Addressing Issues of Heart Disease Prevention: Cholesterol, Fat, Lipids
Vanthaya Gan, MD
Dallas Children's Hospital
PRETEST
Q1. True or False 50% of calories in cow milk, infant formulas and human milk comes from fat.
Q2. True or False. Obese infants should limit fat intake to 30% of total calories.
Q3. True or False. The daily recommended fat intake in school age children is the same as that in adults, i.e. 30% of total calories from fat and cholesterol intake should be < 300 mg/day.
Q4A. True or False. Cholesterol screening is recommended for all children over 5 years of age.
Q4B. Pick one of the following choices out of a hat: A = Screen all; B = Screen only those shown to be "at-risk," and C = Screen none. Debate within a group of three with contrary positions. Explain your answer in a paragraph or a class discussion
Q5A. True or False. Non-obese children do not need to worry about serum cholesterol levels.
Q5B. Explain your answer in a paragraph or a class discussion Again discuss in group.
Q6. True or False Trans-fats are unsaturated, but they can raise total and LDL ("bad") cholesterol and lower HDL ("good") cholesterol.
OBJECTIVES
On completion of this teaching module, resident will be able to:
1. Define/identify the pediatrician's responsibility in the prevention of coronary heart disease (CHD).
2. Identify risk factors for hyperlipidemias and CHD.
3. Define proper screening - who, what, when (at what age).
4. Define hyperlipidemias and interpret lab values.
5. Be able to outline the Non-pharmacological (life style change & nutritionnel management) of hyperlipidemias
FACILITATOR PREPARATION
1. American Academy of Pediatrics, Committee on Nutrition Cholesterol in Childhood. Pediatrics 1998; 101:141-147.
2. American Heart Association- Policy Statement of the AAP. Gidding SS, Dennison BA, Birch L, et al Dietary Recommendations for Children and Adolescents: A Guide for Practitioners. Pediatrics. 2006;117(2):544-559
3. Belay B, Belamarich P, Racine AD. Pediatric Precursors of Adult Atherosclerosis. Pediatrics in Review 2004 25: 4-16.
4. Bao W, Srinivasan SR, Valdez R, Greenlund RK, Wattigney WA, Berenson G S. Longitudinal changes in cardiovascular risk from childhood to young adulthood in offspring of parents with coronary artery disease: the Bogalusa Heart Study JAMA. 1997; 278:1749-1754.
5. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. National Institutes of Health, National Institute of Heart, Lung and Blood Institute, Sept. 2002.
INTRODUCTION
Many adult diseases begin in childhood; this is especially true for coronary heart disease (CHD). Most, though not all, children with lipid abnormalities will have them as adults, increasing their risk for CHD. High serum total cholesterol, LDL cholesterol, and very low-density lipoprotein cholesterol, and low HDL cholesterol levels correlate with the extent of early atherosclerotic lesions in children and adolescents. Evidence from several autopsy reports of adolescents and young adults indicates that the early stages of arteriosclerosis begin in childhood.
The Bogalusa heart study shows that childhood LDL cholesterol levels and obesity -- a body mass index (BMI) in the highest quartile -- were significant risk factors of increased carotid intimal-media thickness (IMT) in adulthood. This is a measure of cardiovascular risk. In adults, high blood cholesterol levels undoubtedly play a role in the development of atherosclerosis and premature coronary heart disease. In order to prevent adult CHD, pediatricians must take an active role in monitoring childhood risk factors and promoting healthy behaviors in children. Maintaining LDL cholesterol levels at those found in childhood would have a profound impact on the occurrence of CHD.
CASE STUDY 1
Sara Smith is a 3-year-old female who came in for a check-up. Her birth weight was 3.5 kg, with a length of 51 cm, and a head circumference (HC) of 35 cm. At one year of age, she weighed 9.5 kg (50th percentile), with a length of 75 cm, and a HC of 45 cm. At age 3 years, her growth percentile has shifted; her weight was 11 kg (less than 5th percentile), with a length of 95 cm, and a HC of 50.5 cm. The BMI curves show her to be at less than 5th percentile.
* percentiles are in parentheses
There is a family history of early death from heart disease on the father's side, and the father's cholesterol and LDL are elevated. Because of this family history, Sara's mother cooks low fat foods and the family follows an American Heart Association Diet. Sara is an only child and she stays home with her mother. Her appetite is good, and she eats a variety of foods.
Feeding History:
She was breast-fed for 6 months, solids were introduced at 5 months, and she began
an infant formula at 6 months of age. At one year, the family used skim milk and low fat table foods.
Q1. Why did Sara fail to thrive?
