and methionine influences on homocyst(e)ine levels
soluble and insoluble
sterols and stanol ester
Cholesterol Education Program and American Heart Association dietary
and lifestyle modification
training, the learner will be able to:
Objectives: Medical Students
how fatty acids and cholesterol are absorbed in the intestine
and how the body controls cholesterol absorption, including
the role of the ABC protein.
the pathways of cholesterol and triglyceride transport between
tissues and identify sites of regulation that influence
VLDL, LDL, and HDL levels.
the role of the three major lipoprotein classes in atherogenesis.
the effects of saturated, monounsaturated and polyunsaturated
fatty acids on plasma LDL and cholesterol levels.
at least three common foods that are high in cholesterol,
saturated, monounsaturated and polyunsaturated fatty acids.
and contrast the structure of saturated fatty acids and
trans fatty acids and their differential effects on atherogenesis.
at least three common foods high in n-3 fatty acids.
the utility of lowering homocyst(e)ine levels to prevent
homocyst(e)ine metabolism and the roles of folate, B6 and B12.
at least two common foods high in folate, B6,
B12, or methionine.
between soluble and insoluble fiber.
at least three common foods that are high in soluble and
the effects of soluble and insoluble fiber on LDL and triglyceride
the effects of soluble and insoluble fiber on the absorption
of bile acids and simple sugars.
and contrast the effects of complex carbohydrates and simple
sugars on plasma glucose and triglyceride levels.
at least five common foods that are high in complex carbohydrates.
the effect of the level of alcohol consumption on VLDL and
HDL in normal and hypertriglyceridemic persons and any subsequent
effect on atherosclerosis.
how plant sterols and stanols influence cholesterol absorption
and LDL levels.
at least three common foods that are high in dietary sodium,
calcium, and potassium.
NCEP ATP-III criteria defining the metabolic syndrome.
how weight loss affects LDL and HDL levels, insulin resistance,
abdominal obesity, glucose intolerance, hypertriglyceridemia,
and the risk of diabetes.
the Therapeutic Lifestyle Change (TLC) diet recommendation
of the National Cholesterol Education Program (NCEP). Compare
the TLC Diet with diets advocating extremely low or high
fat intakes and the expected effects on levels of the major
classes of lipoproteins.
the utility of lowering homocyst(e)ine levels to prevent
at least two examples of individual genetic variations affecting
the efficacy of the nutritional management of cardiovascular
the gender-related differences in energy balance, diet-associated
lipoprotein levels, and the incidence of CVD.
the controversy surrounding the use of antioxidant vitamin
supplements/foods to prevent CVD.
the effects of the metabolic pathways from N-6 and N-3 fatty
acids to prostaglandins on vascular reactivity and platelet
the effects of N-3 fatty acids on plasma triglyceride levels
and cardiac electrical conduction.
the effects of altering dietary folate, B6, B12,
or methionine on homocyst(e)ine levels and CVD risk.
at least five dietary intervention clinical trials and five
observational studies that demonstrated a reduction in the
incidence of CVD, and identify the specific dietary constituents
associated with cardiovascular health in each study.
and justify with scientific evidence the total quantitative
benefit achievable from combining at least five diet and
exercise modifications in the prevention of cardiovascular
the controversy regarding the vascular benefit of adding
antioxidant vitamins and foods to the diet.
a comprehensive patient medical history, and identify any
risk factors and symptoms of cardiovascular disease present.
an appropriate nutrition history to determine the intake
of saturated fat, cholesterol, sodium, soluble fiber, fruits,
vegetables, complex carbohydrates, alcohol and vitamin,
mineral and herbal supplements.
a focused physical examination that includes assessment
of abdominal obesity estimated by waist circumference and
accumulation of cholesterol in the skin, tendons, and eyes.
a patients medical history, select appropriate lipid
laboratory tests to estimate CHD risk using the NCEP ATP
between normal and abnormal serum concentrations of total
cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides
using NCEP ATP-III criteria.
a patients risk using the Framingham Risk Assessment
Tool for Estimating 10-year Risk of Developing CHD.
a patients medical history and the results of appropriate
lipid laboratory tests, propose an optimal set of goals
for nutritional risk factor reduction using the NCEP and
AHA guidelines for nutrition and exercise.
the cumulative significance of appropriate dietary fats
and maintaining a diet in the prevention of CVD.
a commitment to promoting dietary and lifestyle modifications
that can diminish the risk of cardiovascular disease.
the value of a cardiovascular disease prevention diet for
nutritional health in general, including maintaining normal
a personal commitment to serve as a positive role model
for patients by maintaining a healthy diet and active lifestyle
consistent with reducing CVD risk.
fellow physicians to refer patients with CVD or CVD risk
to registered dietitians or other credentialed healthcare
professionals as appropriate to assist with medical nutrition
examples for some of knowledge objectives
egg yolks, shrimp, liver, kidney
fat: Palm oil, coconut oil, whole milk and cheese, fatty
fat: olive oil, avocado, canola oil, nuts
fat: safflower oil, corn oil, soybean oil, sunflower oil
fatty acids: salmon, herring, halibut, flax seed, nuts
brewers yeast, orange juice, liver, legumes, leafy vegetables,
fortified grain products
B6: Meat, poultry, fish, green leafy vegetables,
whole grains, legumes
B12: Meat, poultry, fish, eggs, dairy products
whole grains, sesame seeds, sunflower seeds, brewers yeast
canned, frozen and dehydrated foods, chips, restaurant food
Fruits and vegetables, milk, potatoes
dairy products, calcium-fortified foods (e.g. orange juice, cereals)
of genetic variations/control of cholesterol levels:
Apo E4: raises LDL
Apo A-IV polymorphisms: may reduce response to dietary cholesterol
bold items were ranked in the top 1/3 of all objectives.
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