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New Insights on African-American Cardio Disease
November 12, 2008
The statistics are painfully clear. African-Americans are 40% more likely to die from cardiovascular disease than the white population; including a 250% increased chance for heart failure between ages 45 and 64. Conditions that increase the risk for heart disease such as high blood pressure, high cholesterol, obesity, and diabetes are at epidemic levels in young African-Americans and the general trend of these health issues is worsening.
Public health advice to address these issues is trite and condescending. It tells people to monitor their blood pressure, don't smoke, don't gain weight, and exercise more. It tells them to eat less fat, eat more fiber, reduce salt, and cut down on fried food. None of these proclamations is particularly helpful. After all, just about everyone already knows this information. It's not hard to understand that having too many fast food restaurants in your neighborhood sets you up to become a junk food addict with future heart disease risk.
Big Pharma views the African-American problem as a major business opportunity. This became apparent when the new Medicare prescription drug law went into effect and the African-American population boosted Big Pharma sales by 5%. While Big Pharma drugs for blood pressure, cholesterol, and diabetes can change numbers on paper – they seldom improve health or extend life. In fact, the greater the combination of drugs used for cardiovascular issues and diabetes, the more likely a person is to die from side effects of the medications. There is not a single cardiovascular drug or combination of these drugs that can hold a candle to refreshing aerobic exercise. This is true not only in terms of helping to correct the current health problems, but also in terms of extending life with a better quality of health.
The increase in cardiovascular disease risk in the African-American community is a very real problem. The problem is multi-faceted. Some will point to economic disadvantage and a more stressful living environment as keys to the issue. No doubt, such factors can be a percentage of the problem. In light of many scientific advances such a view is too narrow. To really tackle this problem we must begin with a broad-based understanding of key factors contributing to the problem.
Here are some of the most important cardiovascular risk factors for African-Americans that extend beyond basic topics of diet and exercise:
• Many generations of malnutrition that have turned on thrifty gene switches that influence the rate at which calories are burned.
• Adverse fetal programming due to malnourished and stressed mothers.
• Stress in children, leading to sleep problems, obesity, drug abuse, and serious cardiovascular stress.
This is by no means an all-inclusive list. However, by better understanding the nature of the problems on this list a door is opened for cardiovascular solutions that simply will never happen if all we do is tell people to eat less and exercise more. Don't get me wrong, a good diet and exercise are important – there is just more to it than that.
As soon as anyone starts talking about genetic differences between African-Americans and whites it is like walking though a minefield. However, there are certain aspects of this issue that all African-Americans should understand and this information has nothing to do with one race or the other being genetically superior or inferior (which is a ridiculous notion).
True changes in genes take tens of thousands of years. One example in the African-American population, especially for those descending from sub-Saharan Africa, is that of sickle cell anemia. This means that red blood cells have changed shapes into a sickle shape and become more rigid. This was a clear survival advantage that developed over thousands of years to combat malaria, as this shape and stiffness of red blood cells prevented the malaria parasite from entering the blood cells and causing disease. However, the trade off is that these blood cells don't flow as well in the circulation and this gene-related survival change has no value at all living in America today – in fact it is a detriment to cardiovascular health.
We normally think of red blood cells in the shape of a basketball. In reality, these cells are incredibly flexible and constantly bend and contort as they travel around tight corners in your circulation. Flexibility is the key. Even though flagrant sickle cell problems in the African-American population are less than 1%, there is a genetic weak spot here that says many African-Americans are likely to have higher percentages of irregularly shaped and less flexible red blood cells.
One of the key emerging themes of cardiovascular health for all Americans is that inflammation, caused by a wide variety of factors, results in blood cells becoming stickier and not flowing properly in circulation. This means that African-Americans with a sickle cell predisposition are more likely to have their circulatory systems irritated by various stressors.
How much this accounts for the difference in cardiovascular disease between whites and African-Americans is unknown. It is likely to be a small but relevant issue as part of the overall picture.
My main reason for bringing the topic up is to help you understand the difference between a true genetic change that takes tens of thousands of years and changes in how genes are set that take place in one or two generations, or in a period of a number of generations in a row. I believe the latter has a profound effect on heart disease risk in the African-American community.
Surviving famine has been the largest problem during the evolution of all racial ethnicities. The ability to do so is based on the ability of the hormone leptin to do its job. Leptin is a hormone that is produced in your stored fat, travels up to your brain, and instructs your metabolism how fast it can go. It is a sensor of energy reserves, much like the gas gauge in your car that lets you know how much fuel you have in the tank.
