Fact Sheet 2
Part A: Olive Oil and Cardiovascular Risk
Atherosclerosis and coronary heart disease (CHD) as its main clinical manifestation have a multifactorial origin. The susceptibility to CHD is determined both by genetic and environmental influences. Among the latter, diet is undoubtedly the central factor in the development of CHD. Dietary factors exert their influence largely through their effects on blood lipids and lipoproteins, but also through their great influence on the other established modifiable risk factors (Table 1), with the exception of cigarette smoking.
Table 1: Risk factors for coronary heart disease (CHD)
The dietary factors most directly
implicated are dietary fats. Numerous comparisons between populations have
shown that there is a strong correlation between the intake of saturated fatty
acids (SFA) and CHD morbidity and mortality. A customary diet high in SFA is
associated with high levels of CHD. This is the case for the most Western and
Northern European countries. On the other hand, in the Mediterranean countries,
where people consume their traditional diet in which the majority of fat
calories is derived from olive oil, there is a low incidence of CHD. The
present paper outlines the effects of monounsaturated fatty acids (MUFA), olive
oil, and Mediterranean diet on the different cardiovascular risk factors and on
This topic is covered in Fact Sheet 1.
Cross-cultural comparisons and prospective observational studies identify a strong relationship between diet and blood pressure. The studies show that vegetarians in particular have lower blood pressure than non-vegetarians. There is also evidence that the Mediterranean diet might exert a beneficial influence on blood pressure. For instance, significantly lower blood pressures were observed in Italian population samples as compared to Finnish and Scottish groups (41). Until now it could not be clearly determined which of the many nutrient differences compared to usual Western diets were responsible for the blood pressure lowering effect. The partial substitution of vegetables and grain for meat decreases SFAs which are largely derived from animal sources. The intake of MUFA is increased due to the olive oil consumption. In addition, Mediterranean as well as vegetarian diets are characterised by a higher intake of fibre, carbohydrates and micronutrients (eg. potassium, calcium, magnesium), and a lower salt intake.
As a consequence of these observations a large number of different studies have examined the correlation between dietary intake of different types of fat and blood pressure. The majority of cross-sectional studies measuring blood pressure and self-reported diet at the same time, provide no evidence to support the hypothesis that dietary fats affect blood pressure. However, the results must be qualified by taking some methodological weakness into account. In most studies either the measurement of usual diet (eg. 24-hour recall) or blood pressure (eg. only one measurement) was inaccurate or there was an inadequate control of both dietary and non-dietary confounding factors.
Epidemiological prospective studies show conflicting results. For instance, in the Multiple Risk Factor Intervention Trial (MRFIT) (32) with approximately 1200 participants, systolic blood pressure was independently related to SFA intake and dietary cholesterol (48). In contrast, there was no relationship between dietary fat and blood pressure in two large cohort studies: ie: in the Nurses Health Study (57) the 4-year incidence of hypertension was investigated among 58,218 disease-free nurses who completed a dietary questionnaire at baseline. In multivariate analysis controlled for dietary and non-dietary factors, the development of hypertension was not associated with usual intake of total fat, saturated fat, or unsaturated fat. A similar analysis of a cohort of 30,681 US male health professionals confirmed these results (3).
The large sample size of the two latter studies together with their accurate assessment of usual dietary intake and rigorous statistical control for confounding factors provide support for the absence of an association between dietary fat and hypertension or change in blood pressure.
Experimental data of a relationship between dietary fat and blood pressure are also contradictory (for review see 31). In many studies the dietary intervention simultaneously included several measures (eg. exchange of animal fat with vegetable oils plus increase in vegetable consumption). Thus, it is impossible to attribute changes in blood pressure to a single nutrient. In addition, the majority of studies were conducted with normotensive subjects, and their results may not be applied to hypertensive patients.
