Dietary fat, coronary heart disease, and cancer: a historical review

OBJECTIVES: This report describes the historical development of medical theories and research concerning the relationship between dietary fat intake and breast and colorectal cancer and coronary heart disease (CHD). METHOD: The historical and medical literature on this topic was analyzed with special reference to the Woman's Health Initiative (WHI) studies. RESULTS: After 1900, changes in clothing fashions and life insurance mortality studies created strong preferences for slimness and emphasized reduced dietary fat intake as the preferred method of weight control. After midcentury, ecological correlations of countries found that national average dietary fat intake was related to national breast cancer and CHD rates. These relationships were not found in longitudinal studies of the same countries or in studies of dietary fat intake of individuals, including the WHI study. Dietary fat intake was found to affect colorectal cancer in some studies of individuals, although not the WHI. The WHI, like other intervention studies of dietary fat reduction, used unrepresentative samples and costly lifestyle change techniques that are not economically feasible in the community. CONCLUSION: The WHI concurred with many other studies in finding that dietary fat intake is not a significant risk factor for CHD or breast cancer.     

Dietary fat intake and risk of coronary heart disease: the Strong Heart Study

BACKGROUND: The results of previous studies on the association between dietary fat intake and coronary heart disease (CHD) incidence are inconsistent. OBJECTIVE: The aim of this study was to examine the association between dietary fat intake and CHD incidence in American Indians in the Strong Heart Study. DESIGN: A total of 2938 participants aged 47-79 y and free of CHD at the second examination (1993-1995) were examined and followed for CHD, nonfatal CHD, and fatal CHD events to 31 December 2002. Dietary intake was assessed by using a 24-h diet recall and was calculated as percentages of energy. RESULTS: Participants were followed for a mean (+/-SD) of 7.2 +/- 2.3 y. During follow-up, 436 incident CHD cases (298 nonfatal CHD and 138 fatal CHD events) were ascertained. Participants aged 47-59 y in the highest quartile of intake of total fat, saturated fatty acids, or monounsaturated fatty acids had higher CHD mortality than did those in the lowest quartile [hazard ratio (95% CI): 3.57 (1.21, 10.49), 5.17 (1.64, 16.36), and 3.43 (1.17, 10.04), respectively] after confounders were controlled for. These associations were not observed for those aged 60-79 y. CONCLUSIONS: Total fat, saturated fatty acid, and monounsaturated fatty acid intake were strong predictors of CHD mortality in American Indians aged 47-59 y, independent of other established CHD risk factors. It may be prudent for American Indians to reduce their fat intake early in life to reduce the risk of dying from CHD.     

The effect of dietary protein intake on coronary heart disease risk

There is cumulative evidence that there is a relationship between diet and coronary heart disease (CHD) risk. The majority of studies have focused on the role of carbohydrate and fat on CHD risk; yet the role of protein has, until recently, been neglected. The effects of dietary protein on modulating CHD risk factors are still unclear. The aim of this review is to summarise available data from epidemiological and randomised control trials on the effects of animal and vegetable protein intake on markers of CHD risk; that is, obesity, hyperlipidaemia, glucose intolerance, diabetes and hypertension. Regarding the management of body weight, reviewed data suggest that there is no convincing evidence that higher protein (HP) diets enhance weight loss compared with low protein (LP) diets, but there is some evidence that HP diets may lead to better weight maintenance. Moreover, HP diets seem to have a more favourable effect on triglyceride levels than LP diets, but on the other hand, there is no convincing evidence that there is a significant beneficial effect on total and low‐density lipoprotein cholesterol levels. In the literature, there is also a concern that higher protein intakes may increase blood glucose levels and may aggravate glycaemic control. Currently, data suggest that HP diets may have a favourable effect on postprandial glucose and glycated haemoglobin levels, whereas there is no convincing evidence on their effects on fasting glucose and insulin levels. There has also been concern that higher protein intakes may increase arterial blood pressure because of higher levels of sodium in protein‐rich foods. The data we reviewed suggest that HP diets may be more beneficial in ameliorating hypertension than LP diets. Finally, the effect of a higher protein intake on kidney function has been debated.     