A1. The most likely reason for FTT in this child is an inadequate caloric intake due to a low fat diet. This is not a normal shifting of growth percentiles that is usually seen in toddlers, nor does it represent an organic cause of failure to thrive. The committee on nutrition (CON) of the AAP recommends that total fat intake for children under 2 years of age should not be lower than 30% of total calories for children and adolescents. Dietary fat or cholesterol intake should not be restricted in children during the first two years of life because of high-energy requirements during this time of rapid growth and development. Fat is a substrate for the production of hormones and mediators; it is essential for neurological development and brain function in infancy and early childhood. In fact 50% of calories in breast milk and infant formula comes from fat. Dietary fat supplies essential fatty acids (EFA) and aids in the absorption of fat-soluble vitamins A, D, E and K.
The essential fatty acids, linoleic acid and linolenic acid, are long-chain polyunsaturated fatty acids that are necessary for normal growth and functioning, but they cannot be synthesized by humans or other animals. Vegetable oils are the only source of these essential fatty acids. A minimum of 1% of calories must be provided as linoleic acid, and many suggest that 2% of calories is a safer minimum intake. [HYPERLINK TO RDA AND DRI IN PEDIATRIC NUTRITION NOTES.] The exact requirement for linolenic acid is less clear, but 0.5% of calories have been suggested. Essential fatty acid deficiency can occur in those children with very restricted diets or severe malabsorption.
Essential fatty acid deficiency can lead to dry, thick, scaly skin with desquamation, erythema and oozing in intriginous areas, sparse hair, and hepatomegaly due to fatty infiltration of the liver, brittle nails, and poor wound healing and overall growth.
At age 2 years, ALL children can begin eating fewer high fat foods, so that by age 5, their caloric intake from fat should be no more than 30%. The recommendations of the Committee on Nutrition of the AAP are shown below:
TEACHING CAPTION: These recommendations are evolving. It may be that the provision of a reduced fat and cholesterol diet will be suggested at an earlier age. However the CON recommendations evolve, keep your eye on the child in front of you. If it doesn't sound right, it probably isn't.
Q2. How do we approach children of different ages with respect to taking a family history for CHD?
A2. Under 2 years of age, the review of family history should be casual for fear of creating the psychology affecting Sara's family. We do not want parents reducing fat content too early. The parent should be asked the age of each grandparent and whether any of these or other close relative had a stroke, heart attack, chest pain from heart disease, or high blood fat or cholesterol.
Q3. Should pediatricians working in poor communities where
grandparents are often young and the histories are incomplete use the same protocol for 2 year olds?
Here's a good exercise for the residents. Ask them to break into groups with a request to define the parameters of concern and not just a "yes" or "no" to the question.
A3. Yes! Was that a surprise? As shown in inner city Brooklyn, Coronary heart Disease (CHC) occurs at such young ages among the inner-city poor that the AAP recommendations hold true. The positive predictive value of a positive screen - "did any of the four grandparents have chest pain from heart disease, a heart attack or a stroke before the age of 55?" - was about 40% in the surveys conducted throughout the United States [Louisiana (Bao) and Brooklyn, New York (Wadowski)].
Q4. Should Sara have a lipid profile drawn to check for the presence of a hyperlipidemia syndrome?
See if the residents can appreciate why the answer is "yes."
A4. The answer is "yes/" There is a positive family history of conditions associated with atherosclerosis. A positive family history of premature CHD is defined as a first degree (sib, parent, uncle, aunt) or second degree ( grandparent or first cousin) relative who suffered CHD before the age of 55 in a male or before age 65 in a female. See table below
TEACHING CAPTION: be sure to take a complete family history as sibs, cousins, uncles and aunts count, too.
The AAP endorses an individualized approach to screening, i.e. selective screening in over 2 year of age who are 'at risk' of developing coronary vascular disease as adults. See Wadowski, et al for a description and Tom Newman's challenge to that position.
Q5. What lab tests should be used in screening?
A5. Total cholesterol and HDL cholesterol levels can be measured at any time of day in the non-fasting state because total cholesterol concentrations do not change appreciably after a fat-containing meal and HDL cholesterol levels drop only slightly.
The AAP recommends that all children 2 years of age or older who have a parent with elevated total cholesterol (>240 mg/dL), but no family history of premature CHD have a non-fasting total serum cholesterol level measured. With any actual CHD, however, a fasting lipid profile is required. If the child is obese or showing signs of "diabesity" (e.g., acanthosis nigricans) one would have a fasting blood sugar, insulin and HGB A1C measured, also.