A well-controlled, randomised cross-over trial compared the effects of a high-fat, high-MUFA diet with a high-fat, high-PUFA diet on blood pressure in healthy adults. No change in blood pressure was found after 4 weeks of treatment (42). There was no evidence of a blood-pressure-lowering effect of either dietary MUFA or PUFA in further studies of normotensive individuals. One study compared a low-fat, carbohydrate-rich diet with a high-fat, olive-oil-rich diet, while holding constant PUFA and SFA (28). Another replaced about 10% of energy with either oleic acid or SFA in otherwise similar diets (30), and two separate studies compared diets rich in MUFA with PUFA, with dietary intake of total fat and SFA held constant (29,34). The effects of MUFA on blood pressure were not tested among hypertensive patients.
In an Italian study the dietary intervention consisted of a change from Mediterranean type diet to a high-fat, high-SFA diet. This dietary modification was obtained by substituting specific items of the habitual diet (olive oil, cereals, vegetables) with foods rich in SFA such as butter, dairy products, cheese, and meat. At the end of the 6-week intervention period systolic and diastolic blood pressure had increased significantly. After return to the customary diet a rapid decrease in blood pressure levels to preintervention values was observed (49). However, in this study there was again a multifactorial dietary intervention and not only an exchange of fatty acids.
A recent Spanish study with 20 healthy volunteers evaluated the effects of two high-fat, MUFA-rich diets (40% fat, 22% MUFA), one with virgin olive oil, the other with high-oleic sunflower oil, as compared with the National Cholesterol Education Program (NCEP) Step 1 diet (30% fat, 12% MUFA) (12). SFA content, dietary cholesterol, fibre, and minerals (sodium, potassium, calcium, magnesium) were kept constant throughout the trial. The MUFA diets which were followed for a 4-week period each led to a significant reduction in systolic (from 120 to 110 mmHg) and diastolic (from 73 to 66 mmHg) blood pressure. Both MUFA oils produced similar changes. Thus, the blood pressure lowering effect was likely to be due to the MUFA, and not to unsaponifiable materials mainly present in olive oil. This well-designed, strictly controlled study gives support that MUFA enrichment of an otherwise unchanged diet has a blood pressure lowering effect. The results indicate that there may be a direct and active influence of MUFA on blood pressure. However, they need confirmation by further studies as well as by investigation of the possible underlying mechanisms.
In summary, the question of the
relation between dietary fats and blood pressure has not yet been definitively
answered. Evidence suggests that Mediterranean diets with a high consumption of
olive oil, cereals, vegetables and fruits have favourable effects on blood
pressure. However, it still remains a matter of debate if the protective
influence is primarily caused by single nutrients, eg. dietary fatty acids,
potassium or dietary fibre, or if it can be attributed to the Mediterranean
diet as a whole. There is support for the latter hypothesis suggesting that the
combination of various favourable factors - low SFA content, high MUFA content,
high carbohydrate, fibre and micronutrient content, low salt intake - leads to
lower blood pressure values as compared to typical Western diets. Although the
effects of a single nutrient may be small, dietary MUFA content may play a more
important role in this protective effect than has been assumed in the
The prevalence of non-insulin-dependent diabetes mellitus (NIDDM) is very different throughout the world: it is particularly high in Western industrialised countries whereas it is low. Furthermore, the prevalence of NIDDM, and presumably the insulin resistance that invariably accompanies this disorder, has increased dramatically since World War II in all developed countries of the world. The association of increased incidence with economic affluence observed in international comparisons and studies of migrants have illustrated the significance of environmental factors in addition to a genetic disposition. Nutritional factors and the degree of habitual physical activity appear to be important determinants of this form of diabetes. Evidence suggests that the progression from glucose intolerance to diabetes can be prevented by dietary treatment and increased physical activity.
It is known people living in Mediterranean regions are at a particularly low risk developing the most common degenerative diseases of the industrialised populations. Therefore, the question arises whether or not the Mediterranean diet protects from diabetes. Unfortunately, information on the prevalence of diabetes in Mediterranean countries is rare, because there is a lack of properly designed studies. However, although no direct evidence exists which suggests that Mediterranean diet protects against the development of diabetes, there are clear indications from cross-cultural comparisons and studies on vegetarians that some of its most important characteristics - namely, the high intake of complex carbohydrate and dietary fibre and the low intake of SFA - may be beneficial in reducing the risk of diabetes.
