As I have pointed out in a previous post, there is no reason to take multivitamins or any individual vitamin or supplement to prevent cardiovascular disease.
The U.S. Preventive Services Task Force (USPSTF) has just updated its 2003 recommendation on vitamin supplementation to prevent cardiovascular disease and cancer and published this analysis in the April 15, 2014 Annals of Internal Medicine issue.
Their recommendations agree with mine and those of the American Heart Association, the American Cancer Society and the Academy of Nutrition and Dietetics.
After analyzing all available studies they found insufficient evidence to support
the use of multivitamins to prevent cardiovascular disease or cancer
the use of single or paired nutrients (except β-carotene or vitamin E) for the prevention of cardiovascular disease or cancer (including Vitamins A, C, D, E, folic acid, selenium and beta-carotene)
About half the country is taking these worthless vitamins, supplements and multivitamins and spending 28 billion dollars per year on them.
This money would be much better spent on gym memberships or on the purchase of real, unprocessed food which contains all the vitamins and nutrients you need.
The skeptical cardiologist participated in the Pedaler’s Jamboree this Memorial Day weekend. This is an annual bicycling/music festival centered around a 30 mile bike ride from Columbia to Boonville, MO along the KT trail as it tracks the Missouri River. It ends at Kemper Park in Boonville with a concert and campout (the highlight of which for me was SHEL)
At various stops along the way we were treated to excellent roots/blues/folk
music. Our favorite moment was listening to an awesome duo from Fort Wayne, Indiana, the White Trash Blues Revival, in a downpour at the McBaine stop. The lead singer/guitarist played a home-made lap steel (made from a skate board and a Red Stripe beer bottle) and the drummer played trash cans, a beer keg and a cardboard box with outstanding results.
During the day, I observed thousands of my fellow pedalers consuming hot dogs and bratwursts at the various stops. In America, during Memorial Day weekend, several million brats and dogs will be consumed which made me ponder: is this increasing Americans’ risk of dying from heart disease?
US dietary-guidelines recommend “eating less” red and processed meat. For cardiovascular disease, these recommendations are based largely on expected effects on blood cholesterol of saturated fat and dietary cholesterol in meats. However, multiple recent published analyses have found no relationships of meat intake with cardiometabolic disease outcomes, including coronary heart disease (CHD), stroke, and diabetes.
This is a really important fact to know when making food choices, so I’m going to highlight it and repeat it:
Scientific studies do not show an association between unprocessed red meat consumption and cardiovascular disease.
“Red meat” is usually defined as unprocessed meat from beef, hamburgers, lamb, pork, or game, and excludes poultry, fish, or eggs.
“Processed meat” is any meat preserved by smoking, curing or salting, or addition of chemical preservatives, such as bacon, salami, sausages, hot dogs, or processed deli or luncheon meats, excluding fish or eggs.
A 2010 meta-analysis of American studies on this showed no increased risk of coronary heart disease for the highest consumers of unprocessed meat versus the lowest.
On the other hand, each serving per day of processed meat was associated with a 42% higher risk of coronary heart disease. Restricted to US studies, each serving per day was associated with 53% higher risk of diabetes.
A recent European study of 448,000 people found no association between unprocessed red meat consumption and mortality. For processed meats, there was an 18% higher risk of death per 50 gm/day serving.
Scientists really don’t know what it is about processed red meat that makes it associated with higher mortality.
As the table below indicates, the amount of saturated fat and cholesterol is not higher, so that does not appear to be the cause.
Because sodium nitrite is used to cure most processed meats, processed meats have about 4 times the amount of sodium as red meats.
High dietary sodium intake significantly increases blood pressure. Habitual consumption may also worsen arterial compliance and promote vascular stiffness, so It’s possible this is a factor.
Nitrate and nitrite levels are about 40% higher in processed meats and this has been suggested as a contributor to higher CVD and cancer rates.
However, 80-95% of dietary nitrates come from vegetables sources and a very significant source of nitrites is the breakdown of nitrates to nitrites by bacteria in saliva. Recent studies suggest that the blood pressure lowering effect of vegetables may be mediated by their nitrate content.
At present, it seems that dietary nitrite and nitrate have cardiovascular protective effects. … the effects of nitrite and nitrate to enhance NO bioavailability, to improve endothelial function, to cause vasodilation, and to inhibit platelet aggregation may at least partly mediate their cardiovascular beneficial effects. … Taking the data presented above together with the failure of recent studies to show significant correlation between nitrite and nitrate exposure and cancer, we suggest that the benefits of dietary nitrite and nitrate will strongly outweigh any potential risks, particularly for cardiovascular disease patients.
