Transcript No Slide Title - Michigan State University

HNF 470
Diet Therapy and Coronary Heart Disease (CHD)
I.
Risk Factors for Developing CHD
II.
Diet-Responsive Risk Factors for CHD
A.
B.
American Heart Association “Step” Diets
Role for Dietary Supplements?
III.
Diet Therapy in the Secondary Prevention of IHD
IV.
Diet Therapy in the Primary Prevention of IHD
V.
Are AHA Step I and II Guidelines Enough?
http://www.msu.edu/course/hnf/470
Definitions
and
Terminologies
The Burden
Deaths due to CVD are the #1 cause of death
in the u.s.
(#1 = Coronary heart Disease; #3 = Stroke)
Mortality has dropped DRAMATICALLY in the
past two decades-•
•
1˚ ly due to advances in treatment
Incidence has not changed.
Coronary Heart Disease
Cause:
Formation of Atherosclerotic Plaques
Risk Factors: Maleness (>45 yo), Femaleness (>55 yo)
High LDL (>160 mg/dl); Low HDL (<35 mg/dl)
Hypertension (Diastolic >90 mm Hg)
Smoker
DM
Family Hx
Etiology:
Current hypothesis: Oxidation of the apolipoprotein
component of LDL leads to injury of cells lining
the artery (intima). Damage leads to platelet
activation, excessive clotting, and atherogenesis.
Narrowing of the artery leads to a hypoxic (ischemic)
condition in target organs.
Risk Factors for CHD:
The Framingham Heart Study
Major Risk Factors
“Important” Risk Factors
Cigarette Smoking
Hypertension*
High Total Serum Cholesterol*
Low HDL Cholesterol*
Diabetes Mellitus*
Obesity*
Physical Inactivity
Family Hx of Premature CHD
Hypertriglyceridemia*
Increased Lipoprotein [a]
Increased serum homocysteine*
Abnormal levels of various
coagulation factors
*Dietary factors contribute strongly to the control of or in the etiology
of these risk factors.
Diet-Related Risk Factors
High LDL Cholesterol
Begin treatment
With CHD:
Without CHD + one risk factor:
Without CHD + > 2 risk factors:
Low HDL Cholesterol
Hypertension
Diabetes Mellitus
LDL Cholesterol
(mg/dl)
>100
>160
>130
Blood Lipid Fraction
Desirable Borderline
High
LDL Cholesterol (mg/dl)
<130
130-159
>160
Total Cholesterol (mg/dl)
<200
200-239
>240
Triglycerides (Fasting; mg/dl) <200
200-400
>400
HDL Cholesterol= “Low” (Bad) if 35 mg/dl
LDL:HDL ratio: > 5 indicates risk for men
>4.5 indicates risk for women
Diastolic Pressure (mm Hg)
< 85 = Normal
80-89 = High-Normal
90-99 = Mild
100-109 = Moderate
110-119 = Severe
>120 = Very Severe
Figure 1: Annual trends in incidence and case fatality rate
of CHD by country.
United States
Russia, E. Europe, China
Source: http://www.bmj.com
Source: http://www.bmj.com
Role of Diet in the Modification of Blood Cholesterol Levels
Assumptions:
• Blood cholesterol [ ] is an important and modifiable risk factor
for coronary heart disease.
• Sustained reduction of total cholesterol [ ] of 1% is associated
with a 2-3% reduction in the incidence of coronary heart disease.
Total Cholesterol Levels (mg/dl) in the U.S.
(National Health and Nutrition Examination Surveys)
Age Group
1976-80
1988-1994
Adults
213
203
Adolescents (ages 12-17)
167
160
Role of Diet in the Modification of Blood Cholesterol Levels-3
Efficacy of Dietary Intervention Trials to Lower Total Cholesterol
Diet Types
% Reduction in
Total Cholesterol
AHA Step 2
Lower Total Fat
6.0
Raise PUFA:SFA Ratio
AHA Step 1
3.0
Tang et al. (1998) BMJ 316: 1213-1220
Systematic review of dietary intervention trials to lower blood total cholesterol in free-living subjects.
