Many of us think that heart disease is something that happens to other folks. Well, the fact is that heart disease is the number one killer of both men and women. In this episode of Nutrition Facts we’ll look at how to reverse heart disease, address the role of Omega-3’s for heart health and see if we can extend our lives by slowing our heartbeats.
Have you ever wondered if there’s a natural way to lower your high blood pressure, guard against Alzheimer's, lose weight, and feel better? Well as it turns out there is. Michael Greger, M.D. FACLM, founder of NutritionFacts.org, and author of the instant New York Times bestseller “How Not to Die” celebrates evidence-based nutrition to add years to our life and life to our years.
Hello and welcome to Nutrition Facts – the podcast that brings you the latest in evidence-based nutrition research. I’m your host, Dr. Michael Greger.
I’m often asked what my opinion is about one food or another. I know what people are asking but, you know, I’m not interested in opinions. I’m not interested in beliefs. I’m interested in the science. What does the best available balance of evidence published in the peer-reviewed medical literature show right now? That’s why I wrote my book, “How Not to Die”, and why I created my nonprofit site NutritionFacts.org and, now, this podcast.
Today, we’re going to discuss our hearts. Did you know that by age 10 nearly all kids raised on the standard American diet already have fatty streaks in their arteries? This is the first sign of atherosclerosis, the leading cause of death in the United States for both men and women. So, the question for most of us is not whether we should eat healthy to prevent heart disease, but whether we want to reverse the heart disease we very well may already have.
It was this landmark study published in 1953 that radically changed our view about the development of heart disease forever. A series of 300 autopsies performed on U.S. battle casualties of the Korean War, average age 22. Twenty-two years old, but 77% of their hearts had gross evidence, meaning visible-to-the-eye evidence, of coronary atherosclerosis, hardening of their arteries. Some of them had vessels that were clogged off 90% or more.
As an editorial in the Journal of the American Medical Association concluded: This widely cited publication dramatically showed that atherosclerotic changes appear in the coronary arteries years and decades before the age at which coronary heart disease becomes a clinically recognized problem, before symptoms arise. Follow-up studies on the hearts of thousands more soldiers over the subsequent years confirmed their results.
How young does it go? Fatty streaks, the first stage of atherosclerosis, were found in the arteries of 100% of kids by age ten. What’s accounting for this buildup of plaque, even in childhood? In the ‘80s, we got our first clue, the now-famous Bogalusa Heart Study looking at autopsies of those dying between the ages of 3 years old to age 26, and the number one risk factor was cholesterol.
You could see the stepwise increase in the amount of their arteries covered in fatty streaks as the level of bad cholesterol in the blood increased. As powerful as this was, this was only looking at 30 kids. So, they decided to study 3,000. Three thousand accidental death victims, ages 15 through 34.
After thousands of autopsies, they were able to produce a scoring system, able to predict advanced atherosclerotic lesions in the coronary arteries of young people. The higher your score, the higher the likelihood you have these lesions growing in your heart.
So, if you’re in your teens, twenties, early thirties, and you smoke, your risk goes up a point. If you have high blood pressure at such a young age, that’s four points. If you’re an obese male, six points. But, high cholesterol was the worst. If your non-HDL cholesterol (meaning your total cholesterol minus your good cholesterol) is above, like, 220, that’s like eight times worse than smoking.
So, let’s say you’re a young woman with relatively high cholesterol, but you don’t smoke, you’re not overweight, your blood pressure and blood sugars are fine. At your sweet sixteen, there’s just a few-percent chance you already have an advanced atherosclerotic lesion in your heart, but, if you don’t improve your diet, by your 30th birthday, there may be like a one-in-five chance you have some serious heart disease and, if you have really high cholesterol, it could be closer to one in three.
Bringing your cholesterol down to even just that of a lacto-ovo vegetarian and you’re down to here and, if you exercise to boost your HDL, you can extrapolate down a little further. So, what this shows us is that even in 15- to 19-year-olds, atherosclerosis has begun in a substantial number of individuals, and this observation suggests beginning primary prevention at least by the late teenage years to ameliorate every stage of atherosclerosis and to prevent or retard progression to more advanced lesions.
