A landmark paper in 1953 radically changed our view about the development of heart disease forever. The study looked at a series of 300 autopsies performed on U.S. battle casualties of the Korean War. The average age was 22 years old, but 77% of the soldiers’ 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 (CHD) becomes a clinically recognized problem.” Follow-up studies on the hearts of thousands of 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 in the famous Bogalusa Heart Study. This looked at autopsies of those who died between the ages of 3 to 26 years old, and the #1 risk factor was cholesterol intake. There was a dramatic stepwise increase in the proportion of their arteries covered in fatty streaks as the level of bad cholesterol in the blood increased. As powerful as this was, the study only looked at 30 kids. So they decided to study 3000: three thousand accidental death victims, ages 15 through 34.
After thousands of autopsies, they were able to produce a scoring system that could predict the presence of advanced atherosclerotic lesions in the coronary arteries of young people. The higher our score, the higher the likelihood we have these lesions growing in the arteries that pump blood and oxygen to our heart. So if we’re young and we smoke, our risk goes up by one point. If we have high blood pressure at such a young age, that’s four points. If we’re an obese male, that’s six points, but high cholesterol was the worst of all. If our non-HDL cholesterol (meaning the total cholesterol minus the good cholesterol) is above 220 or so, our risk increased eight times more than if we smoked.
Let’s say you’re a woman with relatively high cholesterol, but you don’t smoke, you’re not overweight, your blood pressure and blood sugars are OK. At your sweet 16 there’s just about a 1 in 30 (3%) chance you already have an advanced atherosclerotic lesion in your heart, but if you don’t improve your diet, by your 30th birthday, it’s closer to a one in five (20%) chance you have some serious heart disease, and if you have really high cholesterol it could be closer to one in three (33%).
In the video, Heart Disease Starts in Childhood, you can see what happens to our risk if we bring our cholesterol down to even just that of a lacto-ovo vegetarian, or if we exercise to boost our HDL, etc. It shows 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.
If we start kids out on a low saturated fat diet, we may see a significant improvement in their arterial function by 11 years old. The study concluded, “Exposure to high serum cholesterol concentration 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.” And by early in life they meant infancy.
Atherosclerosis, hardening of the arteries, begins in childhood. By age ten nearly all kids have fatty streaks, the first stage of the disease. Then the plaques start forming in our 20s, get worse in our 30s, and can start killing us off in middle age. In our hearts it’s a heart attack, in our brains it’s a stroke, in our extremities it can mean gangrene, and in our aorta, an aneurism.
For those of us 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 we want to reverse the heart disease we likely already have.
Drs. Dean Ornish and Caldwell Esselstyn Jr. proved that we can reverse heart disease with a plant-based diet, but we don’t have to wait until our first heart attack to start unclogging our arteries. We can start reversing our heart disease right now. We can start reversing heart disease in our kids tonight.
The bottom line is that we have tremendous control over our medical destinies. How do we go about reversing our heart disease? I address that question in my latest live annual review presentation More Than an Apple a Day. Or, for shorter snippets:
- Resuscitating Medicare
- Eliminating the #1 Cause of Death
- China Study on Sudden Cardiac Death
- Our Number One Killer Can Be Stopped
- Heart Attacks and Cholesterol: Purely a Question of Diet
- Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero
Heart disease is a choice.
-Michael Greger, M.D.
Image Credit: James MacDonald / Flickr
A recent review suggested that plant-based diets may prove to be a useful nutritional strategy for lifespan extension in part because they tend to be naturally low in the amino acid methionine (see my video Starving Cancer with Methionine Restriction). Apparently, the less methionine there is in body tissues, the longer different animals tend to live. But what are the possible implications for humans? See my video Methionine Restriction as a Life Extension Strategy.
I’ve talked before about the free radical theory of aging, the concept that aging can be thought of as the oxidation of our bodies just like rust is the oxidation of metal (see Mitochondrial Theory of Aging). Methionine is thought to have a pro-oxidant effect. The thinking is that lowering methionine intake leads to less free radical production, thereby slowing aging. Fewer free radicals would decrease the rate of DNA damage, which would curtail the rate of DNA mutation, slowing the rate of aging and disease and potentially increasing our lifespan.
There are three ways to lower methionine intake: The first is caloric restriction. By decreasing our overall intake of food, we would reduce our intake of methionine. Or, because methionine is found protein, we could practice protein restriction, eating a relatively protein deficient diet. The third option is eat enough food, eat enough protein, but just stick to proteins that are relatively low in methionine, which tends to mean plant proteins.
Caloric restriction is hard, because we walk around starving all the time. Something like every-other-day eating is described as “never likely to gain much popularity as a pro-longevity strategy for humans, so it may be more feasible to achieve moderate methionine restriction by eating a plant-based diet.” On a population-wide level, folks could benefit from just lowering their protein intake, period. Researchers noted that “the mean intake of proteins [and thus methionine] of Western human populations is much higher than needed. Therefore, decreasing such levels has a great potential to lower tissue oxidative stress and to increase healthy life span in humans while avoiding the possible undesirable effects of caloric restriction.”
We’re eating around double the protein we need, so the first thing doctors can recommend is to decrease the intake of protein, but we can also get our methionine even lower by eating a plant-based diet.
The fact that beans have comparably low methionine has been classically considered a disadvantage. But, given the capacity of methionine restriction to decrease the rate of free radical generation in internal organs, to lower markers of chronic disease, and to increase maximum longevity, this “disadvantage” may actually be a strong advantage. This fits well with the important role of beans in healthy diets like the traditional Mediterranean diet. Interestingly, soy protein is also especially poor in methionine, which may help explain the healthy effects iof soyfoods. Watch my video Increased Lifespan from Beans.
The reason why plant-based diets are so protective is not known. Yes, vegetables contain thousands of phytochemicals, but separately investigating their possible protective roles would be an impossible task. The idea that the protective effect is not due to any of the individual plant food components, but to a synergic “combined effect” is gaining acceptance. However, based on the relationship of excess dietary methionine to vital organ toxicity, as well as its likely mechanism of action through increases in free radical generation, the possibility exists that the protective effects of plant-based diets can be due, at least in part, to their lower methionine content. As one paper concluded, “The low-methionine content of vegan diets may make methionine restriction feasible as a life extension strategy.”
Plant-based diets can also mimic other benefits of caloric restriction, such as improving levels of the “fountain of youth” hormone DHEA. See The Benefits of Caloric Restriction Without the Actual Restricting.
Americans are living longer but sicker lives. That’s why we need a diet and lifestyle that supports health and longevity. I have a whole presentation on the role diet can play in preventing, arresting, and even reversing many of our top 15 killers: Uprooting the Leading Causes of Death.
I’ve touched previously on the irony that animal protein may be detrimental for the same reasons it’s touted as superior in Higher Quality May Mean Higher Risk.
-Michael Greger, M.D.