Role of Diet in the Modification of Blood Cholesterol Levels-4
How Do These Results Compare to Metabolic Ward Studies?
•
Dietary change results in decreases of total cholesterol
up to 15%.
•
Difficulties in complying with the prescribed dietary change
may explain the failure to achieve the expected reductions
in cholesterol concentrations.
•
Even so, diets low in saturated fat and cholesterol are
important adjunctive therapies for lowering population
risk of CHD.
Tang et al. (1998) BMJ 316: 1213-1220
Systematic review of dietary intervention trials to lower blood total cholesterol in free-living subjects.
Role of Diet in the Modification of Blood Cholesterol Levels-2
Chief Determinants of Blood Cholesterol Levels
1.
2.
3.
4.
Certain saturated fatty acids cause a linear increase
in low-density lipoprotein (LDL) cholesterol concentration.
(Total SFA in U.S. Diet: 11-12 % of total energy)
Trans unsaturated fatty acids increase LDL cholesterol
[ ]; not quite as atherogenic as certain SFA.
(Total trans FA in U.S. Diet: ~ 3 % of total energy)
Polyunsaturated fatty acids derived from plant oils do
NOT raise LDL cholesterol [ ].
(Total PUFA in U.S. Diet: ~ 6 % of total energy)
Monounsaturated fatty acids derived from high oleic acid
(cis-18:1) oils (e.g., olive, peanut, canola) do NOT raise
LDL cholesterol [ ].
Deciles of PUFA:SFA Ratio and Risk of CHD in Women
(Hu et al. AJCN 70: 1001-8, 1999)
The eating plan is based on these AHA dietary guidelines:
* Total fat intake should be less than 30 % of calories.
* Saturated fatty acid intake should be less than 10 % of
calories.
* Polyunsaturated fatty acid intake should be no more
than 10 percent of calories.
* Monounsaturated fatty acids make up the rest of
the total fat intake, about 10 to 15 % of total calories.
* Cholesterol intake should be no more than 300 mG per day.
* Sodium intake should be no more than
2400 milligrams (3 grams) per day.
Fruit and Vegetable Intake in the Nurses Health Study and
Relative Risk of CHD
To control the amount and kind of fat, saturated fatty acids, and dietary
cholesterol you eat:
Eat up to 6 ounces (cooked) per day of lean meat, fish and skinless poultry.
The approximately 5 to 8 teaspoon servings of fats and oils per day may be used for
cooking and baking, and in salad dressings and spreads.
Use cooking methods that require little or no fat — boil, broil, bake, roast, poach,
steam, sauté, stir-fry or microwave.
Trim off the fat you can see before cooking meat and poultry. Drain off all fat after
browning.
The 3 to 4 egg yolks per week included in your eating plan may be used alone or in
cooking and baking (including store-bought products).
Choose skim or 1% fat milk and nonfat or low-fat yogurt and cheeses.
Physicians Health Study
Hennekens et al. (1996) N Engl J Med 334:1145.
•
22,071 male physicians randomized to alternate-day
ß-carotene (50 mg), aspirin (325 mg), both active
treatments, or both placebos.
•
Aspirin component terminated early (1988) due to
statistically extreme 44% reduction in risk of first
myocardial infarction.
•
After 12 years of treatment with ßC, there was no
effect on any CA endpoint, MI, stroke, or CHD
deaths.
Vitamin E Supplementation and CHD
•
Evidence from prospective trials (Physicians Health
Study, Nurses Health Study) showed ~40% reduction
in CHD incidence with > 2 yrs intake of >100 I.U. AT.
•
The Iowa Women’s Health Study showed that vitamin E
content in FOOD, not supplements, was inversely
associated with risk of death from CHD (lowest vs.
highest quintile of consumption: RR= 0.38;p=0.004)
Cambridge Heart Antioxidant Study
(Stephens et al. (1996) Lancet 347: 781-86)
*
Double-blinded study of the prevention of CVD death
and non-fatal MI in patients with angiographically proven
coronary atherosclerosis receiving alpha tocopherol or
a placebo.
*
2002 patients
546 (800 I.U.)
489 (400 I.U.)
