknown pathways remains unclear, thus highlighting a crucial and greatly underappreciated area for further investigation."

Dietary Saturated Fats Are Neutral For Coronary heart Disease Risk

Finally, SFA traditionalists often compare the effects of SFAs only with those of vegetable polyunsaturated fats, one of the healthiest macronutrients. Total SFAs, carbohydrate, protein, and monounsaturated fat each seem to be relatively neutral for coronary heart disease risk, likely due to the biological heterogeneity of nutrients and foods within these macronutrient categories.7Comparisons of any of these broad macronutrient categories with healthy vegetable fats would show harm,12 so why isolate SFAs? Indeed, compared with refined carbohydrates, SFAs seem to be beneficial.7

The overall evidence suggests that total SFAs are mostly neutral for health—neither a major nutrient of concern, nor a health-promoting priority for increased intake. 

Focusing On Reducing Saturated Fats Leads To Unhealthy Dietary Choices

I’ve written about this a lot. The most baffling aspect of this is the promotion of low or non-fat dairy.

There is no evidence that low fat dairy products are  healthier than full fat dairy products.

Non-fat yogurt filled with sugar should be considered a dessert, not a healthy food.

"Continued focus on modifying intake of SFAs as a single group is misleading—for instance, US schools ban whole milk but allow sugar-sweetened skim milk; industry promotes low-fat foods filled with refined grains and sugars; and policy makers censure healthy nut-rich snacks because of SFA content.13 "

It is extremely hard to change most people’s opinions on dietary fat.

My patients have been hearing the SFA traditionalist dogma for decades and thus it has become entrenched in their minds.

When I present to them the new progressive and science-based approach to fat and saturated fat some find it so mind boggling that they become skeptical of the skeptical cardiologist!

Hopefully, in the next few years, the progressive SFA recommendations will become the norm and maybe , some day in the not too distant future, the inexplicable recommendations for low-fat or non fat dairy will disappear.

As more data accumulates we may become SFA enthusiasts!

Saturatingly Yours,

-ACP

For another viewpoint (?from an SFA enthusiast) and  a detailed description of both editorials see Axel Sigurdsson’s excellent post here.

Jamón Ibérico and The Mediterranean Diet

The skeptical cardiologist recently spent a week in the Basque region of Spain intensively researching dietary and lifestyle choices of this unique area.

Spain borders the Mediterranean and is often included in those countries that are considered to be the source of the Mediterranean diet (MD) which I recommend to my patients.

For a good summary of the Mediterranean “diet pyramid” check out this 1995 article.

The definition of the MD varies, often based on what  bias the definer has for particular foods or macronutrients, but initially was considered to be the food patterns typical of Crete, much of the rest of Greece and southern Italy in the early 1960s. The reason for choosing this time era and geography was based on:

  • very high adult life expectancy with very low rates of coronary heart disease, certain cancers and diet-related chronic disease
  • Data suggested common characteristics of  food availability and dietary intake
  • Epidemiological studies throughout the world on populations with similar dietary patterns suggested a benefit

The diet is closely tied to traditional areas of olive cultivation in the Mediterranean region.

The MD of the early 1960s had the following characteristics:

  • an abundance of plant foods (fruit, vegetables, breads, other forms of cereals, potatoes, beans, nuts and seeds)
  • minimally processed, seasonally fresh and locally grown foods
  • fresh fruit as the typical daily dessert
  • sweets containing concentrated sugar or honey consumed a few time per week
  • olive oil as the principal source of fat
  • dairy products (principally cheese and yogurt and full fat) consumed in low to moderate amounts
  • fish and poultry consumed in low to moderate amounts
  • zero to four eggs consumed weekly
  • red meat consumed in low amounts
  • wine consumed in low to moderate amounts, normally with meals

I stayed in a small beach town, Deba, in Spain which is half way between Bilbao (famous for its Guggenheim museum) and San Sebastian. There were very few non-Spanish tourists in Deba so  presumably the dietary and lifestyle choices I observed are representative of current Basque choices although likely different from the early 1960s.

I found the Basque people in Deba to be welcoming and joyful and European statistics show the Basque to be among the most satisfied with their overall life and job conditions.

Interestingly, the  life expectancy of the Basque population in  2000 in years was  75.8 for men and 83.8 for women, and by  2011 it had increased to 79.3 and 86.1, respectively. The Basque women live longer than women in any other country in Europe.