Preventive nutrition intervention in coronary heart disease: risk assessment and formulating dietary goals

Risk factor screening and establishing realistic goals are key steps for the dietitian to follow in planning strategies to prevent coronary heart disease. The major risk factors that are responsive to dietary intervention include: elevated plasma total cholesterol and low-density-lipoprotein cholesterol, elevated blood pressure, glucose intolerance, and obesity. The criteria used in assessing nutrition-related risk in coronary heart disease are presented. The long-term goals of preventive nutrition intervention in heart disease are discussed, with emphasis on a unified and progressive approach to diet planning.     

Dietary fat and risk of coronary heart disease: possible effect modification by gender and age

In a 16-year follow-up study (ending in 1998) of 3,686 Danish men and women aged 30-71 years at recruitment, the association between energy intake from dietary fat and the risk of coronary heart disease was evaluated while assessing the possible modifying role of gender and age. In the models used, total energy and protein intake were fixed. Differences in intake of energy from fat thus reflected complementary differences in intake of energy from carbohydrates. A 5% higher level of energy from saturated fat intake was associated with a 36% greater risk of coronary heart disease among women (hazard ratio (HR) = 1.36, 95% confidence interval (CI): 0.98, 1.88). No overall association between saturated fat and coronary heart disease was found among men. However, age-dependent analyses showed that saturated fat was positively associated with coronary heart disease among the younger men (HR = 1.29, 95% CI: 0.87, 1.91) and the younger women (HR = 2.68, 95% CI: 1.40, 5.12) but not among the older men (HR = 0.94, 95% CI: 0.70, 1.28) and the older women (HR = 1.22, 95% CI: 0.86, 1.71). Polyunsaturated fat was inversely associated with coronary heart disease among women and men, although not significantly. In conclusion, the present study suggests that coronary heart disease risk relates to both the quantity and the quality of dietary fats.     

Nutrition imbalance and angiotoxins as dietary risk factors in coronary heart disease.

Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate vegetable oils to a minimum trans fatty acid content and rearrange this fat with polyunsaturated fats to produce high polyunsaturated fats trans-free margarines and shortenings.     

Prospective study of major dietary patterns and risk of coronary heart disease in men

BACKGROUND: Previous studies on diet and coronary heart disease (CHD) focused primarily on individual nutrients or foods. OBJECTIVE: We examined whether overall dietary patterns derived from a food-frequency questionnaire (FFQ) predict risk of CHD in men. DESIGN: This was a prospective cohort study of 44875 men aged 40-75 y without diagnosed cardiovascular disease or cancer at baseline in 1986. RESULTS: During 8 y of follow-up, we documented 1089 cases of CHD (nonfatal myocardial infarction and fatal CHD). Using factor analysis, we identified 2 major dietary patterns using dietary data collected through a 131-item FFQ. The first factor, which we labeled the "prudent pattern," was characterized by higher intake of vegetables, fruit, legumes, whole grains, fish, and poultry, whereas the second factor, the "Western pattern," was characterized by higher intake of red meat, processed meat, refined grains, sweets and dessert, French fries, and high-fat dairy products. After adjustment for age and CHD risk factors, the relative risks from the lowest to highest quintiles of the prudent pattern score were 1.0, 0. 87, 0.79, 0.75, and 0.70 (95% CI: 0.56, 0.86; P: for trend = 0.0009). In contrast, the relative risks across increasing quintiles of the Western pattern score were 1.0, 1.21, 1.36, 1.40, and 1.64 (95% CI: 1.24, 2.17; P: for trend < 0.0001). These associations persisted in subgroup analyses according to cigarette smoking, body mass index, and parental history of myocardial infarction. CONCLUSIONS: These data suggest that major dietary patterns derived from the FFQ predict risk of CHD, independent of other lifestyle variables.     