You start kids out on a low-saturated-fat diet and you may see a significant improvement in their arterial function by 11 years old. Exposure to high serum cholesterol, even in childhood, may accelerate the development of atherosclerosis. Consequently, the long-term prevention of atherosclerosis might be most effective when initiated early in life, as in seven months of age.
Atherosclerosis (hardening of the arteries) begins in childhood. Remember, by age 10, nearly all kids have fatty streaks, the first stage of the disease. Then, the plaques start forming in our 20s and get worse in our 30s, and then can start killing us off. In our hearts, it’s a heart attack; in our brains, it’s a stroke; in our extremities, it can mean gangrene; in our aorta, an aneurism.
If there is anyone watching this video that is older than ten years of age, the choice likely isn’t whether or not to eat healthy to prevent heart disease, it’s whether or not you want to reverse the heart disease you already have.
Ornish and Esselstyn proved you can reverse heart disease with a plant-based diet but we don’t have to wait until our first heart attack to reverse the clogging of our arteries. We can start reversing our heart disease right now. We can start reversing heart disease in our kids, tonight. There’s only one diet that’s ever been proven to reverse heart disease in the majority of patients. If that’s all a plant-based diet could do, reverse the number one killer of men and women, then shouldn’t that be the default diet until proven otherwise?
But what about fish oil, long-chain omega-3 fats, to keep our hearts healthy? There has been a big shift in the science. Here’s the latest: According to two of perhaps the most credible nutrition authorities, the World Health Organization and the European Food Safety Authority, we should get at least a half a percent of our calories from the essential short-chain omega-3 ALA, which is easy, just like a tablespoon a day of chia seeds or ground flax seeds and you’re all set.
Our body can then take the short-chain ALA from our diet, and elongate it into the long-chain omega-3s, EPA and DHA, but the question has long been, can our bodies make enough for optimal health? Well, how would you determine that?
Well, take fiber, for example. A convincing body of literature showed an increased heart disease risk when diets were low in fiber. So, the Institute of Medicine came up with a recommendation for about 30 grams a day, which is an intake observed to protect against coronary heart disease and reduce constipation. Thus, just as cardiovascular disease was used to help establish an adequate intake for dietary fiber, it was used as a way to develop a recommendation for EPA and DHA.
So, with reviews published as late as 2009 suggesting fish oil capsules may help with heart disease, nutrition authorities recommended an additional 250 mg a day of preformed EPA and DHA, since evidently we were not making enough on our own, if taking more helped. So, in addition to the one or two grams of ALA, 250 mg of preformed DHA/EPA, which can be gotten from fish or algae.
Fish is a toughie, because, on one hand, fish has the preformed DHA and EPA but, on the other hand, our oceans have become so polluted that fish may contain various pollutants, including dioxins, PCBs, pesticides like DDT, flame-retardant chemicals, and heavy metals, including mercury, lead, and cadmium, that can negatively affect human health.
This was an editorial comment on a recent study on women that found that dietary exposure to PCBs was associated with increased risk of stroke and an almost three times higher risk of hemorrhagic stroke. Unless you live next to a toxic waste dump, the main source of exposure to PCBs is fish consumption, of which perhaps salmon is the worst, though PCBs can also be found in lesser quantities in other meat sources as well.
This may explain why studies in the U.S. have shown that just a single serving of fish a week may significantly increase one’s risk of diabetes, emphasizing that even levels of these pollutants once considered safe may completely counteract the potential benefits of the omega-3s and other nutrients present in fish, leading to the type of metabolic disturbances that often precede type 2 diabetes.
Now, one could get their 250 mg a day from algae oil, rather than fish oil, which is free from toxic contaminants because it never comes in contact with anything from the ocean. Then, one could get the best of both worlds, right, the beneficial nutrients without the harmful contaminants. But, recently, it was demonstrated that these long-chain omega-3s don’t seem to help with preventing or treating heart disease after all and since that’s the main reason we thought people should get that extra 250 mg of preformed EPA and DHA, why do I still recommend following the guidelines? Because the recommendations were not just based on heart health, but brain health as well.
