Why might healthy lifestyle choices wipe out 90 percent of our risk for having a heart attack, whereas drugs may only reduce risk by 20 to 30 percent?
Can Cholesterol Get Too Low?
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
On the standard American diet, atherosclerosis, hardening of the arteries, the number one killer of men and women, starts in your teens. Investigators collected about 3,000 sets of coronary arteries and aortas—the main artery in the body—from accident, homicide, and suicide victims 15–34 years of age, and this is what they found. The fatty streaks start in our teens, which turn into atherosclerotic plaques in our 20s, which get worse in our 30s, and can then start killing us off. In our heart, it can cause a heart attack. In our brain, it can cause a stroke.
How common is this? A hundred percent of the teens they looked at already had fatty streaks building up inside their arteries, and by their early 30s, most already had those streaks blossoming into atherosclerotic plaques bulging into their arteries. This is what their aortas look like at ages 15 through 19, fatty streaks building up throughout but no plaques yet on average. But the plaques start appearing in our early 20s, get worse in our late 20s, by which time fatty streaks have infiltrated throughout. And by our early 30s, our arteries are in bad shape. But that’s our aorta, the main artery that plunges down through our torso to split off into our legs. What about the coronary arteries feeding our heart?
Same thing. We start out with fatty streaks in our teens, begin to see the first hint of plaque in our early 20s, then late 20s, then look at the average coronary arteries of 30 to 34-year-olds. Most people in their early 30s already have plaques in their coronary arteries. Atherosclerosis begins in youth.
So, that’s why we shouldn’t wait until heart disease becomes symptomatic to treat it. If it starts in youth, we should start treating it in youth. It’s like if you knew you had a cancerous tumor, you wouldn’t want to wait until it grew until a certain size to treat it, or if you had diabetes, you wouldn’t want to wait until you started going blind before you did something about it. Okay. So, how do you treat atherosclerosis? You lower LDL cholesterol through a stringent diet that is low in cholesterol and saturated fat, so a diet that’s low in eggs, meat, dairy, and junk.
If we want to stop this epidemic, we have to alter our lifestyle accordingly, starting as early as possible. Is such a radical proposal totally impractical? I mean, eating more healthfully? Radical! It would, of course, take an all-out commitment, but remember this is our #1 cause of death. I mean, if we’re going to commit to anything. We did pretty good with cigarettes—slashing smoking rates, and lung cancer rates came right down. And yes, healthy eating is safe. According to the Academy of Nutrition and Dietetics, the largest and oldest association of nutrition professionals in the world, even strictly plant-based diets are appropriate for all stages of the lifecycle from pregnancy, infancy through old age. And if you want to learn more, the Academy can suggest a few good websites to visit.
Curing atherosclerosis should be the next major cardiovascular prevention goal. What evidence do we have that a life-long suppression of LDL will do it? There is a genetic mutation of a gene called PCSK9 that about 1 in 50 African Americans are lucky to be born with because it gives them about a 40 percent lower cholesterol their whole lives. And indeed, they have dramatically lower rates of coronary artery disease to show for it: an 88 percent drop in risk—despite otherwise terrible risk factors, on average. Most had high blood pressure and were overweight; almost a third smoked; nearly 20 percent had diabetes. But that just goes to show that a lifelong history of reduced LDL cholesterol levels significantly lowers the risk of coronary heart disease, even in the presence of multiple risk factors.
And this near-90 percent drop in events like heart attacks or sudden death occurred at an average LDL-C 100 mg/dl, compared to 138 mg/dl; so, you could get even lower than 100. Hold on! Why does the lowering of LDL cholesterol by about 40 points in those with that lucky mutation reduce coronary heart disease incidence by nearly 90 percent, whereas that same 40-point drop with statin drugs would reduce coronary heart disease by only about 20 percent? The most likely answer is duration. When it comes to lowering LDL cholesterol, it’s not only how low, but how long it’s been low.
That’s why healthy lifestyle choices may wipe out like 90 percent of our risk for having a heart attack, whereas drugs may reduce it by only 20 to 30 percent. If you’re getting treating with drugs later in life, you may have to get your LDL under 70 to halt the progression of coronary atherosclerosis, but if we start early enough, young enough, it may be sufficient to just lower LDL cholesterol down to 100 mg/dl, which should be attainable for most people. That’s consistent with country-by-country data that suggested heart disease would bottom out at a population average of about 100. But that’s if you can keep it down your whole life.
If you’re just using drugs late in life to try to stop the progression of your disease, you have to get your LDL lower than 70, and if you’re trying to reverse a lifetime of bad food choices, you don’t get to zero until about an LDL of 55. And if your heart disease is so bad you’ve already had a heart attack but you’re trying not to die of another one, ideally you might want to push your LDL down to about 30. Once you get that low, not only would you prevent any new atherosclerotic plaques, but you’d also help stabilize the plaques you already have so they’re less likely to burst open and kill you. Is it even safe to have cholesterol levels that low though? In other words, can LDL cholesterol ever be too low? We’ll find out, next.
Please consider volunteering to help out on the site.