The key importance of quantity and quality of dietary fat on the development of diabetes has been underlined in several recent studies. In the San Louis Valley Diabetes Study, fat consumption, adjusted for total energy intake, predicted the risk for NIDDM in individuals with impaired glucose tolerance (27). A high intake of animal fat and cholesterol was found in Japanese-American men with impaired glucose tolerance progressing to NIDDM (51). In the Nurses Health Study, on the other hand, a high, energy-adjusted intake of vegetable fat was associated with a low relative risk of developing diabetes (7). The metabolic mechanisms responsible for this associations have not been identified yet. Assumptions that a high-fat diet might adversely influence insulin-related glucose disposal, could not be confirmed in controlled studies. However, a high-fat diet clearly promotes weight gain and obesity which has been shown to be the dominating risk factor for the development of diabetes in genetically disposed individuals (for review see 19,54). The prevention of obesity is probably the most important measure for reducing the incidence of NIDDM.
Dietary measures are not only important in the prevention of diabetes, but are the cornerstone in the treatment of diabetes. There is no doubt that the basic measure must be a reduction in the intake of SFA. This recommendation is considered of paramount importance by all experts since diabetic patients are exceedingly prone to atherosclerosis. The current guidelines for the treatment of diabetes mellitus favour a diet with a relatively high proportion of carbohydrate-rich foods for most patients (1,11).
Although prospective studies seem to support this approach, controlled dietary treatment studies with diabetic individuals have shown controversial results. Some investigators found that a high-fat, MUFA-enriched diet with a low proportion of energy from SFA, was associated with better glycaemic control and reduced insulin requirements compared with a high carbohydrate diet (12,15,16,17). Furthermore, high-MUFA diets were advantageous because of their effect on lowering of plasma triglyceride and very low density lipoprotein (VLDL) concentrations whilst increasing HDL cholesterol and apo A-I levels (25,38). Although weight-reduction is usually facilitated with high-carbohydrate diets containing fibre-rich foods, high-MUFA diets may have some advantages over diets with a higher energy-density for overweight patients.
The results of these studies indicate that a normoenergetic high-MUFA diet can be consumed by NIDDM patients without negative effects on glucose and lipid metabolism. In addition it may even have some advantages compared to a very-low fat, high-carbohydrate diet, albeit not for all patients. With respect to carbohydrates, it should be emphasised that there are large differences in the effects on glucose metabolism depending on the type of carbohydrate. Patients should be generally advised to choose fibre-rich sources of complex carbohydrates in preference of refined sugars.
In summary, the type and amount of dietary fat influences the risk of developing obesity, insulin resistance and NIDDM. The most important measures for preventing diabetes are weight reduction in obese people, and the restriction of dietary fat, especially saturated fat (SFA), together with increased physical activity. For treatment of NIDDM a high-carbohydrate (fibre-rich) or a high-MUFA diet can be recommended. The choice between the two diets should be based on individual requirements and management goals.
The traditional Mediterranean diet
meets all the demands for an adequate diabetes diet. It has a low SFA content
and is rich in MUFA due to olive oil . With cereals and vegetables,
carbohydrates are mainly taken up as fibre-rich, complex carbohydrates. The
absolute fat content can easily be varied - depending on the individual needs -
by varying the amount of olive oil in the daily diet.
Overnutrition manifested by obesity has emerged as a major health problem in affluent countries. Although obesity is associated with many risk factors for diseases, the mechanisms whereby it enhances disease risk are not fully understood. However, it is generally agreed that overnutrition and obesity only induce disease states when they are combined with an inherent metabolic weakness or defect. In the absence of obesity such defects may well go unnoticed.
One of the most common consequences of obesity is dyslipidaemia, that is, elevations of very low-density lipoprotein (VLDL) triglycerides, low-density lipoprotein (LDL) cholesterol, and low concentrations of high-density (HDL) cholesterol. The two former effects can be explained by overproduction of VLDL, due to obesity, combined with a genetic defect in clearance of VLDL or LDL. The mechanism whereby obesity causes a lowering of HDL cholesterol is unclear (18).
