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STANFORD, CALIF. – Picture a 15-year-old Hispanic girl who is 152.5 cm tall, weighs 88.7 kg, and has a body mass index of 38 kg/m
Her father has hyperlipidemia, but she has no family history of a premature coronary artery event (such as a myocardial infarction in a family member less than 55 years old) and no physical signs of hypercholesterolemia such as xanthomas under the skin.
Her fasting lipid profile is the following: total cholesterol, 267 mg/dL; triglycerides, 255 mg/dL; HDL cholesterol, 51 mg/dL; and LDL cholesterol, 164 mg/dL.
When would Dr. Clifford Chin consider initiating cholestyramine or a statin medication?
“The short answer is never,” said Dr. Chin, a pediatric cardiologist and codirector of the pediatric heart transplant program at the Lucile Packard Children's Hospital at Stanford (Calif.) University.
“I feel fairly strongly we should not give an individual with obesity a pill. I think it sends a message: 'It's not up to me. It doesn't matter what I do. I'll take this pill and I'll be fine,' “he said at a recent pediatric update sponsored by Stanford University. “[Patients with] hyperlipidemia induced by obesity [in childhood] should have obesity treatment as their primary therapy.”
Children who have genetic abnormalities at the root of their dyslipidemia may well require medical therapy, even at a young age.
But in today's children, dubbed “Generation XXL” by some, hyperlipidemia is far more likely to be caused by obesity.
In this scenario, the evidence favoring drug therapy is far from clear, according to Dr. Chin.
Most obese children do not have significant elevations in LDL cholesterol. “It's triglycerides [that drive up their total cholesterol], and we don't have much evidence that lowering triglycerides has an impact on premature coronary artery disease,” said Dr. Chin.
Indeed, no study to date has demonstrated that lowering lipids in general during childhood has any effect on the end point of preventing coronary events in adults.
The long-term impact of cholesterol-lowering drugs has not been studied in children and “no one knows the optimal timing of when to initiate drug therapy,” he stressed.
Given the dearth of evidence of benefit, Dr. Chin's policy is to focus on dietary therapy and lifestyle changes in obese adolescents and reserve medications for those with such conditions as familial hypercholesterolemia caused by genetic mutations.
At Stanford, obese children can be referred to a specialized teen weight clinic or be seen by a pediatric nutritionist.
Dr. Chin counsels families to follow the American Heart Association Step I diet, which emphasizes a daily intake of no more than 30% of total calories from fat and less than 10% of total calories from saturated fat.
An easy way to begin is to cut starch intake by half in each meal and make up the difference in vegetables, he said.
Close monitoring and encouragement can help, but medication actually may interfere with lifestyle adaptation by making it seem unnecessary, he said.
Even children with a strong family history of premature coronary disease deserve a full lipoprotein profile rather than a simple total cholesterol screen before any decision is reached about initiating cholesterol-lowering therapy, he said.
In a typical cholesterol panel, the LDL cholesterol is not measured directly, but calculated according to a formula based on total cholesterol.
A full lipoprotein profile offered reassuring news to the parents of a 7-year-old Asian American boy who had three relatives who suffered premature coronary events (myocardial infarction, angina pectoris, and established coronary atherosclerosis by imaging, sudden cardiac death, or peripheral or cerebrovascular disease before the age of 55 years).
This child's height was 120 cm; weight, 23 kg; and BMI, normal at 16 kg/m
His total fasting cholesterol was 220 mg/dL, but his triglycerides were in the normal range at 100 mg/dL, his HDL cholesterol 80 mg/dL, and LDL cholesterol 120 mg/dL.
“Although he comes from a family with premature coronary disease, he seems somewhat protected,” said Dr. Chin.
He would follow the child and order a repeat lipoprotein profile at age 12, but for now, this child does not require medical therapy, he concluded.
STANFORD, CALIF. – Picture a 15-year-old Hispanic girl who is 152.5 cm tall, weighs 88.7 kg, and has a body mass index of 38 kg/m
Her father has hyperlipidemia, but she has no family history of a premature coronary artery event (such as a myocardial infarction in a family member less than 55 years old) and no physical signs of hypercholesterolemia such as xanthomas under the skin.
Her fasting lipid profile is the following: total cholesterol, 267 mg/dL; triglycerides, 255 mg/dL; HDL cholesterol, 51 mg/dL; and LDL cholesterol, 164 mg/dL.
When would Dr. Clifford Chin consider initiating cholestyramine or a statin medication?
“The short answer is never,” said Dr. Chin, a pediatric cardiologist and codirector of the pediatric heart transplant program at the Lucile Packard Children's Hospital at Stanford (Calif.) University.
“I feel fairly strongly we should not give an individual with obesity a pill. I think it sends a message: 'It's not up to me. It doesn't matter what I do. I'll take this pill and I'll be fine,' “he said at a recent pediatric update sponsored by Stanford University. “[Patients with] hyperlipidemia induced by obesity [in childhood] should have obesity treatment as their primary therapy.”
Children who have genetic abnormalities at the root of their dyslipidemia may well require medical therapy, even at a young age.
But in today's children, dubbed “Generation XXL” by some, hyperlipidemia is far more likely to be caused by obesity.
In this scenario, the evidence favoring drug therapy is far from clear, according to Dr. Chin.
Most obese children do not have significant elevations in LDL cholesterol. “It's triglycerides [that drive up their total cholesterol], and we don't have much evidence that lowering triglycerides has an impact on premature coronary artery disease,” said Dr. Chin.
Indeed, no study to date has demonstrated that lowering lipids in general during childhood has any effect on the end point of preventing coronary events in adults.