- Brown MS, Goldstein JL. Biomedicine. Lowering LDL—not only how low, but how long? Science. 2006;311(5768):1721-3.
- McGill HC Jr, McMahan CA. Determinants of atherosclerosis in the young. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Am J Cardiol. 1998;82(10B):30T-6T.
- Strong JP, Malcom GT, McMahan CA, et al. Prevalence and extent of atherosclerosis in adolescents and young adults: implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth Study. JAMA. 1999;281(8):727-35.
- Steinberg D, Glass CK, Witztum JL. Evidence mandating earlier and more aggressive treatment of hypercholesterolemia. Circulation. 2008;118(6):672-7.
- Melina V, Craig W, Levin S. Position of the Academy of Nutrition and Dietetics: Vegetarian Diets. J Acad Nutr Diet. 2016;116(12):1970-80.
- Robinson JG, Gidding SS. Curing atherosclerosis should be the next major cardiovascular prevention goal. J Am Coll Cardiol. 2014;63(25 Pt A):2779-85.
- Cohen J, Pertsemlidis A, Kotowski IK, Graham R, Garcia CK, Hobbs HH. Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9. Nat Genet. 2005;37(2):161-5.
- Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med. 2006;354(12):1264-72.
- Kahleova H, Levin S, Barnard ND. Vegetarian Dietary Patterns and Cardiovascular Disease. Prog Cardiovasc Dis. 2018;61(1):54-61.
- Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-72.
- O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004;43(11):2142-6.
- Roberts WC. Cholesterol is the Cause of Atherosclerosis. Am J Cardiol. 2017;120(9):1696.
- Kataoka Y, Hammadah M, Puri R, et al. Plaque microstructures in patients with coronary artery disease who achieved very low low-density lipoprotein cholesterol levels. Atherosclerosis. 2015;242(2):490-5.
- Wiviott SD, Cannon CP, Morrow DA, et al. Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy. J Am Coll Cardiol. 2005;46(8):1411-6.
Video production by Glass Entertainment
Motion graphics by Avo Media
- African Americans
- animal products
- atherosclerosis
- Black Americans
- cardiovascular disease
- children
- cholesterol
- dairy
- eggs
- fat
- heart disease
- infants
- junk food
- LDL cholesterol
- lifespan
- lifestyle medicine
- longevity
- meat
- mortality
- Plant-Based Diets
- pregnancy
- processed foods
- saturated fat
- standard American diet
- stroke
- vegans
- vegetarians
Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
On the standard American diet, atherosclerosis, hardening of the arteries, the number one killer of men and women, starts in your teens. Investigators collected about 3,000 sets of coronary arteries and aortas—the main artery in the body—from accident, homicide, and suicide victims 15–34 years of age, and this is what they found. The fatty streaks start in our teens, which turn into atherosclerotic plaques in our 20s, which get worse in our 30s, and can then start killing us off. In our heart, it can cause a heart attack. In our brain, it can cause a stroke.
How common is this? A hundred percent of the teens they looked at already had fatty streaks building up inside their arteries, and by their early 30s, most already had those streaks blossoming into atherosclerotic plaques bulging into their arteries. This is what their aortas look like at ages 15 through 19, fatty streaks building up throughout but no plaques yet on average. But the plaques start appearing in our early 20s, get worse in our late 20s, by which time fatty streaks have infiltrated throughout. And by our early 30s, our arteries are in bad shape. But that’s our aorta, the main artery that plunges down through our torso to split off into our legs. What about the coronary arteries feeding our heart?
Same thing. We start out with fatty streaks in our teens, begin to see the first hint of plaque in our early 20s, then late 20s, then look at the average coronary arteries of 30 to 34-year-olds. Most people in their early 30s already have plaques in their coronary arteries. Atherosclerosis begins in youth.
So, that’s why we shouldn’t wait until heart disease becomes symptomatic to treat it. If it starts in youth, we should start treating it in youth. It’s like if you knew you had a cancerous tumor, you wouldn’t want to wait until it grew until a certain size to treat it, or if you had diabetes, you wouldn’t want to wait until you started going blind before you did something about it. Okay. So, how do you treat atherosclerosis? You lower LDL cholesterol through a stringent diet that is low in cholesterol and saturated fat, so a diet that’s low in eggs, meat, dairy, and junk.
If we want to stop this epidemic, we have to alter our lifestyle accordingly, starting as early as possible. Is such a radical proposal totally impractical? I mean, eating more healthfully? Radical! It would, of course, take an all-out commitment, but remember this is our #1 cause of death. I mean, if we’re going to commit to anything. We did pretty good with cigarettes—slashing smoking rates, and lung cancer rates came right down. And yes, healthy eating is safe. According to the Academy of Nutrition and Dietetics, the largest and oldest association of nutrition professionals in the world, even strictly plant-based diets are appropriate for all stages of the lifecycle from pregnancy, infancy through old age. And if you want to learn more, the Academy can suggest a few good websites to visit.