Another disease associated with obesity is cholesterol gallstones. The presence of obesity more than doubles the risk for gallstones. Overnutrition promotes the synthesis of whole-body cholesterol, and the only way for excretion of this excess cholesterol is via the biliary tree. Thus, obesity leads to an increased output of cholesterol in the bile. When this reaction is combined with either a deficiency of bile acids or a propensity to crystal formation, the risk for gallstones is greatly increased (18).
Among patients with NIDDM a high incidence of obesity is well known. It appears that obesity is not the underlying cause of NIDDM, but when combined with a primary defect in insulin metabolism - (a progressive decline in the ability to secrete insulin by beta cells of pancreatic islets or a primary insulin resistance) - NIDDM develops (18).
Approximately 50% of patients with essential hypertension are obese. The mechanisms whereby obesity raises blood pressure are still uncertain. Since many obese patients do not have hypertension, there must be underlying defects in blood pressure control for hypertension to become manifest in obese individuals (18).
Finally, limited data suggest that overnutrition increases the risk for certain types of cancer, namely breast, colon, and prostate cancer. If so, it seemingly is a promoter of cancer development rather than a primary initiator. However, the present data are insufficient to conclude that obesity is definitely a risk factor for human cancer.
The role of obesity as an independent risk factor for cardiovascular morbidity and mortality is also a matter of debate up until now. On the other hand, there is no doubt that obesity strongly increases the cardiovascular risk through its detrimental effects on frequency and severity of the other described risk factors. The obesity-mediated risk is not only determined by the degree of obesity, but also by the body-fat distribution. It has been shown that especially abdominal (visceral) obesity is closely related to cardiovascular risk factors and coronary heart disease (4). Abdominal obesity seems to be associated with a cluster of risk factors, such as dyslipidaemia, NIDDM, and hypertension. This metabolic syndrome is closely linked to visceral fat mass and indicates a very high risk for coronary heart disease.
Obesity is a complex disease with multiple causes. Lifestyle, environment and genetics contribute to its manifestation. Although the pathophysiological mechanisms underlying obesity are not fully understood, it is proven that obesity results from an imbalance in energy intake and energy expenditure. There are many possible causes for this imbalance such as disturbed regulation of food intake, low basal metabolic rate, impaired thermogenesis, and low rates of fat oxidation (39). Numerous studies have shown that the diet of the majority of obese people is not unusually high in calories, but that the fat content is too high. Since dietary fats - in contrast to carbohydrates and protein - are rather stored than oxidised in the postprandial state, a high-fat diet regularly causes weight gain.
In industrialised countries energy-rich foods are easily available, ubiquitous, and, due to their palatability, are given high preference. The calorific foods are believed to be a major cause of obesity. These foods are low in complex carbohydrates and fibre, and rich in fat. The main sources in the diet of most Western countries are foods from animal origin with a high content of invisible fat. Furthermore, an increasing intake of snacks and sweets leads to a further increase in dietary fat as well as in simple carbohydrates. Consumption of vegetable foods rich in complex carbohydrates and fibre is very low.
Epidemiological data convincingly show that there is a strong inverse relationship between carbohydrate intake and relative body weight. Populations with a high carbohydrate intake in general have lower obesity rates as compared to countries with a high fat intake. Epidemiological studies dating from the beginning of the 1960s noted that the prevalence of overweight and obesity in Mediterranean countries was less than that of other industrialised nations. However, since 1960 both lifestyle and dietary habits have changed in most Mediterranean countries. They have moved from a diet based on cereals, vegetables, and olive oil towards a diet rich in animal products. Consequently, the incidence of obesity in Mediterranean countries is increasing (5).
Olive oil is a main component in the traditional Mediterranean diet. As well as other pure fats it has a high energy content and provides 9 kcal (38 kJ) per gram. And, theoretically, an excessive consumption of olive oil could therefore also lead to weight gain and obesity. But, in practice, the amount of olive oil in the usual Mediterranean diet is not large enough to cause obesity. Olive oil is the principle fat source in the diet: intake of animal fat is very low, and the diet contains abundant foods of plant origin. As a consequence, the diet has a high complex carbohydrate and fibre content. Such a diet is usually not hypercaloric, but has an energy content according to the individual energy need.