So, there is a signal from observational data that processed meats may increase cardiovascular disease and death, but exactly which ones might be the culprits and how this might work is entirely unclear. I’m still consuming brats, sausages, and hot dogs on occasion. Riding a bike, listening to music and drinking beer is a fine occasion for that.
I would advise the following
Don’t worry about nitrates/nitrites in processed meats. Science has not determined whether this is good or bad for you. Brands of bacon/sausage that claim no nitrates/nitrites are often using “natural” forms of nitrates that come from sources such as celery powder or sea salt.
Processed meats contain a lot of salt. Your body likely senses that and cuts back on salt consumption in other food choices during the day, especially if you indulge moderately. If you eat too much, too often, you put yourself at risk for high blood pressure and its attendant consequences. What is “too much” is uncertain, but the higher rates of heart disease and death don’t really seem to kick in until you eat the equivalent of greater than 80 grams per day.
Personally, I choose sustainably, humanely, “naturally” and locally raised processed meats whenever possible but there is no evidence-based medicine supporting this choice.
A new documentary movie, Fed UP, released May 9 and a New York Times Editorial published today are helping to focus the country’s attention on a new paradigm for what makes us fat and the importance of added sugar in causing obesity and chronic diseases. I highly recommend both viewing the movie and reading the editorial.
As I’ve pointed out here and here and as eloquently summarized by Gary Taubes in “Good Calories, Bad Calories” and “Why We Get Fat”, the concept of replacing fat with carbohydrates is not making America healthier.
The NY Times editorial and an article published by the same authors in JAMA focus on an alternative view of why people get fat. The generally accepted view is based on the (seemingly immutable) first law of thermodynamics, that you gain weight because you have consumed more calories than you have burned with exercise. People get fat due to lack of willpower in either consuming too many calories or not exercising enough. In this paradigm, all calories are equal in their effects. To lose weight you merely need to cut back on how many calories you consume. Unfortunately, calorie restriction for weight loss fails almost all the time.
The alternative view of obesity posits that underlying genetic factors exacerbated by lifestyle factors such as inadequate sleep, stress and by poor quality of diet are the major reasons for obesity. These factors lead to increase in fat storage which , in turn, means less metabolic fuels available for activity. This causes an increase in hunger and a reduction in metabolic activity, muscular efficiency and physical activity. The combination of increased energy intake and reduced energy expenditure causes obesity.
Insulin is the major hormone involved in fat metabolism and of all the things we eat highly refined and rapidly digestible carbohydrates cause the greatest insulin response. Thus, the authors write
By this way of thinking, the increasing amount and processing of carbohydrates in the American diet has increased insulin levels, put fat cells into storage overdrive and elicited obesity-promoting biological responses in a large number of people. Like an infection that raises the body temperature set point, high consumption of refined carbohydrates — chips, crackers, cakes, soft drinks, sugary breakfast cereals and even white rice and bread — has increased body weights throughout the population.
Fed Up, the movie, focuses on how American diets became awash in added sugar and what the consequences of that has been. Dr. Robert Lustig a pediatric endocrinologist at the University of California, San Francisco is an advisor to the film and has spoken and written eloquently on this new paradigm for obesity and the dangers of processed food, fructose and sugar as in this video.
Here’s the trailer for Fed Up.
The film has a limited release and may not be showing in your town, but you can check out some actions the film’s web site proposes (supporting a proposed tax on soda and sugary beverages, investigating your school’s nutrition policy, taking a 10 day no-sugar challenge) here.
The skeptical cardiologist recently participated in the 5 Boro New York City Bike Tour. It was quite cool.
This annual event allows 32,000 bike riders to stream from Manhattan to the Bronx to Queens, Brooklyn and Staten Island along 40 miles of traffic-free (except for thousands of cyclists) roads
Unlike my previous rides in Brooklyn and Manhattan (under the guidance of legendary Park Slope flaneur, NYC biking advocate, and old high school chum David Alquist) I was not in constant peril from automobile encounters because we cyclists had the mean streets of New York all to ourselves.
Take a look at this video to understand “why cyclists come from around the world for an experience of the Big Apple unlike any other”.