Curing atherosclerosis should be the next major cardiovascular prevention goal. What evidence do we have that a life-long suppression of LDL will do it? There is a genetic mutation of a gene called PCSK9 that about 1 in 50 African Americans are lucky to be born with because it gives them about a 40 percent lower cholesterol their whole lives. And indeed, they have dramatically lower rates of coronary artery disease to show for it: an 88 percent drop in risk—despite otherwise terrible risk factors, on average. Most had high blood pressure and were overweight; almost a third smoked; nearly 20 percent had diabetes. But that just goes to show that a lifelong history of reduced LDL cholesterol levels significantly lowers the risk of coronary heart disease, even in the presence of multiple risk factors.
And this near-90 percent drop in events like heart attacks or sudden death occurred at an average LDL-C 100 mg/dl, compared to 138 mg/dl; so, you could get even lower than 100. Hold on! Why does the lowering of LDL cholesterol by about 40 points in those with that lucky mutation reduce coronary heart disease incidence by nearly 90 percent, whereas that same 40-point drop with statin drugs would reduce coronary heart disease by only about 20 percent? The most likely answer is duration. When it comes to lowering LDL cholesterol, it’s not only how low, but how long it’s been low.
That’s why healthy lifestyle choices may wipe out like 90 percent of our risk for having a heart attack, whereas drugs may reduce it by only 20 to 30 percent. If you’re getting treating with drugs later in life, you may have to get your LDL under 70 to halt the progression of coronary atherosclerosis, but if we start early enough, young enough, it may be sufficient to just lower LDL cholesterol down to 100 mg/dl, which should be attainable for most people. That’s consistent with country-by-country data that suggested heart disease would bottom out at a population average of about 100. But that’s if you can keep it down your whole life.
If you’re just using drugs late in life to try to stop the progression of your disease, you have to get your LDL lower than 70, and if you’re trying to reverse a lifetime of bad food choices, you don’t get to zero until about an LDL of 55. And if your heart disease is so bad you’ve already had a heart attack but you’re trying not to die of another one, ideally you might want to push your LDL down to about 30. Once you get that low, not only would you prevent any new atherosclerotic plaques, but you’d also help stabilize the plaques you already have so they’re less likely to burst open and kill you. Is it even safe to have cholesterol levels that low though? In other words, can LDL cholesterol ever be too low? We’ll find out, next.
Please consider volunteering to help out on the site.
- Brown MS, Goldstein JL. Biomedicine. Lowering LDL—not only how low, but how long? Science. 2006;311(5768):1721-3.
- McGill HC Jr, McMahan CA. Determinants of atherosclerosis in the young. Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Am J Cardiol. 1998;82(10B):30T-6T.
- Strong JP, Malcom GT, McMahan CA, et al. Prevalence and extent of atherosclerosis in adolescents and young adults: implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth Study. JAMA. 1999;281(8):727-35.
- Steinberg D, Glass CK, Witztum JL. Evidence mandating earlier and more aggressive treatment of hypercholesterolemia. Circulation. 2008;118(6):672-7.
- Melina V, Craig W, Levin S. Position of the Academy of Nutrition and Dietetics: Vegetarian Diets. J Acad Nutr Diet. 2016;116(12):1970-80.
- Robinson JG, Gidding SS. Curing atherosclerosis should be the next major cardiovascular prevention goal. J Am Coll Cardiol. 2014;63(25 Pt A):2779-85.
- Cohen J, Pertsemlidis A, Kotowski IK, Graham R, Garcia CK, Hobbs HH. Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9. Nat Genet. 2005;37(2):161-5.
- Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med. 2006;354(12):1264-72.
- Kahleova H, Levin S, Barnard ND. Vegetarian Dietary Patterns and Cardiovascular Disease. Prog Cardiovasc Dis. 2018;61(1):54-61.
- Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-72.
- O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004;43(11):2142-6.
- Roberts WC. Cholesterol is the Cause of Atherosclerosis. Am J Cardiol. 2017;120(9):1696.
- Kataoka Y, Hammadah M, Puri R, et al. Plaque microstructures in patients with coronary artery disease who achieved very low low-density lipoprotein cholesterol levels. Atherosclerosis. 2015;242(2):490-5.
- Wiviott SD, Cannon CP, Morrow DA, et al. Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy. J Am Coll Cardiol. 2005;46(8):1411-6.
Video production by Glass Entertainment
Motion graphics by Avo Media
- African Americans
- animal products
- atherosclerosis
- Black Americans
- cardiovascular disease
- children
- cholesterol
- dairy
- eggs
- fat
- heart disease
- infants
- junk food
- LDL cholesterol
- lifespan
- lifestyle medicine
- longevity
- meat
- mortality
- Plant-Based Diets
- pregnancy
- processed foods
- saturated fat
- standard American diet
- stroke
- vegans
- vegetarians
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Can Cholesterol Get Too Low?
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Content URLDoctor's Note
Didn’t know atherosclerosis could start at such a young age? See Heart Disease Starts in Childhood.
For more on drugs vs. lifestyle, check out my video The Actual Benefit of Diet vs. Drugs.
Want to learn more about so-called primordial prevention? See When Low Risk Means High Risk.
Does Cholesterol Size Matter? Watch the video to find out.
Stay tuned for Are PCSK9 Inhibitors for LDL Cholesterol Safe and Effective? next.
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