Be sure to check out the results of the new trial data on the effectiveness of omega-3s on brain function at our website NutritionFacts.org.
Here’s a question for you: Can our lives be extended by actually slowing our heartbeat? Here’s what we found out.
Immanuel Kant, the 18th century philosopher, described the chemistry of his day as a science, but not really science, because it wasn’t grounded in mathematics, at least not until a century later. The same could be said for biology, the study of life.
In math, and physics, quantum physics, there are constants, physical quantities thought to be both universal and unchanging. Biology, though, was considered too complex, too messy to be governed by simple, natural laws. But in 1999, a theoretical high-energy physicist from Los Alamos joined up with two biologists to describe universal scaling laws that appear to apply across the board. Are there any clinical implications of these kind of theories?
Well, a fascinating observation was published. The number of heartbeats per lifetime is remarkably similar, whether you’re a hamster, all the way up to a whale. So, even though mice only live less than two years, their heart rate is like 500 to 600 beats a minute, up to ten beats a second, whereas the heart of a Galapagos tortoise beats 100 times slower, but they live about 100 times longer.
There’s such a remarkable consistency in the number of heartbeats animals get in their lifetimes. that a provocative question was asked: Can human life be extended by cardiac slowing? In other words, if humans are predetermined to have about three billion heartbeats, period, in a lifetime, then would a reduction in average heart rate extend life? This is not just some academic question. If that’s how it worked, then one might estimate that a reduction in heart rate from more of an average, you know, 70 beats per minute, down to what many athletes have, 60 beats per minute, could theoretically increase lifespan over a decade.
Seems a bit off the wall, but that’s how the scientific method works; you start out with an observation, like these striking heartbeat data, and then you make an educated guess, or hypothesis, that you can then put to the test. How might one demonstrate a life-prolonging effect of cardiac slowing in humans?
Well, perhaps a first attempt in this direction would be to see if people with, you know, slower hearts live longer lives, lamenting the fact that there is no drug that just lowered heart rate that they could give to people, since drugs like beta-blockers lower heart rate but also lower blood pressure. So, wouldn’t be ideal for testing the question at hand; but, at least, we could do that first part, about do people with slower hearts live longer lives and, indeed, from the evidence accumulated so far, we know that a high resting heart rate, meaning how fast our heart beats when you’re just sitting at rest, is associated with an increase in mortality in the general population, as well as those with chronic disease. A faster heart rate may lead to a faster death rate. Faster resting heart rates are associated with shorter life expectancies, considered a strong independent risk factor for heart disease and heart failure.
You can see how those with the higher heart rates were about twice as likely over the next 15 years to experience heart failure, in middle-aged people, and older people, in men and women, and what’s critical is that this link between how fast our heart goes and how fast our life goes is independent of physical activity.
I mean, at first, I was like, well duh, of course, lower resting heart rates are associated with a longer lifespan. Who has a really slow pulse? Athletes. As you can see, the more physically fit we are, the lower our resting pulse, but, no, they found that, irrespective of level of physical fitness, people with higher resting heart rates fare worse than people with lower heart rates. So, it appears it’s not just a marker of risk, but a bona fide risk factor, independent of how fit we are or how much we exercise. Why? Well, if our heart rate is up, you know, 24 hours a day, even when we’re sleeping, all that pulsatile stress may break some of elastic fibers within the arterial wall, causing our arteries to become stiff. It doesn’t allow enough time for our arteries to relax between beats and, so, the faster our heart, the stiffer our arteries. But there are all sorts of theories how an increased resting heart rate could decrease our time on earth. Regardless, this relationship is now well recognized. It’s not just a marker of an underlying pathology. It’s not merely a marker of inflammation.
The reason it’s important to distinguish a risk factor from a risk marker is that if you control the risk factor, you control the risk, but if it is just a risk marker, it wouldn’t matter if we brought our heart rate down. But now, we even have evidence from drug trials (now that there actually are medications that just affect heart rate) that lowering our heart rate lowers our death rate.