Urban Cycling as Transportation
The NYC event, and the fact that this is “bike to work week,” lead me to ponder aspects of urban bike riding, specifically, cycling as transportation. Since cycling is physical exercise and there is scientific evidence (observational studies only) linking regular physical activity to a significant cardiovascular risk reduction, we might expect that it would help us live longer.
A reasonable physical activity goal , endorsed by most authorities, is to engage in moderate-intensity aerobic physical activity for a minimum of 30 min on 5 days each week or vigorous-intensity aerobic activity for a minimum of 20 min on 3 days each week. This level of exercise helps with weight control, fitness and is associated with lower mortality from cardiovascular disease .
The metabolic equivalent of task (MET) is a measure of the energy cost of physical activity. The chart to the left gives METs for various activities. Individuals should be aiming for 500–1,000 MET min/week. Leisure cycling or cycling to work (15 km/hr) has a MET value of 4 and is characterized as a moderate activity A person shifting from car to bicycle for a daily short distance of 7.5 km would meet the minimum recommendation (7.5 km at 15 km/hr = 30 min) for physical activity in 5 days (4 MET × 30 min × 5 days = 600 MET min/week).
Thus, cycling to work for many individuals would provide the daiy physical activity that is recommended for cardiovascular benefits. However, cycling in general, and urban cycling in particular, carries a significant risk of trauma and death from accidents and possibly greater exposure to urban pollutants.
This table shows the estimated numbers of traffic deaths per age category per billion passenger kilometers traveled by bicycle and by car (driver and passenger) in the Netherlands for 2008. These data suggest that there are about 5.5 times more traffic deaths per kilometer traveled by bicycle than by car for all ages. Interestingly, there is no increase in risk for individuals aged 15-30 years. On the other hand , those of us in the “baby-boomer” generation (?slowed reflexes, poor eyesight, impaired hearing) and older are at an 8 to 17 fold increase risk.
In the Netherlands, where a very large percentage of the population regularly rides bikes, there has been considerable scientific study of the overall health consequences of biking and we have reasonably good data on the question of relative safety of biking versus driving a car for short distances. You can watch the happy people of Groningen (“the world’s cycling city”, where 57% of the journeys in the city are made by bicycle) riding their bikes below.
Health Impact of Transition from Car to Bike for Short Trips
One study quantified the impact on all-cause mortality if 500,000 people made a transition from car to bicycle for short trips on a daily basis in the Netherlands and concluded
For individuals who shift from car to bicycle, we estimated that beneficial effects of increased physical activity are substantially larger (3–14 months gained) than the potential mortality effect of increased inhaled air pollution doses (0.8–40 days lost) and the increase in traffic accidents (5–9 days lost). Societal benefits are even larger because of a modest reduction in air pollution and greenhouse gas emissions and traffic accidents.
Apart from the highest average distance cycled per person, the Netherlands is also one of the safest countries in terms of fatal traffic accidents so it’s reasonable to ask whether these data apply to other countries. This study concluded
When traffic accident calculations for the United Kingdom were utilized, where the risk of dying per 100 million km for a cyclist is about 2.5 times higher, the overall benefits of cycling were still 7 times larger than the risks.
If you decide to bike to work this week, braving the elements , the possible automobile collisions and the automobile exhaust you can rest comfortably with the thought that not only are you prolonging your own life but by reducing greenhouse gas emissions and air pollution you are contributing to the health of everyone around you.
Aspirin is a unique drug, the prototypical two-edged sword of pharmaceuticals. It has the capability of stopping platelets, the sticky elements in our blood, from forming clots that cause strokes and heart attacks when arterial plaques rupture, but it increases the risk of serious bleeding into the brain or from the GI tract. Despite these powerful properties, aspirin is available over the counter and is very cheap, thus anyone can take it in any dosage they want.
Who Should Take Aspirin?
For the last five years I’ve been advising my patients who have no evidence of atherosclerotic vascular disease against taking aspirin to prevent heart attack and stroke. Several comprehensive reviews of all the randomized trials of aspirin had concluded by 2011 that
The current totality of evidence provides only modest support for a benefit of aspirin in patients without clinical cardiovascular disease, which is offset by its risk. For every 1,000 subjects treated with aspirin over a 5-year period, aspirin would prevent 2.9 MCE and cause 2.8 major bleeds.