- Acceptable total cholesterol (TC) levels are <170 mg/dL. Children whose total cholesterol level is less than 170 mg/dL require no further intervention, but should be re-evaluated in 5 years. Children whose total cholesterol levels are between 170 and 200 mg/dL should have a repeat test; if the average of the two tests is greater than 170 mg/dL, a fasting lipoprotein profile is recommended. Children whose TC level is greater than 200 mg/dL should have an immediate fasting lipid profile performed.
- A fasting lipid profile allows quantification of LDL and HDL levels, which is important because up to 15% of children who have total cholesterol levels greater than 200 mg/dL may have an elevated HDL cholesterol (HDL-C) level and a normal value for LDL cholesterol (LDL-C), a condition that confers a decreased risk of CHD.
- For children with a positive family history of premature CHD regardless of parental cholesterol level, the screening test is a fasting lipoprotein analysis. Sara needs to have a lipoprotein analysis, i.e. a 12-hour fasting level of total cholesterol, total triglycerides (TG), HDL cholesterol and LDL cholesterol. LDL-C can be calculated by using Friedewald's equation:
LDL-C =Total cholesterol - (HDL-C) - (triglycerides/5)
This equation is ONLY considered accurate when TG levels are less than 400.
It is important to remember that the HDL cholesterol level must be interpreted in light of the levels of triglyceride-rich lipoproteins in the plasma.
As shown below, HDL cholesterol decreases as an inverse logarithmic function of the triglyceride level because triglycerides are substituted for cholesterol esters in the cores of the HDL molecule as plasma triglyceride levels rise.
A person who eats very little fat or a diet rich in polyunsaturated FA tends to have moderate decreases in HDL cholesterol. Strict vegetarians, in the United States where corn and other vegetable oils are used rather than mono-unsaturated olive oil, tend to have decreased levels of both HDL and LDL. See the `home plate diet' in nutrition notes for more discussion of an appropriate diet for children and `the problem of the USDA food pyramid.'
Q6. How should lab results be interpreted?
A6. LDL-C levels less than 110 mg/dL are considered acceptable.
Levels greater than 130 mg/dL are considered elevated.
LDL-C levels of 110 to 130 mg/dL are borderline and REQUIRE repeat measurements yearly. The finding of elevated LDL-C values should trigger an individualized treatment plan, including dietary advice.
* From the National Cholesterol Education Program (NCEP)
TEACHING CAPTION: Keep your head up for changing recommendations.
Q7. What advice do you give to Sara's mother?
Create groups of three. Let one resident interview another with the third resident being an outside observer. Let each critique the guidance from the perspective of guide, guided, and outside observer.
A7. The dietary patterns presented do not represent a cultural or alternative diet approach to nutrition. It is likely that her mother will be responsive to a strictly scientific approach to Sara's need for more fat and more calories. Still, it will be necessary to give the mother a chance to explain why she made her choices and be totally non-judgmental and supportive of her choices.
Take a careful diet history. She may be heavily invested in her low fat regimen. "Give my child ice cream? You do know that her father died of a heart attack!" A simple approach is to suggest use of olive and canola oil supplementation of the foods she is already using. A Mediterranean diet has a reasonable fat content but is not associated with coronary heart disease.
TEACHING CAPTION: Note that East Finland stands well below the regression line while Crete stands well below.
COMMENT: As Keys writes, "The correlation coefficient of 0,8 between the cohort median cholesterol value and the death rate from CHD means that 64% [r2] of the variances coronary heart death rates is accounted for by the median cholesterol level of the cohort"
CASE STUDY 2
Her mom who is concerned about her daughter's cholesterol brings Maria, a 16-year-old, into your office. She was first alerted to this after cholesterol screening at the local mall warned that Maria's cholesterol was high at 195mg/dL. Her mother is health conscious and worries that her daughter eats unhealthy food: cold pizza for breakfast; school lunches with chocolate milk; afternoon snacks of chocolate bars, chips and soda; and for, dinner, hotdogs, fries and shakes. Maria is in the 11th grade, and participates in her school computer and math teams. She avoids sports and does not exercise at all. Maria denies taking any illicit drugs, but began smoking in high school. She has been on birth control pills since the 8th grade.
Family Hx/Social Hx: single mom, no family Hx of CHD on the mother's side, but the family history is unknown on the dad's side.
Physical exam reveals a pleasant young lady whose weight (55 kg) and height (162 cm) are at the 50% percentile, BMI 21, BP 110/75. Her general physical examination is within normal limits. The BMI curves show her to be at the 60th percentile and she is not obese.
Marie states that she does not have a weight problem and she does not need to be on a "diet". She has no worries about cholesterol.
Q8. Are there any concerns about high cholesterol level in Maria?
A8. Here is a common myth: "Only overweight people have to worry about elevated cholesterol."