In summary, obesity is one of
the principal public health problems of affluent societies. It is a complex
disease with multiple causes. One of the major causes is a high fat content in
the habitual diet. In Western countries, consumption of fat, particularly fat
derived from animal food, is almost twice as high as the recommended amount,
while the carbohydrate content is too low. This is the most important
nutritional anomaly of the Western world leading to overnutrition and obesity.
A diet rich in complex carbohydrates and fibre, on the other hand, means a
protection against the development of obesity. The obvious implications are
that obesity could be prevented, or treated through use of a diet rich in grain
and vegetables such as the traditional Mediterranean diet.
The importance of factors influencing blood clotting and fibrinolysis in preventing coronary events is now well established. There is also evidence that platelet aggregation, plasma fibrinogen concentration and other haemostaseological factors may be influenced by diet. A high intake of saturated fatty acids is believed to increase the risk of arterial thrombosis. The role of unsaturated fatty acids in thrombogenesis still remains controversial (20,33,44).
Dietary supplementation with type n-3 (omega-3) polyunsaturated fatty acids has been shown to modify platelet function, as evidenced by a prolongation of the bleeding time, diminished platelet aggregation and secretion, and attenuated thromboxane production. These diet-related effects on platelets are considered to be beneficial for the prevention of cardiovascular disorders (20,33,44).
Results concerning the effects of n-6 (omega-6) polyunsaturated fatty acids on thrombosis are contradictory. There are some studies which reported a reduced platelet aggregation, while others found an increase (33). It seems that not only the absolute content of linoleic acid is of importance with regard to their thrombotic or antithrombotic effects, but also the content of other fatty acids, eg. the amount of saturated fatty acids and the ratio of n-6 to n-3 fatty acids.
There have been hardly any thorough evaluations of the influence of monounsaturated fatty acids on the coagulation system. The studies conducted so far do not give an indication either of a significant pro- or antithrombotic effect of MUFA. Thus, there is no scientific basis to encourage the consumption of olive oil for reducing the risk of thrombosis (44).
However, the majority of fatty acid
and thrombosis studies suggest that both a low-fat or a vegetable-fat diet are
preferable to a high-fat diet or a diet high in saturated fatty acids. In this
respect, the Mediterranean diet meets the requirements and is a recommendable
diet for the prevention of thrombosis.
Part B: Olive Oil and Coronary Heart Disease
The first hypothesis about a possible
relationship between the typical diet of a country and a low incidence of
coronary heart disease, including the intermediate role of low serum
cholesterol levels, was based on exploratory surveys conducted by Ancel Keys
and colleagues in the 1950s in Southern Italy, Spain and Greece. They reported
a rarity of cases of hospitalised myocardial infarction which was paralleled by
low mean levels of serum cholesterol. These observations were particularly
impressive when compared with similar data reported from the United States and
Finland, where higher levels of serum cholesterol corresponded to many cases of
myocardial infarction. Simultaneously, the Mediterranean populations showed a
dietary pattern different from that of North American and Northern European
These non-systematic observations became the basis for methodologically more valid approaches which led to the conduction of the Seven Countries Study. This study probably represents until nowadays the major investigation contributing to knowledge about the relationship between the Mediterranean diet and CHD.
The Seven Countries Study was conducted with almost 13,000 men, aged 40 to 59 years, and healthy at entry examination, enrolled in 15 population samples located in seven different countries (Italy, Greece, former Yugoslavia, the Netherlands, Finland, United States, and Japan) (22). Dietary data were collected at different time points. Serum lipids and other risk parameters were measured at baseline and at 5- and 10-year follow-up. The collection of data on mortality and death was continuous from the beginning.