(MCE=major cardiovascular events, e.g. stroke, heart attack, death from cardiovascular disease)
Dr. Oz, on the other hand, came to St. Louis in 2011 to have lunch with five hundred women and advised them all to take a baby aspirin daily (and fish oil, which is not indicated for primary prevention as I have discussed here). When I saw these women subsequently in my office I had to spend a fair amount of our visit explaining why they didn’t need to take aspirin and fish oil.
After reviewing available data, the FDA this week issued a statementrecommending against aspirin use for the prevention of a first heart attack or stroke in patients with no history of cardiovascular disease (i.e. for primary prevention). The FDA pointed out that aspirin use is associated with “serious risks,” including increased risk of bleeding in the stomach and brain. As for secondary prevention for people with cardiovascular disease or those who have had a previous heart attack or stroke (secondary prevention), the available evidence continues to support aspirin use.
Subclinical Atherosclerosis and Aspirin usage
As I’ve discussed previously, however, many individuals who have not had a stroke or heart attack are walking around with a substantial burden of atherosclerosis in their arteries. Fatty plaques can become quite advanced in the arteries to the brain and heart before they obstruct blood flow and cause symptoms. In such individuals with subclinical atherosclerosis aspirin is going to be much more beneficial.
Guided Use of Aspirin
We have the tools available to look for atherosclerotic plaques before they rupture and cause heart attacks or stroke. Ultrasound screening of the carotid artery, as I discussed here, is one such tool: vascular screening is an accurate, harmless and painless way to assess for subclinical atherosclerosis.
In my practice, the answer to the question of who should or should not take aspirin is based on whether my patient has or does not have significant atherosclerosis. If they have had a clinical event due to atherosclerotic cardiovascular disease (stroke, heart attack, coronary stent, coronary bypass surgery, documented blocked arteries to the legs) I recommend they take one 81 milligram (baby) uncoated aspirin daily. If they have not had a clinical event but I have documented by either
vascular screening (significant carotid plaque)
coronary calcium score (high score (cut-off is debatable, more on this in a subsequent post)
Incidentally discovered plaque in the aorta or peripheral arteries (found by CT or ultrasound done for other reasons)
then I recommend a daily baby aspirin (assuming no high risk of bleeding).
There are no randomized trials testing this approach but in the next few years several large aspirin trials will be completed and hopefully we will get a better understanding of who benefits most from aspirin for primary prevention.
Until then remember that aspirin is a powerful drug with potential for good and bad effects on your body. Only take it if you and your health care provider have decided the benefits outweigh the risks after careful consideration of your particular situation.
The skeptical cardiologist was planning on attending Moogfest 2014 in Asheville, North Carolina last weekend. I was going with the old friend and life coach of the skeptical cardiologist (OFLCSC) and planned on taking in electronic and synthesizer legends like Kraftwerk and Keith Emerson, riding bikes and drinking lots of craft beer. Unfortunately, a very bad upper respiratory infection took hold of me, progressing to what felt like a pneumonia (shaking chills, fever, coughing up dark, thick sputum, rattling emerging from the depths of my lungs) and I had to cancel the trip.
After processing multiple factors of risk versus benefit (not to mention the contribution to resistant bacteria), I decided to start myself on a Z-pak which is commonly utilized for community acquired pneumonia (does this mean I have a fool for a doctor?)
Azithromycin (the macrolide antibiotic in the Z-pak) , due to its broad antibiotic spectrum and perceived favorable safety profile, became one of the top 15 most prescribed drugs and the best-selling antibiotic in the United States, accounting for 55.4 million prescriptions in 2012.
Between 2004 to 2011, the FDA received 203 reports of azithromycin-associated QT prolongation (see graphic to the left) Torsades de Pointes (graphic) ventricular arrhythmia, or, in 65 cases, sudden cardiac death.
This prompted a review of Tennessee medicaid data which was published in 2012.
This study found that people taking azithromycin over the typical 5 days of therapy, had a rate of cardiovascular death 2.88 times higher than in people taking no antibiotic, and 2.49 times higher than in people taking amoxicillin. Most of the risk appeared to be those patients who had a baseline high risk of cardiovascular disease and the excess risk of death resolved after the 5 days of therapy.
As a result, the FDA added a warning to the azithromycin package insert and urged health care professionals to use caution when prescribing it to patients known to have risk factors for drug-related arrhythmias, including those with long QT intervals, either congenitally or induced by drugs, low potassium or magnesium levels, slow heart rates or on other medications drugs used to control abnormal heart rhythms (amiodarone, sotalol and dofetilde).