Target value of intraabdominal fat area for improving coronary heart disease risk factors

OBJECTIVE: The goal of this study was to determine an intraabdominal fat (IF) area target value for improving coronary heart disease (CHD) risk factors in response to weight reduction. RESEARCH METHODS AND PROCEDURES: Subjects were 279 obese Japanese women, 21 to 66 years old, who were divided into diet-alone and diet-plus-exercise groups and participated in a 14-week weight reduction program. The IF area was measured by computerized tomography scans. Systolic blood pressure > or = 140 mm Hg, diastolic blood pressure > or = 90 mm Hg, total cholesterol > or = 5.70 mM, triglycerides > or = 1.70 mM, and fasting plasma glucose > or = 6.99 mM were defined as CHD risk factors. RESULTS: The best trade-off between sensitivity (probability of correctly detecting true positive) and specificity (probability of correctly detecting true negative) was found at 100 cm2 pretreatment in combined data of the two groups. At posttreatment, although a slight difference was found in the target value between the treatment groups (60 cm2 for diet alone and 50 cm2 for diet plus exercise), the combined data showed that the best trade-off occurred at 60 cm2 (sensitivity and specificity were 0.55 and 0.63, respectively). The percentage of subjects having no CHD risk factors was significantly lower in the group that had large IF areas (> or = 60 cm2) (46%) compared with the group that had normal IF areas (<60 cm2) (65%). However, the percentage of subjects having multiple CHD risk factors was significantly greater in the group that had large IF areas (16%) compared with the group with normal IF areas (7%) at posttreatment. DISCUSSION: Our longitudinal data suggest that obese Japanese women should reduce their IF areas to < 60 cm2 through weight reduction to improve CHD risk factors independent of treatment.     

Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements

Previous cohort studies of fat intake and risk of coronary heart disease (CHD) have been inconsistent, probably due in part to methodological differences and various limitations, including inadequate dietary assessment and incomplete adjustment for total energy intake. The authors analyzed repeated assessment of diet from the Nurses' Health Study to examine the associations between intakes of four major types of fat (saturated, monounsaturated, polyunsaturated, and trans fats) and risk of CHD during 14 years of follow-up (1980-1994) by using alternative methods for energy adjustment. In particular, the authors compared four risk models for energy adjustment: the standard multivariate model, the energy-partition model, the nutrient residual model, and the multivariate nutrient density model. Within each model, the authors compared four different approaches for analyzing repeated dietary measurements: baseline diet only, the most recent diet, and two different algorithms for calculating cumulative average diets. The substantive results were consistent across all models; that is, higher intakes of saturated and trans fats were associated with increased risk of CHD, while higher intakes of monounsaturated and polyunsaturated fats were associated with reduced risk. When nutrients were considered as continuous variables, the four energy-adjustment methods yielded similar associationS. However, the interpretation of the relative risks differed across models. In addition, within each model, the methods using the cumulative averages in general yielded stronger associations than did those using either only baseline diet or the most recent diet. When the nutrients were categorized according to quintiles, the residual and the nutrient density models, which gave similar results, yielded statistically more significant tests for linear trend than did the standard and the partition models.     

Familial hypercholesterolemia and coronary heart disease: a HuGE association review

Familial hypercholesterolemia (FH) is an autosomal disorder characterized by increased levels of total cholesterol and low density lipoprotein cholesterol. The FH clinical phenotype has been shown to be associated with increased coronary heart disease and premature death. Mutations in the low density lipoprotein receptor gene (LDLR) can result in the FH phenotype, and there is evidence that receptor-negative mutations result in a more severe phenotype than do receptor-defective mutations. Mutations in the apolipoprotein B-100 gene (APOB) can result in a phenotype that is clinically indistinguishable from familial hypercholesterolemia, and mutations in this gene have also been shown to be associated with coronary heart disease. Preliminary research indicates that the FH phenotype is influenced by other genetic and environmental factors; however, it is not clear if these are synergistic interactions or simply additive effects.     