967 (placebo)
*
Median follow-up:
510 days (range 3-981)
CHAOS Results
1.
Alpha tocopherol treatment decreased risk of CVD death
and non-fatal MI:
Relative Risk (RR):
2.
Most of this benefit was due to decreased risk of non-fatal
MI:
RR:
3.
0.53 (95% CI 0.34-0.83; p=0.005)
0.23 (95% CI 0.11-0.47; p=0.005)
Non-significant INCREASE or excess in cardiovascular
deaths in the treatment group compared to the placebo group.
Vitamin E: A Review
Function: Cell Membrane Antioxidant
(prevents lipid peroxidation/free radical generation)
Alpha-Tocopherol
Gamma-Tocopherol
•
•
•
•
• principal form of
vitamin E in U.S. diet
• more rapid uptake and
cellular turnover
• traps mutagenic
electrophiles like NOx
higher vitamin E activity
more potent antioxidant
primary form of supplemental vitamin E
low plasma levels are strong predictors of
risk of certain cancers and CHD
• displaces gamma-T in plasma/other tissues
• 5-fold higher plasma levels than gamma-T
Dietary Effectors of Endothelial Cell Function
(“NOT ready for prime time”)
•
Arginine:
substrate for endothelial nitric oxide
synthase
HeartBar®:
3 grams arginine per bar
Purports “Heart Healthy” benefits
•
Pharmacologic Doses of Vitamins A and C
•
Negative Effector: High Fat Diets
Frequent nut consumption and risk ofcoronary heart disease
in women: prospective cohort study
Frank B Hu et al. Harvard University School of Public Health
BMJ 1998;317:1341-1345 ( 14 November )
After adjusting for age, smoking, and other known
risk factors for CHD:
Women consuming > five ounces of nuts a week
(frequent consumption)
vs.
women who never ate nuts or who ate < one ounce a month
(rare consumption)
had a significantly lower risk of total coronary heart disease
(RR = 0.65, 95% confidence interval 0.47 to 0.89, P for
trend=0.0009).
The magnitude of risk reduction was similar for both
fatal coronary heart disease (0.61, 0.35 to 1.05, P for trend=0.007)
& non-fatal MI (0.68, 0.47 to1.00, P for trend=0.04).
Further adjustment for intakes of dietary fats, fibre,
vegetables, and fruits did not alter these results.
The inverse association persisted in subgroups
stratified by levels of smoking, use of alcohol, use of
multivitamin and vitamin E supplements, body mass index,
exercise, and intake of vegetables or fruits.
Key messages
Nuts are high in fat, but most of the fatty acids are unsaturated
This study suggests that frequent consumption of nuts,
including peanuts, may reduce the risk of coronary heart disease
This protective effect may be partly mediated through serum
lipids because unsaturated fats have benefical effects on
serum lipids. Other potentially protective constituents include
vegetable protein, magnesium, vitamin E, fibre, and potassium
Nuts can be included as part of a healthy diet
Lyon Diet Heart Study
(de Lorgeril et al., Arch Int Med 158: 1181-1187)
• Randomized secondary prevention trial;
• 605 patients with coronary artery disease
randomized to either a Meditarranean-type
diet or control (A.H.A. Step 1-like) diet;
• After ~ 4 years of follow-up, Cox
proportional hazards model was used to
estimate risk ratios for cancer, total or
cardiac death, combined total death,
nonfatal cancer, and nonfatal MI.
Table 1: Number of Events and Risk Ratios
de Lorgeril et al. (1998) Arch. Int. Med. 158: 1181-1187.
Table 2: Characteristics of patients who developed
cancer in the two groups
Figure 1: Cumulative survival without nonfatal cancer among patients
in the experimental and control groups.
Figure 2: Cumulative survival without nonfatal cancer and
recurrent acute MI among patients in the experimental
and control groups.
Eat a variety of foods.
Choose most foods from plant sources.
Eat at least 5 servings of fruits and vegetables every day.
Eat at least 6 servings of whole grain foods each day.
Minimize the consumption of high-fat foods, especially
those from animals.
Choose low-fat, low-cholesterol foods.
imit the amount of simple sugars in the diet.