In addition to genetic, cultural and socioeconomic (environmental) factors, dietary factors, caloric intake and distribution are the risk factors for CAD. Eating patterns affect blood cholesterol levels and the risk of coronary heart disease. The 3 major dietary factors contributing to high cholesterol are high intake of dietary cholesterol, high intake of saturated fat, and an imbalance between caloric intake and energy expenditure leading to obesity. Fast food, diets low in fruits and vegetables and lack of exercise are the suspected reasons for the increase in obesity. Obesity is also associated with medical conditions including Metabolic Syndrome.
Metabolic syndrome, a set of maladies recognized as a consequence of insulin resistance, is characterized by the presence of elevated serum triglycerides, low HDL cholesterol, increased fasting blood glucose, obesity, and elevated blood pressure,. The combination of any 3 factors listed below leads to a diagnosis of Metabolic Syndrome. Diagnostic criteria for Metabolic Syndrome are evolving. The table below shows one set. Modifications are provided.
TEACHING CAPTION: It is essential to remember that insulin resistance is both a cause and a consequence of truncal obesity and the sequelae that follow.
* For children, JT Fernandez and colleagues suggests a waist circumference >90% of standard (see J Pediatr 2004;145;439).
For adult men, the waist circumference is greater than his hip circumference. For women, the waist should not be greater than 84% of hips. In absolute terms, for adult men, 40 in (100 cm) waist circumference is the maximum; for adult women 35 in (88 cm) is the upper limit.
Fernandez, et al. have determined %ile measures for waist circumferences by gender and ethnicity calculated from NHANES III data. The table below shows the mixed population 90th percentiles by gender, The numbers have been rounded and are appropriate for clinical use, only.
** Lambert, et al, suggest that insulin resistance, a defining characteristic for Metabolic Syndrome, is an essential part of the diagnosis. They require an elevated insulin level on a fasting blood sample be present plus 2 additional criteria from the above list. Serum insulin should be below 14 U/dL on a fasting blood sugar (FBS) below 110 mg/dL, an acceptable level for FBS. An elevation in FBS would suffice to document disordered glucose metabolism..
See Lambert V, et al. Int J Obese Relat Metab Disorders 2004;28:833.
The Case continues
Although Maria is not overweight, her high fat diet, smoking, sedentary lifestyle and her borderline high cholesterol level increase her risk of becoming obese and having CHD.
The two types of risk factors of CHD, the modifiable risk factors and non- modifiable risk factors (age, male sex, and family history of premature CHD) are listed below.
TEACHING CAPTION: Note that these factors range from those over which one has no control to those for which there is complete control as well as those with a mix of genetic and social overlay.
Testing for lipid abnormalities is recommended for children who have these cardiovascular risk factors. Testing children whose family histories are unknown is discretionary. A fasting lipid profile rather than a total cholesterol determination should be obtained for all obese children.
Q9. what types of fat in Maria's diet affect her blood cholesterol levels?
A9. The relationship between dietary fat and CHD is complicated. The debate continues over whether concerns about fat should focus on total fat intake or on the relative proportion of saturated, monounsaturated and polyunsaturated fatty acids (PUFA). There are also questions about trans-fatty acids and CHD.
Current recommendations include maintaining a lean body weight and having fat contribute no more than 30% of calories with an equal distribution (1:1:1) of saturated, mono-, and poly-unsaturated fats.
Brief descriptions of fat, lipids and lipoproteins follow in order to review key points and identify Maria's dietary risks:
Fat and lipids are a class of compounds soluble in organic solvents (e.g. acetone, ether, chloroform). These compounds range from hydrophobic triglycerides (TG's) and steroid esters to more water-soluble phospholipids (PL) and cardiolipins. Triglycerides are naturally produced and stored in the body as fat. Most fats in foods are in the form of triglycerides. Elevated triglycerides have been shown to be an independent risk factor for CHD. High levels are also associated with obesity, diabetes, and high blood pressure.
Cholesterol is a fat-like substance (lipid) that is present in cell membranes and is a precursor of bile acids and steroid hormones. Cholesterol travels in blood in distinct particles containing both lipid and proteins. These particles are cell lipoproteins.
Lipoproteins: each lipoprotein contains a lipid core surrounded by a surface monolayer of phospholipids, unesterified cholesterol and apolipoproteins. Lipoproteins are necessary to make fats soluble so they can be transported in the plasma. The major classes of lipoproteins in the blood are shown in the following table.
- Chylomicrons are formed from dietary fat and catabolism by the liver or stored in adipose tissue as triglyceride.