Walking around the squares of Deba I observed two activities which I would ordinarily have presumed would result in a low life expectancy: lots of cigarette smoking and lots of Jamón consumption.

hanginghamsHam was everywhere in Deba, from the supermarkets to the cafes. A typical appetizer choice was a plate full of Jamón Ibérico. Most of the pintxos (Basque-style tapas) we saw consisted of Jamon on bread.

From  jamon.com (dedicated to the fine art of ham):

jamon“Picture paper-thin strips of dark red ham like petals ringing a hand painted plate. Imagine big honest hams curing in the mountain air. Picture individual hams resting on stands in family kitchens throughout Spain with a long slim knife at hand for any and all to slice a treat.

In Spain, Jamón is hospitality. Jamón is Spain. Of all the European hams, jamón from Spain is the Gold Standard.”

Jamón, dry-cured ham, has been eaten in Spain and other Mediterranean countries since ancient times. There are basically two kinds: hams from rustic and free range  pigs (Iberia, Corsican or Cinta Senese) and hams from intensively-reared white pigs (Serrano, Parma, Bayonne).

Both hams involve a moderate salting and a ripening period of 7-14 months for white pigs and over 20 months for Iberian hams.

When they are finished curing, they have an incredibly complex taste,  distinct marbling, a deep red color and an intense ham flavor.

The most sought after ham is Jamón Ibérico de Bellota: a sub category of Jamón Ibérico” where the pigs are free to roam the meadows of the ‘dehesa’. During the autumn prior to their sacrifice, they are encouraged to gorge on acorns (bellotas) from the holm oak and cork trees, sometimes gaining as much as a kilo of weight a day.”

Health Consequences of Eating Jamón Ibérico.

A 100 g serving of Jamon Iberico contains 375 calories, 200 of them from fat. Of the total 22 grams of fat, 6.5 grams is saturated, 2 grams polyunsaturated, and 13 grams monounsaturated . There are 43 grams of protein and a lot of sodium ( 1.1 grams).

If we follow most current nutritional guidelines we would be advised to avoid Jamon because it is a considered a processed meat and it contains lots of salt and saturated fat.

Despite eating lots of Jamon,  however, the Spanish and Basque do very well in terms of longevity and rates of heart disease.

joxeancider
Our Basque host, Joxean, pouring cider from a giant wooden barrel at a “sagardotegi” or Basque cider house after yelling “Txotx”. See here (http://www.euskoguide.com/food-drink-basque-country/sagardotegi-sidreria-cider-house/)

The Basque good health could be related to any number of factors. They consume lots of fresh fish caught in nearby ports and prepared with lots of garlic and olive oil. (I had the best monkfish of my life in a cider house in the hills near Deba). Fish and olive oil are clearly beneficial dietary components.

They also drink alcohol in varied forms, including locally sourced apple cider, beer and fine local wines from Rioja.

moreflyschThey are active and they have long stretches of beautiful coastline to hike (including this geopark), some of the best surfing beaches in the world, and hills for cycling.

Ultimately, a healthy lifestyle consists of enjoyable and sustainable exercise and an enjoyable, sustainable  and palatable diet composed of  a combination of foods (mostly plants) , interacting in myriad unmeasurable ways. Focusing on specific fat (other than industrially produced trans fats) or sodium content is not a particularly useful approach.

I think Jamon can be considered part of a healthy Mediterranean diet when consumed in moderation and when combined with an active physical lifestyle. It makes a wonderful addition to anyone’s diet.

Jamónly yours,

-ACP

 

 

Since Dietary Cholesterol Isn’t Important Can I Stop Taking My Cholesterol Drug

A year ago one of my patients began experiencing  chest pain when he walked up hills. Subsequent evaluation revealed that atherosclerotic plaque (95% narrowing of a major coronary artery ) was severely reducing the blood flow to his heart muscle and was the cause of his chest pain. When this blockage was opened up with a stent he no longer had the pain.

Along with other medications (aspirin and plavix to keep his stent open) I had him start atorvastatin, the generic version of Lipitor, a powerful statin drug that has been shown to prevent progression of atherosclerotic plaque and thereby reduce subsequent heart attacks, strokes and death in patients like him

I saw him in the office the other day in follow up and he was feeling great . He asked me “Doc I read  your post yesterday.s Since you say that cholesterol in the diet doesn’t matter anymore, does that mean I don’t have to take my cholesterol drug anymore.?”