During times of famine you start to break down stored fat to use for energy. As your stored fat supply lessens, less leptin is made on a daily basis. This signifies to your brain that there is a food scarcity, and thus your metabolism must slow down so that you don't starve. To withstand starvation your body must get along with less food. This is the idea behind the thrifty metabolic type1. It is a type of hibernation.
A metabolic problem for African-Americans, as compared to whites of European descent, is that Africa has suffered at least 13 generations with significant times of famine whereas during the same time Europeans have been the best nourished people. This is not a long enough time for a true genetic change, like the sickle cell issue, but it is a long enough time to create changes in how gene switches are set.
In other words, if while in the womb the mother has inadequate nutrition then the baby will set metabolic gene switches to be thrifty, knowing that the likelihood of famine is higher during that child's life. These gene switch settings are more like computer hardware than easily changed software, as they are happening as the child's nervous system is forming.
When these problems exist for a number of generations over an extended period of time they become a metabolic weak spot. The biggest problem with a thrifty setting of the metabolic switches is that your metabolism runs best on a smaller amount of food. As soon as you starts eating too much the extra calories are stored as fat, as your body subconsciously thinks it is fighting famine even if it is not. Such weight can be very hard to lose, as your body holds on to it as an insurance policy against starvation.
There is scientific evidence indicating that African-Americans have thrifty settings of their gene switches. Leptin has a best friend, another hormone that comes from fat, called adiponectin. These hormones must be released in balance for optimal metabolism of calories. Adiponectin levels control blood sugar, insulin resistance, and risk for diabetes. It is an established fact that African-American children2 have low levels of adiponectin regardless of their body weight or any health problem, indicating that the adiponectin levels are set by gene switches relating to thrifty metabolism. The problem is worse in African-American boys3 who have 37% lower adiponectin than white boys. As soon as such a child eats too much food, especially sugar and fat-laden junk food, they will develop insulin resistance and increase their risk for diabetes, high blood pressure, obesity, and future heart disease.
Major leptin problems show up in African-American adults4, who have higher levels of leptin than Whites – once factors like obesity are taken into account. When leptin levels go too high (leptin resistance) then adiponectin levels go low which causes diabetes.
There are receptors for leptin on red blood cells, meaning that leptin talks directly to your red blood cells. Unfortunately, when leptin levels are too high (from eating too much) it promotes red blood cells to become sticky, resulting in reduced circulation and increased risk for stroke and heart disease. In fact, problems with leptin may be the driving force and most important risk factor for cardiovascular disease. This applies to everyone. However, if you have a thrifty metabolic type, as many African-Americans do, it is easier to fall into this trap.
Fetal programming5 is the setting of gene switches while in the womb based on nutritional adequacy and stress. There is overwhelming science to show that mothers who are overweight (over nourished), malnourished, and/or stressed are much more likely to have children at risk for obesity6, diabetes7, and heart disease. These findings apply to all ethnicities.
There is also the issue of fetal damage from smoking, alcohol, and street drugs. This is a form of stress, but more than just emotional stress. Not only does this cause gene-related disruptions that result in birth defects and brain-related issues, the effects can be directly passed to several generations if the child is a girl. That is because the eggs that will become her children are forming while she is in the womb of her mother, and subject to toxic damage.
Leptin is a multi-faceted hormone that not only governs your response to starvation, it enables successful pregnancy. Leptin problems in the mother, especially women who are overweight entering pregnancy, set the stage for leptin problems in her child and future heart disease risk.
Leptin is the key hormone that enables the growth of the placenta. Leptin problems during pregnancy are the primary cause for high blood pressure (preeclampsia), gestational diabetes, thyroid problems, and premature delivery.
The poor nutritional status of many African-American mothers is resulting in premature babies. A baby born prematurely is at much higher risk for thrifty-related metabolic problems and future heart disease.
In summary, it is a combination of poor nutrition during pregnancy along with too much stress that predisposes any child to future risk of heart disease. This weak spot is greater for African-Americans than whites, in part because of an ancestral history of many generations of famine in the recent past.
The stability of the home environment as well as the quality of nutrition in the first few years of life also has a large bearing on future cardiovascular health. It is during these early years that nerves continue to form their core circuits for dealing with life.
New science is pointing out that the earliest sign of future risk for cardiovascular disease is trouble sleeping8, which raises blood pressure. The worse the sleep problems9, the more likely changes in circulation are already occurring that are setting the stage for cardiovascular disease. Many of these changes are already underway by age 6. For example, young children who sleep less than 10 hours per night are 4 times more likely to be obese.