CHD death rates were related to serum cholesterol, blood pressure, smoking habits, and mean age. The death rates, as well as the average diets differed among the cohorts. The major differences in food consumption between the Mediterranean areas and northern Europe and the United States were in the proportions of saturated fat and not necessarily in overall fat consumption. The polyunsaturated fat consumption had relatively minor relevance since the intercohort differences were limited. The monounsaturated fat consumption showed large differences among the cohorts.
15-year CHD death rates were related positively to average percentage of dietary energy from SFA, negatively to dietary energy percentage from MUFA, and were unrelated to dietary energy percentage from PUFA, proteins, carbohydrates, and alcohol. They were also negatively related to the ratio of monounsaturated to saturated fatty acids. All-cause and CHD death rates were low in cohorts with olive oil as the main fat and as the main source of MUFA (Greece, Italy, former Yugoslavia). The intake of SFA, on the other hand, was low, thus resulting in a high MUFA to SFA ratio. A relatively high MUFA intake was also observed in the US cohort, but there it was accompanied by a high SFA intake, a low MUFA/SFA ratio, and, as a consequence, high CHD mortality rates (22).
Among all cohorts from southern Europe, Crete showed the lowest mortality from CHD and all causes. More than other Mediterranean diets, the Cretan diet was, at least in the 1960s, rich in legumes, fruit, and edible fats that were mostly olive oil. The Cretan diet contained much less meat, but supplied moderate amounts of fish and alcohol, mostly in form of red wine (Table 2). The extremely low CHD mortality rates were particularly surprising, since the average serum cholesterol concentrations in the Cretan population were similar to those in the other Mediterranean cohorts.
Table 2: Seven Countries Study: Dietary intake and mortality rates in selected cohorts1
1 Adapted from
From the results of the Seven Countries Study, Keys (22) drew the main conclusion that the Mediterranean diet would be ideal for decreasing serum cholesterol concentrations, with most of the cholesterol-lowering effects attributed to both a low intake of saturated fats and to a relatively high intake of monounsaturated fatty acids, specifically oleic acid, which is supplied by olive oil. With regard to the results in Crete, however, it should be emphasised that besides the very important cholesterol-lowering effects due to its favourable fatty acid composition, the Mediterranean diet yields further cardioprotective effects because of the large amounts of cereals, legumes, vegetables, and fruit. These foods contain a variety of nutrients and non-nutrients (antioxidative vitamins and other antioxidants such as polyphenols1) that have been recently shown to play an important role in the prevention of CHD and other chronic diseases.
Since the 1960s, ongoing changes in eating habits have occurred in the Mediterranean region. In Italy, eg. food survey data demonstrate a pronounced increase in the consumption of animal foods (meat, milk, and dairy products), and of edible fats other than olive oil during the past 40 years. Consumption of sugar, fruits, and vegetables has also increased, whereas that of cereals has decreased slightly (14). Comparative changes have been observed in other Mediterranean countries. Increasing evidence suggests that these dietary changes have been accompanied by increases in several cardiovascular risk factors: higher concentrations of serum cholesterol, hypertension, and obesity. In turn, investigators have observed raising rates of CHD and diabetes in various Mediterranean countries (47). These trends confirm the well-established relations between diet and CHD risk and suggest the need to reverse current practices through widespread efforts to preserve and promote traditional diets within the Mediterranean area.
But despite the unfavourable changes in diet, particularly the observed increase in consumption of animal foods, the dietary profile of the Mediterranean countries has still maintained many of its basic features, and recent vital statistics still demonstrate an advantage of eating behaviour, associated with lower CHD mortality rates (Table 3) as compared to Western Europe and the United States (14).
Table 3. CHD mortality rates in Europe and the United States in the 1990s1.
1 non age-adjusted mortality rates per year per 100.000 persons; data from 1990, 1991 or 1992.