I survived my 5 day brush with a three-fold increased risk of sudden death and I really think the Z-pak substantially helped me get over the bacterial lung infection I felt I had. I knew my risk factors in detail and they were low. I was totally aware of any interacting drugs that could prolong my QT interval.
You can survive too. Make sure you definitely need the drug (i.e. you have a bacterial infection not just the common cold) and be cautious if you have any of the following
Family history of sudden death
Personal history of unexplained passing out or dizziness
Use of other medications that prolong QT interval (PDF)
Low potassium or magnesium levels (not uncommon in heart failure patients who are on water pills)
Many of my patients believe that coffee is bad for them. I’m not sure where this belief comes from; perhaps the general belief that anything that they really like and are potentially addicted to cannot be healthy.
It’s not uncommon for a patient to tell me after a heart attack that they have “really cleaned up their act” and have stopped drinking alcohol and cut back on coffee. They seem disappointed when I tell them that moderate alcohol consumption and coffee consumption are heart healthy behaviors.
In contrast to what the public believes, the scientific evidence very consistently suggests that drinking coffee is associated with living longer and having less heart attacks and strokes. Multiple publications in major cardiology journals in the last few years have confirmed this.
You can read the details here and here. The bottom line is that higher levels of coffee consumption (>1 cup per day in the US and >2 cups per day in Europe) are NOTassociated with:
Hypertension (if you are a habitual consumer)
Higher total or bad cholesterol (unless you consume unfiltered coffee like Turkish, Greek or French Press types, which allow a fair amount of the cholesterol-raising diterpenes into the brew)
Increase in dangerous (atrial fibrillation/ventricular tachycardia) or benign (premature ventricular or supra-ventricular contractions) irregularities in heart rhythm
Higher levels of coffee consumption compared to no or lower levels IS associated with:
lower risk of Type 2 Diabetes
lower risk of dying, more specifically lower mortality from cardiovascular disease
So, if you like coffee and it makes you feel good, drink it without guilt, there is nothing to suggest it is hurting your cardiovascular health. It’s a real food. These tend to be good for you.
Making Coffee Unhealthy: Dessert as Stealth Food
People have always added things to coffee – cream, half and half, milk, skim milk, sugar, artificial sweeteners. The coffee data doesn’t reveal to us what the consequences of these additions are, but given the consistent positive health associations of coffee, they must have had a minor effect.
However, in the last 20 years, the food industry, led by the behemoth Starbucks (which controls 1/3 of the coffee served in the US and has 11,000 stores and growing) has turned coffee into a stealth dessert. Starbucks offers the consumer (by their own admission) 87,000 different choices of coffee drinks.
A basic coffee house drink is a latte’. This consists of one or more shots of espresso combined with steamed milk (skim, 2% or whole) and topped with foam. According to Starbucks, the 16 ounce, medium (I refuse to use their size terminology), cafe latte’ made with 2% milk, contains 17 grams of sugar and 7 grams of fat, yielding a reasonable 190 calories. Those who drink these should understand that they are consuming a glass of milk, plus coffee. Dairy products have consistently been associated with lower cardiovascular risk. They would arguably be better off consuming a whole milk (11 grams fat, 16 grams sugar, 220 calories) latte’ as I’ve pointed out in previous blogs here and here.
Most of the latte’s consumed at Starbucks aren’t plain latte’s, however; they are nightmares of added sugar. Let’s take the Cinnamon Dolce Latte’: (A complete nutritional breakdown is available from Starbucks’ website (I do congratulate Starbucks for finally capitulating and presenting nutritional data on their products at stores, allowing the public to draw back the curtain on the Starbucks Oz. Their website provides a cool way to compare your drink with whole/2%/skim/soy milk or with and without whipped cream)) It contains 38 grams of sugar, 6 grams of fat, and 11 grams of protein, yielding 260 calories, 152 of which are coming from sugar. That’s 22 grams more sugar, compared to their unadulterated latte’. (There must be an internet site devoted to promoting the health benefits of cinnamon since I hear about them so often from my patients but this claim is not evidence-based)
My 17 year old daughter’s drink of choice at Starbucks is the Mocha Frappuccino® Blended Beverage, which, according to Starbucks, is “Coffee with rich mocha-flavored sauce, blended with milk and ice. Topped with sweetened whipped cream.” It contains 60 grams of sugar, 15 grams of fat and has 400 calories.