Another aspect of this problem is that a lack of sleep also sets up a child to go down a path of alcohol and drug abuse. We now understand that early stress10 and food-related malnutrition problems cause your arousal thermostat to be set too high. This makes a person feel more anxious and less able to sleep. Unfortunately, the nerves that are wired up in this aroused situation (hypocretins) are soothed by a burst of pleasure or a reward11. While there are many healthy behaviors that could be employed to bring balance and a more relaxed feeling – food, alcohol, and drugs are all quick fixes.
It is now clear that sleep problems, poor nutrition, and stress are the recipe for future cardiovascular disease. The thrifty metabolic type of many African-Americans, based on many generations of famine and/or recent pregnancy-related fetal programming problems, goes a long way towards helping to explain why African-Americans have higher risks for cardiovascular disease.
The common denominator of all of these problems is that your blood cells become inflamed and sticky. Preventing or reversing the problem means that you take steps to help your blood flow better.
For example, stress chemicals in your circulation are highly inflammatory and irritating to your red blood cells. Anything you can do to manage stress more effectively will help reduce the irritation and improve cardiovascular health. Likewise, anything you can do to ensure you get enough sleep will improve cardiovascular health.
Since a history of famine is part of the problem, improving the function of leptin (and adiponectin) are vital to reducing cardiovascular disease risk. While the quality of your diet is important, the real keys to improving leptin have more to do with when you eat than what you eat. Snacking is the worst issue, as is eating after dinner at night. To improve leptin you need to eat three meals a day (or two), not snack between meals, and not eat after dinner. Doing so will reduce inflammation in your circulation and reduce your risk for heart disease. The details of this strategy are explained in my book, The Leptin Diet. Certain foods like high fructose corn syrup, which accounts for 20% of the calories in many kids and teens diets, induces leptin problems and sets the stage for thrifty-related gene issues to manifest. Thus, a combination of improved dietary quality along with eating in harmony with leptin is the best strategy.
In order to change the trend of cardiovascular disease in the African-American community the focus of solutions must be placed on young children and women of child bearing age. If we can improve the health of women before and during pregnancy and the stressors and nutrition of young children, we can address this problem at its source and save future generations a great deal of trouble. For those of us who know we already have problems, it is important to do the right things on a regular basis. Yes, you have less margin for error and dietary abuse, and it may not seem fair. On the other hand, there is a clear path to better health that you can take if you want to. Gene-related programming issues are not written in concrete. You can change them. There are no medications or quick fixes. It just takes a bit more work.
Public health advice to address these issues is trite and condescending. It tells people to monitor their blood pressure, don't smoke, don't gain weight, and exercise more. It tells them to eat less fat, eat more fiber, reduce salt, and cut down on fried food. None of these proclamations is particularly helpful. After all, just about everyone already knows this information. It's not hard to understand that having too many fast food restaurants in your neighborhood sets you up to become a junk food addict with future heart disease risk.
Big Pharma views the African-American problem as a major business opportunity. This became apparent when the new Medicare prescription drug law went into effect and the African-American population boosted Big Pharma sales by 5%. While Big Pharma drugs for blood pressure, cholesterol, and diabetes can change numbers on paper – they seldom improve health or extend life. In fact, the greater the combination of drugs used for cardiovascular issues and diabetes, the more likely a person is to die from side effects of the medications. There is not a single cardiovascular drug or combination of these drugs that can hold a candle to refreshing aerobic exercise. This is true not only in terms of helping to correct the current health problems, but also in terms of extending life with a better quality of health.
The increase in cardiovascular disease risk in the African-American community is a very real problem. The problem is multi-faceted. Some will point to economic disadvantage and a more stressful living environment as keys to the issue. No doubt, such factors can be a percentage of the problem. In light of many scientific advances such a view is too narrow. To really tackle this problem we must begin with a broad-based understanding of key factors contributing to the problem.
Here are some of the most important cardiovascular risk factors for African-Americans that extend beyond basic topics of diet and exercise:
• Many generations of malnutrition that have turned on thrifty gene switches that influence the rate at which calories are burned.
• Adverse fetal programming due to malnourished and stressed mothers.
• Stress in children, leading to sleep problems, obesity, drug abuse, and serious cardiovascular stress.
This is by no means an all-inclusive list. However, by better understanding the nature of the problems on this list a door is opened for cardiovascular solutions that simply will never happen if all we do is tell people to eat less and exercise more. Don't get me wrong, a good diet and exercise are important – there is just more to it than that.
What Does Genetics Have To Do With It?
As soon as anyone starts talking about genetic differences between African-Americans and whites it is like walking though a minefield. However, there are certain aspects of this issue that all African-Americans should understand and this information has nothing to do with one race or the other being genetically superior or inferior (which is a ridiculous notion).