- Pre-B-lipoproteins or very low-density lipoproteins (VLDL) are formed in the liver and carry the triglycerides synthesized there. VLDL is catabolized through a common pathway with chylomicrons that involve the lipoprotein lipase system (LPL). Some VLDL remnants are further metabolized to form LDL. Pancreatitis and arteriosclerosis are both associated with an elevated level of VLDL. VLDLs are precursors of LDL. VLDL typically contains 10-15% of total serum cholesterol.
- Low-density lipoprotein is formed in the liver from VLDL. LDL is the principal carrier of cholesterol in serum and is removed primarily by specific receptors on the liver and other tissues. Excess levels of LDL carry a risk of premature arteriosclerosis. The LDL typically contains 60-70% of total serum cholesterol.
- The liver and small intestine secrete HDL. It is important in removing the excess cholesterol from the peripheral tissues to the liver and has an inverse correlation with risk of arteriosclerosis. The HDL typically contains 20-30% of total serum cholesterol.
Only the number of hydrogen atoms on the molecule separates saturated and unsaturated fats, but they are strikingly different in how they affect the body. Both plants and animals provide sources of saturated fat. Animal fats (butter, lard, cheese) and tropical oils (coconut, palm oil) are high in saturated fat and cholesterol.
Consumption of too much saturated fat elevates circulating total and LDL-C levels. Higher levels of free cholesterol in the liver suppress LDL receptor activity resulting in an increased circulatory level. Dietary triglyceride varies widely in their fatty acid composition. Short chain fatty acids (4 carbons) and medium chain FA (6-12 carbons) are found in vegetable oils and dietary fats, whereas fish oil and certain plants such as walnuts contain FA of the n-3 family. Consumption of n-3 PUFA is strongly inversely correlated with the incidence of heart disease. Consumption of n-6 PUFA lowers circulating cholesterol values.
Of note, epidemiological data fail to demonstrate any direct protective effects of dietary PUFA on coronary heart disease risk. Consumption of mono- unsaturated fats also results in lower cholesterol levels.
Trans-fatty acids are not commonly found in nature. They are in widespread use in commercial and home cooking. Trans-fatty acids are created when fats from vegetable oils are hydrogenated or partially hydrogenated. The hydrogenation process is used to increase the viscosity of vegetable oils. The partially hydrogenated vegetable oils (also identified as vegetable shortening or margarine) are solid at room temperature, unlike the natural vegetable oils where they originated. Trans-fatty acids have been shown to raise LDL cholesterol and lowers HDL cholesterol, with the overall effect on the lipid profile being more adverse than that of the saturated fats. Consumption of trans-FA raises LDL and lowers HDL levels in a dose-dependent fashion.
Q10. Other than fat intake, what other dietary factors influence plasma lipoproteins and affect the risk of developing CHD?
A10. Dietary antioxidants, especially vitamin C and vitamin E have been shown to prevent LDL oxidation and endothelial cell dysfunction. Dietary fiber also influences cholesterol levels. More soluble forms of fiber such as gums and pectins found in legumes and fruit possess more cholesterol lowering properties than insoluble fiber. Fiber exhibits cholesterol-lowering action by at least 3 mechanisms. Fiber:
1. Acts as a bile acid-sequestering agent.
2. Reduces the rate of insulin rise by slowing carbohydrate absorption, thus slowing CH synthesis.
3. Produces short chain fatty acids that are absorbed by partial circulation and inhibit cholesterol synthesis.
Q11. Marie wants to know whether chocolate plays any beneficial role in reducing the risk of CHD.
[Conflict of interest warning: never trust research performed by a chocoholic researcher (or teacher) on chocolates' health effects.]
A11. There are whole schools of thought on national paradoxes.
They all may relate to various flavonoids in food. Flavonoids are naturally occurring compounds that are widely distributed in plants, appearing in fruits, vegetables, and plant-derived beverages, such as tea and red wine. Flavonoids have been claimed to be powerful antioxidants in a number of different biological systems, protecting against damage by free radicals. In addition to red wine, chocolate has been identified as a rich source of flavonoids. Cocoa powder and cocoa-derived products, especially dark chocolate, are good sources of flavonoids, mainly epicatechin and its oligomers, called procyanidins. Dark chocolate has the highest total procyanidins content. Procyanidins strongly correlate with the antioxidant activity of chocolate observed in vitro. Cocoa flavonoids may decrease the oxidation of LDL and modulate platelets and they may positively affect the balance of certain substances involved in hemostatic and inflammatory processes with the possibility of inhibition of atherosclerosis in those who regularly consume cocoa products. While chocolate alone can have beneficial effects, high intake of the combination of milk and chocolate (whether it be through chocolate milk or milk chocolate) increases the amount of fat, adding to the risks for high cholesterol.
Q12. What type of foods should Maria add to make her diet healthier?