Such concoctions have no right to consider themselves coffee, they should be labeled as a sugar-laden dessert that happens to have some coffee in it. To give some perspective, the typical 20 ounce soda contains 40 grams of sugar (the equivalent of 10 packs of sugar). Starbucks has added 44 grams of sugar to coffee and milk in order to draw children, teens and unsuspecting adults to consume more “coffee.”
There is growing evidence that sugar, not fat, is the major toxin in our diet. The misguided concept that cutting fat in the diet and replacing it with anything, including sugar, will reduce cardiovascular disease is gradually being rolled back. Nutritional advocates are now zeroing in on appropriate targets like sugary beverages.
It’s sad that Starbucks, which started out making a good, real product that was actually good for you, has morphed into an international, growth-obsessed, behemoth that is pumping billions of grams of added sugar into our stomachs.
But, as the significant other of the skeptical cardiologist (SOSC) often muses, people are always looking for new ways to con themselves into thinking they are eating/drinking something healthy, when in fact, they are just eating/drinking cleverly disguised desserts. Starbucks has made a huge success for themselves by providing people what they want: a way to kid themselves.
I reviewed in a previous post the importance of detecting sublinical atherosclerosis when trying to assess someone’s risk of heart attack and of dying suddenly. Subclinical atherosclerosis refers to the build-up of plaque in the lining of our arteries which occurs long before any symptoms of atherosclerosis occur.
Since the process tends to be diffuse, occurring in all the large arteries of the body, it makes sense that if we can easily visualize one artery this will give us a window into what is happening in other arteries (including the coronary arteries supplying blood to the heart muscle).
The vascular screening I offer in my office uses high frequency ultrasound to image the large artery, the carotid artery, that supplies blood to the brain.
Normally the lining of that artery is smooth and thin as in the example to the left. As the process of atherosclerosis works its damage on the artery lining it becomes thicker and plaque begins to develop. High frequency ultrasound is an excellent tool for identifying these early, subclinical stages of atherosclerosis because it is painless, harmless, inexpensive, and quick.
Identifying Higher Risk Patients
Mr. M is a 60 year old man who I was seeing for an abnormal heart rhythm. Using the ACC risk estimator I calculated his 10 year risk of atherosclerotic cardiovascular disease (ASCVD) as <7.5%. However, he had a brother who had cardiac stents placed in his coronary arteries (indicating coronary artery disease (CAD)). His carotid artery screening (shown below) shows a large, soft plaque
This indicates that although his known risk factors for atherosclerosis were not tremendously high, the combination of known and unknown factors (likely genetic, given his brother’s premature CAD) were damaging the lining of his arteries leaving him at a high risk for stroke and heart attack.
A patient like Mr. M I consider to have documented atherosclerotic cardiovascular disease (ASCVD)and I will strongly recommend statin therapy along with a baby aspirin
Several studies have shown in those patients who are reluctant to start statin therapy, documenting subclinical atherosclerosis serves as a strong motivational factor for lifestyle change or compliance with medications.
Identifying Lower Risk Patients
Equally important as identifying advanced subclinical atherosclerosis, imaging the carotid artery can identify those patients who are at lower risk and save them from a lifetime of unnecessary treatment.
Ms N is 64 years old whom I see h for high blood pressure and supra ventricular tachycardia (an abnormal heart rhythm). She has a total cholesterol of 219, HDL(or good) cholesterol of 74, systolic blood pressure of 130 and the ACC risk estimator gives her an 8.4% risk of ASCVD over the next 10 years. She greatly dislikes taking medications, but her mother died in her early fifties from a “massive heart attack” .
Her carotid exam shows the carotid thickness as less than average for her age and gender, equivalent to that of a 58 year old. There is no plaque anywhere in her carotid system. I feel comfortable not recommending statins to this type of patient. In many cases, I often stop cholesterol treatment in patients with no evidence for subclinical atherosclerosis who have marginal cholesterol levels and intermediate risk.
What vascular screening allows me is the ability to see if my patients do or do not have the disease that we are trying to prevent or mitigate: atherosclerosis.
As the skeptical cardiologist I must point out that national guidelines do not endorse vascular screening primarily because there are no randomized controlled trials showing that it influences outcomes. I’ll talk more about potential pitfalls of vascular screening when done by for profit ventures in a subsequent post and we’ll discuss the other good way of assessing for subclinical atherosclerosis: coronary calcium.