True changes in genes take tens of thousands of years. One example in the African-American population, especially for those descending from sub-Saharan Africa, is that of sickle cell anemia. This means that red blood cells have changed shapes into a sickle shape and become more rigid. This was a clear survival advantage that developed over thousands of years to combat malaria, as this shape and stiffness of red blood cells prevented the malaria parasite from entering the blood cells and causing disease. However, the trade off is that these blood cells don't flow as well in the circulation and this gene-related survival change has no value at all living in America today – in fact it is a detriment to cardiovascular health.
We normally think of red blood cells in the shape of a basketball. In reality, these cells are incredibly flexible and constantly bend and contort as they travel around tight corners in your circulation. Flexibility is the key. Even though flagrant sickle cell problems in the African-American population are less than 1%, there is a genetic weak spot here that says many African-Americans are likely to have higher percentages of irregularly shaped and less flexible red blood cells.
One of the key emerging themes of cardiovascular health for all Americans is that inflammation, caused by a wide variety of factors, results in blood cells becoming stickier and not flowing properly in circulation. This means that African-Americans with a sickle cell predisposition are more likely to have their circulatory systems irritated by various stressors.
How much this accounts for the difference in cardiovascular disease between whites and African-Americans is unknown. It is likely to be a small but relevant issue as part of the overall picture.
My main reason for bringing the topic up is to help you understand the difference between a true genetic change that takes tens of thousands of years and changes in how genes are set that take place in one or two generations, or in a period of a number of generations in a row. I believe the latter has a profound effect on heart disease risk in the African-American community.
The Thrifty Gene Problem
Surviving famine has been the largest problem during the evolution of all racial ethnicities. The ability to do so is based on the ability of the hormone leptin to do its job. Leptin is a hormone that is produced in your stored fat, travels up to your brain, and instructs your metabolism how fast it can go. It is a sensor of energy reserves, much like the gas gauge in your car that lets you know how much fuel you have in the tank.
During times of famine you start to break down stored fat to use for energy. As your stored fat supply lessens, less leptin is made on a daily basis. This signifies to your brain that there is a food scarcity, and thus your metabolism must slow down so that you don't starve. To withstand starvation your body must get along with less food. This is the idea behind the thrifty metabolic type1. It is a type of hibernation.
A metabolic problem for African-Americans, as compared to whites of European descent, is that Africa has suffered at least 13 generations with significant times of famine whereas during the same time Europeans have been the best nourished people. This is not a long enough time for a true genetic change, like the sickle cell issue, but it is a long enough time to create changes in how gene switches are set.
In other words, if while in the womb the mother has inadequate nutrition then the baby will set metabolic gene switches to be thrifty, knowing that the likelihood of famine is higher during that child's life. These gene switch settings are more like computer hardware than easily changed software, as they are happening as the child's nervous system is forming.
When these problems exist for a number of generations over an extended period of time they become a metabolic weak spot. The biggest problem with a thrifty setting of the metabolic switches is that your metabolism runs best on a smaller amount of food. As soon as you starts eating too much the extra calories are stored as fat, as your body subconsciously thinks it is fighting famine even if it is not. Such weight can be very hard to lose, as your body holds on to it as an insurance policy against starvation.
There is scientific evidence indicating that African-Americans have thrifty settings of their gene switches. Leptin has a best friend, another hormone that comes from fat, called adiponectin. These hormones must be released in balance for optimal metabolism of calories. Adiponectin levels control blood sugar, insulin resistance, and risk for diabetes. It is an established fact that African-American children2 have low levels of adiponectin regardless of their body weight or any health problem, indicating that the adiponectin levels are set by gene switches relating to thrifty metabolism. The problem is worse in African-American boys3 who have 37% lower adiponectin than white boys. As soon as such a child eats too much food, especially sugar and fat-laden junk food, they will develop insulin resistance and increase their risk for diabetes, high blood pressure, obesity, and future heart disease.
Major leptin problems show up in African-American adults4, who have higher levels of leptin than Whites – once factors like obesity are taken into account. When leptin levels go too high (leptin resistance) then adiponectin levels go low which causes diabetes.
There are receptors for leptin on red blood cells, meaning that leptin talks directly to your red blood cells. Unfortunately, when leptin levels are too high (from eating too much) it promotes red blood cells to become sticky, resulting in reduced circulation and increased risk for stroke and heart disease. In fact, problems with leptin may be the driving force and most important risk factor for cardiovascular disease. This applies to everyone. However, if you have a thrifty metabolic type, as many African-Americans do, it is easier to fall into this trap.
