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Could Adipose Tissue Be a Better Measure for Obesity Than BMI?
Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI).
The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate.
But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity.
For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.
Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.
BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
Assessing Risks From Obesity Beyond BMI
Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.
For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.
A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes.
A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.
In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however.
Will New Body Fat Tools Change Practice?
In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient?
Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.
The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings.
A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes.
In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease.
So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.
Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.
A version of this article appeared on Medscape.com.
Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI).
The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate.
But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity.
For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.
Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.
BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
Assessing Risks From Obesity Beyond BMI
Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.
For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.
A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes.
A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.
In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however.
Will New Body Fat Tools Change Practice?
In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient?
Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.
The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings.
A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes.
In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease.
So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.
Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.
A version of this article appeared on Medscape.com.
Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI).
The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate.
But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity.
For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.
Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.
BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
Assessing Risks From Obesity Beyond BMI
Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.
For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.
A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes.
A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.
In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however.
Will New Body Fat Tools Change Practice?
In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient?
Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.
The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings.
A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes.
In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease.
So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.
Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.
A version of this article appeared on Medscape.com.
Are Carbs Really the Enemy?
Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?
First, a quick review of the history of diet and macronutrient content.
A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.
Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.
Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.
This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers.
Back to Carbohydrates: Do We Need Them? How Much? What Kind?
Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet.
Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context.
So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes.
Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need?
Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates.
In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy).
If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?
We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available.
For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western.
We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients.
How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!
It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods.
Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!
Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.
A version of this article appeared on Medscape.com.
Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?
First, a quick review of the history of diet and macronutrient content.
A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.
Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.
Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.
This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers.
Back to Carbohydrates: Do We Need Them? How Much? What Kind?
Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet.
Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context.
So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes.
Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need?
Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates.
In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy).
If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?
We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available.
For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western.
We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients.
How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!
It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods.
Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!
Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.
A version of this article appeared on Medscape.com.
Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?
First, a quick review of the history of diet and macronutrient content.
A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.
Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.
Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.
This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers.
Back to Carbohydrates: Do We Need Them? How Much? What Kind?
Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet.
Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context.
So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes.
Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need?
Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates.
In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy).
If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?
We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available.
For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western.
We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients.
How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!
It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods.
Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!
Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.
A version of this article appeared on Medscape.com.
Keto for life? Reasons to think twice
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.