This container of Yoplait comes from the refrigerator in the Doctor’s Lounge at my hospital. It is often the go-to snack for busy doctors and health conscious consumers.
I used to consider Yoplait about as healthy a snack as I could get. After all, it was low in fat, owned by French farmers and it had pictures of fruit on it. How could I go wrong?
“Ultimately, we’re focused on making so good yogurt, and here’s how we see it: you can eat something that tastes amazing but isn’t that good for you. You can eat stuff that’s really good for you, but doesn’t always leave you yummed up. So good yogurt does both. All of you is happy, not just your tongue. And while so goodness will never be perfect, we’ll keep working on ways to make our yogurt more so good than it is today.”
The significant other of the skeptical cardiologist (SOSC) made the claim recently that women who felt they were having a healthy lunch by consuming fat free yogurt and salad with sugary, fat-free salad dressing might as well be eating a candy bar. At least they would enjoy it more! Could this be true?
Yoplait made the bold step in 2012 of taking out the high fructose corn syrup they had been adding to their yogurt (or yoghurt as they like to spell it), but it’s still chock full of added sugar (which is probably why it leaves you “yummed up”)
What is now in “original” Yoplait?
Original Yoplait has 12 ingredients. They are Cultured pasteurized Grade A Low Fat Milk, Sugar, Blueberries, Modified Corn Starch, nonfat milk, kosher gelatin, citric acid, tricalcium phosphate, pectin, natural flavor colored with beet juice concentrate, Vitamin A and Vitamin D3.
Indeed, the fat has been taken out but in its place – added sugar, 26 grams of sugar to be precise.
Of the 170 calories you are consuming, 104 of them are coming from sugar.
How healthy is a Snickers Bar?
A regular-sized Snickers candy bar has a total of 280 calories with 13.6 grams of fat (5 grams saturated fat), 35 grams of carbohydrates (29 grams of sugar) and 4.3 grams of protein. It is made with peanuts, milk chocolate, egg whites and hydrogenated soybean oil. If we ate 2/3 of the bar to make the calories the same as the Yoplait, there would be 19 grams of sugar (compared to 26 for Yoplait) and 8 grams of fat.
A recent review of the cardiovascular effects of tree nuts and peanuts concluded:
there is impressive evidence from epidemiological and clinical trials and in vitro studies of beneficial effects of nut consumption and their constituents on the risk of CVD (cardiovascular disease), including sudden death, as well as on major and emerging CVD risk factors.
This is because in addition to a favorable fatty acid profile, nuts and peanuts contain other bioactive compounds that provide cardiovascular benefits. Other macronutrients include plant protein and fiber; micronutrients including potassium, calcium, magnesium, and tocopherols; and phytochemicals such as phytosterols, phenolic compounds, resveratrol, and arginine.
So, consuming 2/3 of a Snickers bar is arguably healthier than Yoplait. It contains peanuts, which have demonstrable benefits in lowering cardiovascular disease despite a high fat content. Yoplait has had the heart healthy dairy fat removed and replaced with added sugars. As I mentioned in a previous post, added sugar is clearly related to increased cardiovascular risk. The higher fat and fibre content of the peanuts in the Snickers bar will increase satiety and arguably be less likely to cause obesity due to rebound overeating later in the day.
A much healthier choice than low fat, added sugar products like Yoplait (and candy bars) is full fat, plain yogurt (preferably from grass-fed cows) as I’ve discussed in previous posts. It can be combined with real fruit or even with nuts. Full fat yogurt is surprisingly hard to find on a grocery shelf. Even at Whole Foods, the vast majority of yogurt and dairy products are low fat. I’ve only been able to find two brands, Supernatural and Trader’s Point Creamery, which consistently offer full fat yogurt.
Disclaimer and clarifications
I do not receive any payments from Snickers nor from Mars, Inc., one of the most known and beloved brands of chocolate. I do not plan on seeing Godzilla, May 16. Although Snickers loves you, you do not need to like Snickers.
Nearly every day I see a patient in the office who has just experienced a friend or relative suddenly “dropping dead.” Understandably, they are very concerned about this and want to know “Is this going to happen to me?”