A12. The AHA makes the following recommendations for a Heart Healthy Diet:
Limit foods high in saturated fat, trans-fat and/or cholesterol, including full fat milk products, fatty meats, tropical oils, partially hydrogenated vegetable oils and egg yolks. It is important to choose foods low in saturated fat, trans- fat and cholesterol.
Some helpful tips are:
1. Eat a variety of fruits and vegetables. Choose 5 or more servings per day.
2. Eat a variety of grain products, including whole grains. Choose 6 or more servings per day.
3. Eat fish at least twice a week, particularly fatty fish.
4. Include fat-free and low-fat milk products, legumes (beans), skinless poultry and lean meats.
See America's home plate diet in nutrition notes and the module on hypertension and nutrition showing A Dietary Approach to Stopping Hypertension (DASH).
Q13. What are the common types of lipid disorders seen in children?
A13. Lipid disorders, or dyslipoproteinemias, refer to any abnormal blood lipid levels e.g., total cholesterol, triglyceride and lipoproteins. This can be either hypo or hyperlipoproteinemia. Low lipoprotein conditions are mostly due to enzymatic/metabolic defects and are not a common issue for general pediatricians. Hyperlipidemia, or hyperlipoproteinemia, is a more common problem.
The general patterns of hyperlipidemias observed clinically are shown in the following table.
Note that the WHO classification is simply a biochemical phenotypic classification based on which lipoprotein is raised. Also the classification was devised before the importance of HDL as a prognostic indicator was recognized.
* IDL = intermediate-density lipoproteins; LDL = low-density lipoproteins; TC = total cholesterol; TG = triglycerides; VLDL = very low-density lipoproteins;
+ = increased; ++ = greatly increased; N= normal; N+ = normal or increased
The most common type of familial hyperlipidemia manifested in childhood is type II-a hyperlipoproteinemia (elevated Cholesterol and LDL-C). The second most common type is type IV "familial hypertriglyceridemia". Type II-b hyperlipoproteinemia that includes familial combined hyperlipidemia (elevated TG and cholesterol levels) with concomitant increased LDL and VLDL.
For any child with high cholesterol (either total cholesterol or LDL-C), screening tests for secondary causes of hypercholesterolemia should be considered. It is important to separate the hyperlipidemias that are secondary (table 9) to various diseases, diets and drugs from those that are primary and/or familial. Although the distinction of primary from secondary etiologies is useful, there is overlap, since genetic and environmental agents interact. Dietary excesses probably represent the largest proportion of secondary hyperlipidemias in children.
Q14. What are the recommended approaches for the management and prevention of hyperlipidemias in children?
A14. The keys to prevention and management are elimination or modification of risk factors, and if possible, in combination with specific therapy. Dietary therapy is the cornerstone of cholesterol lowering management. The goal of dietary therapy is to reduce elevated serum cholesterol while maintaining adequate eating patterns. Diet therapy is designed to
1. progressively reduce intake of saturated fatty acids and cholesterol.
2. promote weight loss in patients who are overweight by eliminating excess total calories and increasing physical activity.
Both weight reduction and exercise not only promote reduction of cholesterol levels, but have other benefits in reducing triglycerides, raising HDL-C, reducing blood pressure, and decreasing the risk of CHD. Exercise tends to increase HDL-C and may decrease LDL-C. Exercise may have anti-CHD effects that are unrelated to change in lipoproteins or lipids.
For children who have hypercholesterolemia, the treatment begins with dietary intervention by instituting the AHA Step 1 diet (Table 10). The goal of this therapy is to lower the LDL-C to below 130 mg/dL. If this goal is not achieved with a Step 1 diet, a Step 2 diet (Table 10) is initiated. This diet limits the amount of saturated fat calories to less than 7% of total calories and the amount of cholesterol to less than 200 mg/dL.
NOTE: Diets restricting fat intake to less than 20% of total calories should not be used in children unless there is proper dietary and medical supervision.
The Dietary Intervention Study for Children (DISC) has demonstrated the safety of low-fat diets in children when implemented under medical supervision. In contrast, unsupervised parental implementation of low-fat hypocaloric diets in young children has been reported to result in failure to thrive in young children and inadequate caloric intake in older children. Therefore, dietitians should be involved in the implementation of Step 2 diets. Weight and growth parameters need to be carefully monitored for the children who have been prescribed a diet.
The National Cholesterol Education Program (NCEP) Expert Panel On Detection, Evaluation And Treatment Of High Blood Cholesterol In Adults (ATPIII) recommends multifaceted lifestyle changes to reduce the risk for CHD. These therapeutic lifestyle changes (TLC) include:
* Consideration of LDL-lowering dietary options including consumption of plant stanols/sterols (2g/day),
* Weight management, and
* Increased Physical Activity and modification of diet (as shown in the TABLE below).