Trends in dietary fat and cigarette smoking and the decline in coronary heart disease in New Zealand

Coronary heart disease (CHD) mortality declined by approximately 23.5% in New Zealand men aged 35-64 years between 1968 and 1980. The contributions of secular trends in dietary fat and tobacco consumption to this decline were examined using data from national consumption statistics and population based studies of risk factor levels. Per capita saturated fat and dietary cholesterol consumption fell by approximately 12% and 10% respectively during this period while polyunsaturated fat consumption increased by 73%. Per capita tobacco consumption fell by approximately 15%. Using equations developed by Keys and Hegsted it was calculated that the mean serum cholesterol level declined by between 6.6 and 10.3 mg/dl (2.9%-4.4%) during this period. The potential impact of these risk factor changes on CHD mortality was estimated using a Framingham multivariate logistic risk function. Between 38% and 51% of the observed decline in CHD mortality in men aged 35-64 years in New Zealand between 1968 and 1980 could be accounted for by the calculated changes in serum cholesterol and tobacco consumption. If serum cholesterol and cigarette smoking were reduced further to meet current recommendations, it is estimated that CHD mortality would decline by a further 26%-30% from the 1980 level.     

Moderate dietary fat consumption as a risk factor for ischemic heart disease in a population with a low fat intake: a case-control study in Korean men

BACKGROUND: Dietary fat intake is associated with the incidence of ischemic heart disease (IHD) in Western countries. In populations in which both the average dietary fat consumption and the incidence of IHD are lower than in Western countries, the association of dietary fat intake with IHD incidence remains unknown. OBJECTIVE: We conducted a case-control study to examine the association of dietary fat with IHD incidence in Korean men. DESIGN: The case group consisted of 108 patients with electrocardiogram-confirmed myocardial infarction or angiographically confirmed (> or =50% stenosis) IHD who were admitted to a university teaching hospital in Seoul, Republic of Korea. The controls were 142 age-matched patients admitted to the departments of ophthalmology and orthopedic surgery at the same hospital. Dietary fat intake was assessed by a nutritionist using a semiquantitative food-frequency questionnaire. Body mass index (BMI), cigarette use, alcohol intake, exercise, and history of disease were determined during an interview and examination. RESULTS: In a univariate analysis, the mean percentages of energy from total fat, saturated fatty acids, and monounsaturated fatty acids were significantly higher in the cases than in the controls. BMI, smoking, and a history of hypertension were associated with the occurrence of IHD. In multiple logistic analyses, total fat intake was a significant risk factor (odds ratio: 1.08 for 1% of energy intake; 95% CI: 1.02, 1.14) after adjustment for BMI and smoking. CONCLUSION: In a population with a relatively low fat intake (19% of energy intake), a moderate increase in total fat intake may be a risk factor for IHD.     

Carbon monoxide and coronary heart disease: A review

The most vulnerable target organ for low level carbon monoxide exposure appears to be the heart. Thus, what physiologists have inferred years ago and epidemiologists suspected only recently, is being proven by clinical investigators. A new role for carbon monoxide in heart disease is emerging from new research findings.     

Earthquake and coronary heart disease risk factors: a longitudinal study.

The longitudinal association between a number of coronary heart disease risk factors and the experience of a natural disaster (earthquake) was analyzed in a group of workers participating in a longitudinal epidemiologic investigation. The 5-year follow-up examination was interrupted by a major earthquake, and examinations were resumed 2 weeks after the quake. Participants screened after the quake had, on average, higher heart rates, serum cholesterol, and triglycerides than participants examined before the quake; these differences were independent from the coronary heart disease risk factor values measured 5 years previously during the baseline examination. The data collected during the 12-year examination indicated that the observed short-term increase in serum lipids and heart rate was not present long-term (7 years after the quake). These longitudinal data indicate that exposure to a natural disaster can be associated with short-term increases in heart rate, serum cholesterol, and triglycerides but that there is no apparent long-term effect on these coronary heart disease risk factors.