His question gets at the heart of the  “diet-heart hypothesis”. The concept that dietary modification, with reduction of cholesterol and fat consumption can reduce coronary heart disease.

The science supporting this hypothesis has never been strong but the concept was foisted on the American public and was widely believed. It was accepted I would  say because it has a beautiful simplicity which can be summarized as follows:

“If you eat cholesterol and fat it  will enter  your blood stream and raise cholesterol levels. This excess cholesterol will then  deposit in your arteries, creating fatty plaque , clogging them and leading to a heart attack.”

This concept was really easy to grasp and simplified the public health recommendations.

However, cholesterol blood levels are determined more by cholesterol synthesized in the liver and predicting  how dietary modifications will effect these levels is not easy.

Since the public has had the diet-heart hypothesis fed to them for decades and given its beautiful simplicity it is hard to reverse this dogma. My patient’s question reflects a natural concern that if science/doctors got this crucial question so wrong, is everything we know about cholesterol treatment and heart disease wrong?

In other words, are doctors promoting a great cholesterol hoax?

Evidence Strongly Supports Statins in Secondary Prevention 

For my patient the science supporting taking a  cholesterol-lowering statin drug is very solid. There are multiple excellent studies showing that in patients with established coronary artery disease taking a statin drug substantially reduces their risk of heart attack and dying.

These studies are the kind that provide the most robust proof: randomized, prospective and blinded.

level of evidenceWhen cardiologists rate the strength of evidence for a certain treatment (as done for lifestyle intervention here) we use  a system that categorizes the evidence as Level A, B, or C quality.

LeveleA quality (or strong) evidence consists of multiple,large, well-done, randomized trials such as exist for statins in patients with coronary heart disease.

Level B Evidence comes from a single randomized trial or nonrandomized studies.

Level C evidence is the weakest and comes from “consensus opinion of experts, case studies or standard of care.”

When treatment recommendations are based on Level C evidence they are often reversed as more solid data is obtained. Level A recommendations almost always hold up over time.

The level of evidence supporting restricting dietary cholesterol and fat to reduce heart attacks and strokes has always been at or below Level C and now it is clear that it is insufficient and should be taken out of guideline recommendations.

Evidence Strongly Supports Atherogenic Cholesterol is Related to Coronary Heart Disease

There are other lines of evidence that strongly support  the concept that  LDL cholesterol (bad cholesterol) or an atherogenic form of LDL cholesterol is strongly related to the development of atherosclerosis. If you are born with really high levels you are at very high risk for coronary heart disease, conversely if you are born with mutations that cause extremely low levels you are highly unlikely to get coronary heart disease.

Thus, the cholesterol hypothesis as it relates to heart disease is very much till intact although the diet-heart hypothesis is not.

Conflating the Diet-Heart Hypothesis and the Cholesterol Hypothesis

There is an abundance of misinformation on the internet that tries to conflate these two concepts. Sites with titles like “The Great Cholesterol Lie” , “The”  Cholesterol Hoax”, The Cholesterol Scam”  abound .

These sites proclaim that cholesterol is a vital component of cell membranes (it is) and that any attempt by diet or drugs to lower levels will result in severe side effects with no benefit

Doctors, according to these types of sites, in collusion with Big Pharma, have inflated the benefits of statin drugs and overlooked the side effects in the name of profit. Often, a “natural” alternative to statins is promoted.  In all cases a book is promoted.

The Great Cholesterol Truths

It’s unfortunate that nutritional guidelines have promoted restriction of cholesterol and fat for so long. These guidelines (like most of nutritional science)  were based on flawed observational studies. They should not have been made public policy without more consensus from the scientific community.  The good news is that ultimately the truth prevails when enough good scientific studies are done.

It is right to question the flimsy foundation of nutritional recommendations on diet and heart disease but the evidence for statin benefits in patients with established coronary heart disease is rock solid.

Hopefully, the less long-winded explanation I provided my patient in the office will persuade him to keep on taking his atorvastatin pills while simultaneously allowing him to eat eggs, shrimp and full fat dairy without guilt.

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.