If the patient does not respond to TLC's, drug treatment may be needed. TLC's should be continued even if drug therapy is needed. The two go hand in hand in prevention and decreasing risk of CHD.
The use of lipid-lowering medication can be considered for children ages 10 years and older if an adequate dietary trial fails and:
a) LDL-C levels remain greater than 190 mg/dL,
b) LDL-C levels remain greater than 160 mg/dL and there is a family history of premature CAD, or
c) LDL-C levels remain greater than 160 mg/dL and the patient has two or more of the following six risk factors: diabetes mellitus, smoking, hypertension, obesity, HDL-C less than 35 mg/dL, or physical inactivity.
It is beyond the scope of the Teacher's Guide modules to address the pharmacologic treatment of high risk for CHD.
Two considerations related to nutrition are:
1. Use of Plant Stanol/Sterols: They are known to bring about a 10-14% reduction in LDL- and Total Cholesterol without reducing HDL-Cholesterol. They include margarines (Benecol, Take Control) or Tablet (Reducol, Cholestoff). They are "natural substances" that are not absorbed and have no side effects.
2. Antioxidant Therapy is lso used. This includes high doses of Vitamins C and E, beta carotene, and flavonoids. Other "alternative" nutrients sold in the marketplace witout substantation include "CoQ 10," Grape Seed Extract, Pycgnogenol, Bilberry. [See modules on alternative medicine and hypervitamin use.]
SUMMARY
Cardiovascular risk is significantly increased by abnormalities in lipids and lipoproteins, including LDL-C, HDL-C and triglycerides. There is compelling evidence that the atherosclerotic process begins in childhood as asymptomatic silent disease and progresses slowly into adulthood.
Prevention of CHD, a major health problem in the United States, should begin in childhood. Limitation of fat intake in children less than 2 years of age can lead to problems of inadequate nutrients and poor growth. After 2 years of age, there is a gradual transition of fat intake to a recommended adult type diet of no more than 30% total calories from fat, less than 10% saturated FA and less than 300mg/day of cholesterol. Pediatricians have the greatest opportunity for providing the safe and feasible intervention for CHD in early childhood by guiding children towards life long healthy eating habits: a diet low in fat, with limitations of foods high in saturated fats, trans-fat and cholesterol, and with a variety of fruits, vegetables and grain products. Advocacy by pediatricians and other clinicians of healthy eating habits along with increased physical activities, decreases exposure to the known risk factors and selective screening for hyperlipidemia in high risk children can help prevent CHD.
*Pediatric Nutrition Handbook 5th edition. AAP
**For Children > 2 Years
Age considerations
" Children < 2 years of age should NOT undergo ANY restriction of fats.
" Dietary and risk factor modification alone is recommended for children 2-10 years of age.
" Children >10 years of age should consume no less than 20% of total calories as fat and may be considered for drug therapy after dietary modification is practiced for 6-12 months without success.
REFERENCES:
1. American Academy of Pediatrics, Committee on Nutrition Cholesterol in Childhood. Pediatrics 1998; 101:141-147.
2. American Heart Association- Policy Statement of the AAP. Gidding SS, Dennison BA, Birch L, et al Dietary Recommendations for Children and Adolescents: A Guide for Practitioners. Pediatrics. 2006;117(2):544-559
3. Belay B, Belamarich P, Racine AD. Pediatric Precursors of Adult Atherosclerosis. Pediatrics in Review 2004 25: 4-16.
4. Bao W, Srinivasan SR, Valdez R, Greenlund RK, Wattigney WA, Berenson G S. Longitudinal changes in cardiovascular risk from childhood to young adulthood in offspring of parents with coronary artery disease: the Bogalusa Heart Study JAMA. 1997; 278:1749-1754.
5. Milner JA, and Allison RG. The Role of Dietary Fat in Child Nutrition and Development: Summary of an ASNS Workshop J. Nutr., November 1, 1999; 129(11): 2094 - 2105.
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7. Knopp RH. Drug Treatment of Lipid Disorders. NEJM 1999; 341:498-511.
8. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. National Cholesterol Education Program. National Heart Lung and Blood Institute, Public Health Service, U.S. Department of Health and Human Services, NIH Publication No. 91-2732, Bethesda, MD, September 1991.
9. Third Report of the National Cholesterol Education Program (NCEP)
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. National Institutes of Health, National Institute of Heart, Lung and Blood Institute, Sept. 2002.
10. Wadowski S, Karp R, Senft C, Murray-Bachmann R. Family History of CHD and Cholesterol Screening in a Disadvantaged population. Pediatrics 1994;93:109-113.