Adverse Fetal Programming and Heart Disease
Fetal programming5 is the setting of gene switches while in the womb based on nutritional adequacy and stress. There is overwhelming science to show that mothers who are overweight (over nourished), malnourished, and/or stressed are much more likely to have children at risk for obesity6, diabetes7, and heart disease. These findings apply to all ethnicities.
There is also the issue of fetal damage from smoking, alcohol, and street drugs. This is a form of stress, but more than just emotional stress. Not only does this cause gene-related disruptions that result in birth defects and brain-related issues, the effects can be directly passed to several generations if the child is a girl. That is because the eggs that will become her children are forming while she is in the womb of her mother, and subject to toxic damage.
Leptin is a multi-faceted hormone that not only governs your response to starvation, it enables successful pregnancy. Leptin problems in the mother, especially women who are overweight entering pregnancy, set the stage for leptin problems in her child and future heart disease risk.
Leptin is the key hormone that enables the growth of the placenta. Leptin problems during pregnancy are the primary cause for high blood pressure (preeclampsia), gestational diabetes, thyroid problems, and premature delivery.
The poor nutritional status of many African-American mothers is resulting in premature babies. A baby born prematurely is at much higher risk for thrifty-related metabolic problems and future heart disease.
In summary, it is a combination of poor nutrition during pregnancy along with too much stress that predisposes any child to future risk of heart disease. This weak spot is greater for African-Americans than whites, in part because of an ancestral history of many generations of famine in the recent past.
Childhood Stress and Heart Disease
The stability of the home environment as well as the quality of nutrition in the first few years of life also has a large bearing on future cardiovascular health. It is during these early years that nerves continue to form their core circuits for dealing with life.
New science is pointing out that the earliest sign of future risk for cardiovascular disease is trouble sleeping8, which raises blood pressure. The worse the sleep problems9, the more likely changes in circulation are already occurring that are setting the stage for cardiovascular disease. Many of these changes are already underway by age 6. For example, young children who sleep less than 10 hours per night are 4 times more likely to be obese.
Another aspect of this problem is that a lack of sleep also sets up a child to go down a path of alcohol and drug abuse. We now understand that early stress10 and food-related malnutrition problems cause your arousal thermostat to be set too high. This makes a person feel more anxious and less able to sleep. Unfortunately, the nerves that are wired up in this aroused situation (hypocretins) are soothed by a burst of pleasure or a reward11. While there are many healthy behaviors that could be employed to bring balance and a more relaxed feeling – food, alcohol, and drugs are all quick fixes.
It is now clear that sleep problems, poor nutrition, and stress are the recipe for future cardiovascular disease. The thrifty metabolic type of many African-Americans, based on many generations of famine and/or recent pregnancy-related fetal programming problems, goes a long way towards helping to explain why African-Americans have higher risks for cardiovascular disease.
Solutions
The common denominator of all of these problems is that your blood cells become inflamed and sticky. Preventing or reversing the problem means that you take steps to help your blood flow better.
For example, stress chemicals in your circulation are highly inflammatory and irritating to your red blood cells. Anything you can do to manage stress more effectively will help reduce the irritation and improve cardiovascular health. Likewise, anything you can do to ensure you get enough sleep will improve cardiovascular health.
Since a history of famine is part of the problem, improving the function of leptin (and adiponectin) are vital to reducing cardiovascular disease risk. While the quality of your diet is important, the real keys to improving leptin have more to do with when you eat than what you eat. Snacking is the worst issue, as is eating after dinner at night. To improve leptin you need to eat three meals a day (or two), not snack between meals, and not eat after dinner. Doing so will reduce inflammation in your circulation and reduce your risk for heart disease. The details of this strategy are explained in my book, The Leptin Diet. Certain foods like high fructose corn syrup, which accounts for 20% of the calories in many kids and teens diets, induces leptin problems and sets the stage for thrifty-related gene issues to manifest. Thus, a combination of improved dietary quality along with eating in harmony with leptin is the best strategy.
In order to change the trend of cardiovascular disease in the African-American community the focus of solutions must be placed on young children and women of child bearing age. If we can improve the health of women before and during pregnancy and the stressors and nutrition of young children, we can address this problem at its source and save future generations a great deal of trouble. For those of us who know we already have problems, it is important to do the right things on a regular basis. Yes, you have less margin for error and dietary abuse, and it may not seem fair. On the other hand, there is a clear path to better health that you can take if you want to. Gene-related programming issues are not written in concrete. You can change them. There are no medications or quick fixes. It just takes a bit more work.
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