It’s now been shown in at least a dozen trials so far, basically, we don’t want our heart to be beating more than about one beat per second at rest. You can measure your pulse right now! For the maximum lifespan, the target is like one beat a second to beat the clock, but don’t worry if you’re too fast, heart rate is a modifiable risk factor. Yes, there are drugs, but there are also lifestyle regimens that can bring our resting pulse down, which I’ll cover next.
Since we don’t like to induce unnecessary anxiety here at Nutrition Facts, here is part two of that story on resting heart rate, or as we like to call it, beans versus exercise.
The accumulated weight of evidence linking elevated resting heart rate to a shortened lifespan, even in apparently healthy individuals, makes a strong case for it to be considered in the assessment of risk. It’s got strong advantages. Taking one’s pulse is cheap, takes little time, it’s understandable to people, and it’s something everyone can do at home to measure their progress to become an active participant in their own health management.
Every ten beats per minute increase is associated with a 10 to 20% increase in the risk of premature death. There seems to be a continuous increase in risk with increasing heart rate, at least for values above about a beat a second. So, we can just look at our watch and if our heart is beating faster than the seconds go by, even when we’re sitting quietly, then we have to do something about it, especially when we start getting up around 80 or 90. Men with no apparent heart disease evidence with a pulse of 90 may have five times higher risk of sudden cardiac death, meaning their first symptom is their last, compared to those down in the safety zone. Living up around 90 increases heart disease risk at a level similar to smoking.
If you ask most doctors, though, 90 is considered normal. The accepted limits of heart rate have long been set at 60 to 100 beats per minute. How’d they come up with that? It was adopted as a matter of convenience, just based on the scale of the squares on EKG paper. A historical accident, like the QWERTY keyboard, that just became the norm.
Sixty to 100 doesn’t even represent the Bell curve. These cardiologists measured the heart rate of 500 people and concluded that 45 to 95 was a better definition of normal, rounding to 50 to 90, which a survey of leading cardiologists concurred with. Now, we know that normal doesn’t necessarily mean optimal, but doctors shouldn’t be telling people with heart rates in their 50s that they’re too low. In fact, they may be right where they should be.
Certainly, a heart rate higher than 80 should ring an alarm bell, but what can we do about it? Well, exercise is one obvious possibility. Ironically, you make the heart go faster so that the rest of the time your heart beats slower.
The public health benefits of physical exercise, especially for heart protection, widely accepted, and among the many biological mechanisms proposed to account for this risk-reducing effect is autonomic nervous system regulation of the heart. That’s your brain’s ability to slow down the resting beat of our heart.
If you put people through a 12-week aerobic conditioning program of cycling, StairMaster, and running on a treadmill, you can drop their resting heart rate down from about 69 to about 66; so, three beats per minute drop. Of course, you have to keep it up; stop exercising and your resting heart rate goes right back up.
Exercise is just one way to drop our heart rate, though. The way to our heart may also be through our stomach. What if, instead of three months of exercise, you did three months of beans? A cup a day of beans, chickpeas, or lentils. The first randomized controlled trial of beans for the treatment of diabetes and indeed, successfully improved blood sugar control, dropping A1c levels from 7.4 to 6.9, but this was also the first study to ever assess the effect of bean consumption on heart rate and, indeed, one of the few to determine the effect on heart rate of any dietary intervention. Now, this is particularly important in diabetics, since having a higher resting heart rate not only increases their risk of death, just like everybody else, but also appears to predict greater risk of diabetic complications, such as damage to the nerves and eyes.
So, how did beans do? A 3.4-beat drop in heart rate, just as much as the 250 hours on a treadmill. We’re not sure why beans are as powerful as exercise in bringing down one’s resting heart rate. In addition to the potential direct beneficial effects of all the good stuff in legumes, you know, there is also the potential displacement value of reducing some of the animal protein foods by eating so many beans instead. Regardless, we should consider eating pulses for our pulse.
I hope you’re feeling great and ready to keep listening to more podcasts here at Nutrition Facts.
Thanks for listening to this episode of Nutrition Facts. To see any graphs, charts, graphics, images, or studies mentioned here, please go to the Nutrition Facts podcast landing page. There, you’ll find all the videos I highlighted with links to all the sources cited.
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Thanks for listening to Nutrition Facts. I’m Dr. Michael Greger.