The long-term impact of cholesterol-lowering drugs has not been studied in children and “no one knows the optimal timing of when to initiate drug therapy,” he stressed.
Given the dearth of evidence of benefit, Dr. Chin's policy is to focus on dietary therapy and lifestyle changes in obese adolescents and reserve medications for those with such conditions as familial hypercholesterolemia caused by genetic mutations.
At Stanford, obese children can be referred to a specialized teen weight clinic or be seen by a pediatric nutritionist.
Dr. Chin counsels families to follow the American Heart Association Step I diet, which emphasizes a daily intake of no more than 30% of total calories from fat and less than 10% of total calories from saturated fat.
An easy way to begin is to cut starch intake by half in each meal and make up the difference in vegetables, he said.
Close monitoring and encouragement can help, but medication actually may interfere with lifestyle adaptation by making it seem unnecessary, he said.
Even children with a strong family history of premature coronary disease deserve a full lipoprotein profile rather than a simple total cholesterol screen before any decision is reached about initiating cholesterol-lowering therapy, he said.
In a typical cholesterol panel, the LDL cholesterol is not measured directly, but calculated according to a formula based on total cholesterol.
A full lipoprotein profile offered reassuring news to the parents of a 7-year-old Asian American boy who had three relatives who suffered premature coronary events (myocardial infarction, angina pectoris, and established coronary atherosclerosis by imaging, sudden cardiac death, or peripheral or cerebrovascular disease before the age of 55 years).
This child's height was 120 cm; weight, 23 kg; and BMI, normal at 16 kg/m
His total fasting cholesterol was 220 mg/dL, but his triglycerides were in the normal range at 100 mg/dL, his HDL cholesterol 80 mg/dL, and LDL cholesterol 120 mg/dL.
“Although he comes from a family with premature coronary disease, he seems somewhat protected,” said Dr. Chin.
He would follow the child and order a repeat lipoprotein profile at age 12, but for now, this child does not require medical therapy, he concluded.
STANFORD, CALIF. – Picture a 15-year-old Hispanic girl who is 152.5 cm tall, weighs 88.7 kg, and has a body mass index of 38 kg/m
Her father has hyperlipidemia, but she has no family history of a premature coronary artery event (such as a myocardial infarction in a family member less than 55 years old) and no physical signs of hypercholesterolemia such as xanthomas under the skin.
Her fasting lipid profile is the following: total cholesterol, 267 mg/dL; triglycerides, 255 mg/dL; HDL cholesterol, 51 mg/dL; and LDL cholesterol, 164 mg/dL.
When would Dr. Clifford Chin consider initiating cholestyramine or a statin medication?
“The short answer is never,” said Dr. Chin, a pediatric cardiologist and codirector of the pediatric heart transplant program at the Lucile Packard Children's Hospital at Stanford (Calif.) University.
“I feel fairly strongly we should not give an individual with obesity a pill. I think it sends a message: 'It's not up to me. It doesn't matter what I do. I'll take this pill and I'll be fine,' “he said at a recent pediatric update sponsored by Stanford University. “[Patients with] hyperlipidemia induced by obesity [in childhood] should have obesity treatment as their primary therapy.”
Children who have genetic abnormalities at the root of their dyslipidemia may well require medical therapy, even at a young age.
But in today's children, dubbed “Generation XXL” by some, hyperlipidemia is far more likely to be caused by obesity.
In this scenario, the evidence favoring drug therapy is far from clear, according to Dr. Chin.
Most obese children do not have significant elevations in LDL cholesterol. “It's triglycerides [that drive up their total cholesterol], and we don't have much evidence that lowering triglycerides has an impact on premature coronary artery disease,” said Dr. Chin.
Indeed, no study to date has demonstrated that lowering lipids in general during childhood has any effect on the end point of preventing coronary events in adults.
The long-term impact of cholesterol-lowering drugs has not been studied in children and “no one knows the optimal timing of when to initiate drug therapy,” he stressed.
Given the dearth of evidence of benefit, Dr. Chin's policy is to focus on dietary therapy and lifestyle changes in obese adolescents and reserve medications for those with such conditions as familial hypercholesterolemia caused by genetic mutations.
At Stanford, obese children can be referred to a specialized teen weight clinic or be seen by a pediatric nutritionist.
Dr. Chin counsels families to follow the American Heart Association Step I diet, which emphasizes a daily intake of no more than 30% of total calories from fat and less than 10% of total calories from saturated fat.
An easy way to begin is to cut starch intake by half in each meal and make up the difference in vegetables, he said.
Close monitoring and encouragement can help, but medication actually may interfere with lifestyle adaptation by making it seem unnecessary, he said.
Even children with a strong family history of premature coronary disease deserve a full lipoprotein profile rather than a simple total cholesterol screen before any decision is reached about initiating cholesterol-lowering therapy, he said.
In a typical cholesterol panel, the LDL cholesterol is not measured directly, but calculated according to a formula based on total cholesterol.
A full lipoprotein profile offered reassuring news to the parents of a 7-year-old Asian American boy who had three relatives who suffered premature coronary events (myocardial infarction, angina pectoris, and established coronary atherosclerosis by imaging, sudden cardiac death, or peripheral or cerebrovascular disease before the age of 55 years).
This child's height was 120 cm; weight, 23 kg; and BMI, normal at 16 kg/m
His total fasting cholesterol was 220 mg/dL, but his triglycerides were in the normal range at 100 mg/dL, his HDL cholesterol 80 mg/dL, and LDL cholesterol 120 mg/dL.
“Although he comes from a family with premature coronary disease, he seems somewhat protected,” said Dr. Chin.
He would follow the child and order a repeat lipoprotein profile at age 12, but for now, this child does not require medical therapy, he concluded.