11. Keys A. (1980) Seven Countries: A Multivariate Analyses of Death and Coronary Heart Disease. Harvard Press, Boston. p. 122 Permission for reproduction has been saught.
POSTTEST QUESTIONS
Q1. Cholesterol screening should be performed in which of the following conditions?
a. All children at 2-4 year check up.
b. Any child whose grandfather died at age 65 from myocardium infarction.
c. Any child whose parent's cholesterol is > 180.
d. Obese children.
e. All of the above
Answer = d
Q2. Strategies for preventing hyperlipidemias in children, include all of the following, except:
a. Promote healthy diet.
b. Decrease fat intake to no more than 30% of total calories by 5 years of age.
c. Encourage exercise.
d. Limit cholesterol intake after weaning at 1 year of age.
Answer = d
Q3. Which of the following is the important determinant of risk factor for screening of CHD?
a. Cigarette smoking
b. Cholesterol level of >240 mg/dL in parent
c. Unattainable family history
d. Obesity
e. All of the above
Answer = e
Q4. Most Americans eat too much fat. How much fat is recommended daily for most adults and children>5 years of age?
a. Total fat intake should be between 20-30% of total calories.
b. Saturated fat should be less than 10% of total calories.
c. Dietary cholesterol should be no more than 300 mg/day.
d. All of the above.
Answer = d
Q5. Which of these are examples of foods high in trans-fats?
a. Vegetable shortening, margarines
b. Many processed foods
c. French fries, donuts and other commercial fried foods
d. Cookies, crackers and other commercial baked goods
e. All of the above
Answer = e
ANNOTATED PRETEST ANSWERS
A1. The answer is True. The macronutrient contents, by percentage and energy content, of all mammalian species vary greatly. Seals and other sea mammals having milk that is mostly fat with some protein and little carbohydrate. By coincidence (cow moil) and by choice (formulae), the fat content of all provide ½ of the energy content.
T or F. Obese infants should limit fat intake to 30% of total calories.
A2. The answer is False. The Committee on Nutrition of the American Academy of pediatrics and other monitoring bodies are wary of low fat diets in infancy. See Pediatric Nutrition Notes for an exposition on the importance of fat, per se for the growing child. Moreover, foods naturally high in fat are carriers for micronutrient minerals such as zinc, iron , and calcium that would be deficient in a fat restricted diet.
A3. The answer is False. The Committee on Nutrition of the American Academy of pediatrics and other monitoring bodies are wary of low fat diets in infancy. See Pediatric Nutrition Notes for an exposition on the importance of fat, per se for the growing child. Moreover, foods naturally high in fat are carriers for micronutrient minerals such as zinc, iron , and calcium that would be deficient in a fat restricted diet. Currently, the recommended age to limit fat intake is two years. It is likely that this will drop, but infant feeding will certainly maintain fat content through one year of age.
A4 (A and B).
The answer, at present, is False. Screening recommendations are different at different ages. No screening below 2 years of age; screening children "at-risk" for coronary heart disease from two to adolescence; routine screening is recommended as children go through puberty with some disagreement as to the actual age.
There continues to be a debate, however, among advocates of "screen all," "screen none" and "screen those at risk." Those who recommend "screen all" do so because risk indices are not sufficiently sensitive, e.g., there are many false negative screens. "No screen" advocates say that we should be using a public health approach for prevention so screening is irrelevant. The "at-risk" advocates look for risk factors in the family and screen accordingly. See Wadowski, 1995 (screen at risk) and Newman, 2002 (no screen) for further discussion. [Disclosure, The editor was a co-author of the Wadowski paper and continues to advocate a mix of "at-risk" and public health prevention.]
A5. The answer is False. Risk follows heredity more than somatic measures. Moreover, there are data to suggest that a relatively lean person with a "normal" BMI but a waist-to-hip ration greater than 1.0 for a male or 0.84 for a female has a higher risk than a person with an elevated BMI and gynecoid obesity. Other nutritional risk is a diminished HDL-Cholesterol or HDL to Total ratio as well as defects in clot clearing or an elevated in Apo(A) lipoproteins.
A6. The answer is True. Unfortunately, the inexpensive spreads such as commercial peanut butter and margarines have used all or partial trans saturation processes to harden their products at room temperature. This includes some of the "soft spreads." Trans-saturated fats are a special concern for commercially available fried and baked foods including fast food French fries, cookies and cakes. The role of the pediatrician as an advocate for the poor is essential here.
An entire generation was raised on various butter and milk substitutes that were lower in saturated fat and cholesterol but loaded with trans fats. Butter and full cream milk would have been a healthier choice. The lesson: be humble about you recommendations. You may just be wrong!