There is very good reason to be concerned. Cardiac disease is the leading cause of death in America. Despite considerable progress, regrettably 50% of deaths occur suddenly, without any previous symptoms which would have suggested a cardiac problem. It doesn’t just hit the overweight or the smoker. It not uncommonly strikes the very fit and seemingly healthy, as in the case of the St. Louis Cardinal pitcher, Daryl Kile, who was found dead in his hotel room at the age of 34. This question of who is going to suddenly drop dead (sudden cardiac death or SCD) is one of the fundamental unsolved mysteries in current cardiology.
Atherosclerosis and Dropping Dead
Most SCD in individuals over the age of 35 is related to the development of fatty plaques (atherosclerosis) in the arteries that supply blood to the heart (coronary arteries) and the subsequent sudden rupture of these plaques (thrombosis). The result of this rupture is the complete blockage of the artery and the total cessation of blood flow to a portion of the heart muscle. When that heart muscle portion becomes starved for oxygen, the muscle cells start dying and a myocardial infarction (MI) or heart attack occurs. You can view an animation of this process here With any MI, the dying muscle cells can become electrically irritable and initiate an abnormal heart rhythm called ventricular tachycardia (VT) or ventricular fibrillation (VF). This abnormal rhythm is what causes people to “drop dead” suddenly. Basically, the heart cannot pump blood efficiently in VT or VF; thus, there is no blood flowing to the brain and other vital organs. This is a long, complicated chain of events, but basically it begins with the development of fatty plaques or atherosclerosis. It makes sense that we can stop people dropping dead from MI by stopping the development and progression of atherosclerosis. Atherosclerosis develops long before any clinical signs or symptoms of disease. You can feel totally fine and have a huge build up of plaque in all of the arteries of your body. This is termed subclinical atherosclerosis. It makes sense, and it has been scientifically proven, that those with a huge buildup of plaque (high plaque burden) are at higher risk for MI and death than those with low or no plaque burden. It also makes sense that treating those patients with high plaque burden will be most beneficial.
How Do you know if you have atherosclerosis
I discussed the standard recommended method for determining risk of MI/SCD in my last post on statins. Basically, this is simply adding up the factors we know contribute to atherosclerosis: diabetes, cigarette smoking, hypertension, age, gender and cholesterol levels. However, most heart attacks and strokes occur in people who are classified by traditional risk factor scoring as low or intermediate risk. Conversely, others are misclassified as high risk and mistakenly advised to take drugs to reduce their risk factors for the rest of their lives.
How Can We Detect Subclinical Atherosclerosis?
In my office practice I offer patients two tests which directly detect and quantify subclinical atherosclerosis. One looks for plaque and thickening in the larger arteries of the neck, the carotid arteries, and one looks for calcium in the coronary arteries. I’ll go into detail about both of these in subsequent posts. For now, I will just say that the carotid screening technique uses harmless ultrasound while the coronary calcium technique uses ionizing radiation from a CT scan. Neither test is covered by insurance or Medicare. Both tests have been shown to improve our ability to identify those at risk for MI and stroke.
These tests are helpful in two general areas:
*The first scenario is the patient who appears to be at low or intermediate risk for atherosclerosis based on the risk estimator, but who has a strong family history of MI, sudden death or stroke. If we identify significant subclinical atherosclerosis in this patient, statin therapy is more likely to be beneficial.
*The second scenario is the patient who has been put on statins for primary prevention based on standard risk estimator but has no family history of ASCVD and is questioning the need for treatment. In this patient if we find no subclinical atherosclerosis, a strong argument can be made to stop the statin drug.
There is an organization dedicated to promoting the detection of SA by these tests and an algorithm for treatment called SHAPE (Society for Heart Attack Prevention and Education). Interestingly, after a female Texas state representative suffered an MI, in 2009, Texas Governor Ricky Perry signed off on the Texas Heart Attack Prevention Bill mandating health-benefit plans to cover screening tests for SA. No other state to my knowledge has such a law.
How to Stop Sudden Cardiac Death
The two tests I mentioned are a good second step towards identifying the individual at risk for MI and SCD but we still don’t know who among those with advanced subclinical atherosclerosis is going to experience a sudden rupture of plaque, have an MI and drop dead.
We need a way to identify those patients with vulnerable plaque (one that is about to rupture) and aggressively treat those patients. This is an area of intense research focus. You can view a fascinating video (accompanied by weirdly cool music) created by SHAPE here and another (featuring a gun shooting a heart) here emphasizing the importance of the vulnerable plaque.