Source: Statistisches Jahrbuch
Although there is a large body of epidemiological evidence supporting the diet-heart-hypothesis, a causal relationship between CHD and the intake of saturated fatty acids or the level of serum cholesterol can only be established by randomised intervention trials. From the 1950s to the 1990s, many intervention trials have been targeted at reducing CHD incidence and mortality. Sometimes, changing a current diet has been used as a single tool for the preventive experiment (such as the Veterans Administration Study (8), the Finnish Mental Hospital Study (52)); sometimes it has been used in combination with other measures (such as the Multiple Risk Factor Intervention Trial (32), the North Karelia Project (37), the WHO European Multifactor Preventive Trial of CHD (56), the Oslo Preventive Trial (21)). In the latter case, it has not been easy to distinguish the role of diet (and of the subsequent cholesterol changes) from that of the other measures.
In most cases, the suggested or implemented changes in dietary habits were oriented towards a reduction in saturated fat, accompanied by an increase in polyunsaturated fat. None of the original Mediterranean diets were particularly rich in polyunsaturated fat. Also, none of the experimental diets were particularly rich in monounsaturated fat, typical of Mediterranean diets due to high consumption of olive oil. Thus, not a single trial including hard end-points has been conducted with the purpose of testing typical Mediterranean diets for the primary prevention of CHD. However, the positive results of saturated fat-reduction obtained in the majority of the trials mentioned above demonstrate the need to reduce the amount of saturated fat in the diet. Furthermore, other intervention studies with soft end-points, such as changes in blood lipids, support, at least indirectly, the benefit of a diet resembling that used in the 1950s and 1960s in the Mediterranean region (for review see 10). Besides, there is much evidence from numerous controlled dietary studies that MUFA-rich diets efficiently lower serum total and LDL cholesterol without changing HDL cholesterol levels2.
In summary, in all dietary intervention studies the cholesterol-lowering effects have been shown to be lower than expected. Metabolic ward studies have shown the high efficacy of a cholesterol-lowering diet3. However, dietary intake can be maximally controlled and confounding variables, such as changes in body weight and physical activity, are removed. Several requirements must be met before generalisation of the results from metabolic ward studies to free-living populations can be made - the most important is compliance to the dietary regimen. In general, the more intensive the dietary counselling, the greater the compliance. The greater the compliance, the more likely will the results achieved in outpatients approximate the results observed in the metabolic ward setting.
It is well established that a
reduction in the cholesterol level will lead to a reduction in morbidity and
mortality from CHD4. Most of the
studies conducted to test this hypothesis have indeed demonstrated a reduction
in the incidence of ischaemic cardiac events, and some have also shown a
reduction in mortality from cardiovascular disease (26). In addition, there is also evidence that an
intensive lipid-lowering therapy in men with moderate hypercholesterolaemia and
no history of myocardial infarction reduces the incidence of myocardial
infarction and CHD mortality without adversely affecting the risk of death from
noncardiovascular causes (46).
All these findings convincingly
underline the importance of diet in the prevention of CHD. Statements have been
made by different national and international bodies and organisations that
recommend preventive diets that are similar to the traditional Mediterranean
diet (13,35). The
intake of total fat should be reduced to 30% of energy, SFA intake below 10%.
The intake of PUFA should not be more than 10% of energy (7-10%), whereas the
remaining fat proportion should be provided by MUFA (10-15% of energy). Dietary
cholesterol content should be below 300 mg/day. Furthermore, the intake of
complex carbohydrates and dietary fibre should be increased. The Mediterranean
diet provides an excellent example how these guidelines could be converted into
a tasty and appetising diet. It contains an abundance of plant foods such as
bread and grain products, vegetables, legumes, and fruit. The amounts of animal
products are only low to moderate. Olive oil is the principle source of fat.
This diet is low in SFA, rich in carbohydrate and fibre, and has a high MUFA
content. The MUFA are primarily derived from olive oil5.
In patients with established CHD the European Atherosclerosis Society as well as the National Cholesterol Education Program have recommended more aggressive cholesterol-lowering measures because these individuals are at the highest risk of a CHD event. Several large trials have evaluated the efficacy of cholesterol reduction in secondary prevention of cardiovascular events. Secondary prevention trials are more likely to include subjects who are highly motivated to comply with dietary modifications, thus reducing the problems of nonadherence to diet that is observed in unselected populations or even in high-risk individuals without CHD. The majority of dietary intervention studies achieved at least a 10% reduction in cholesterol levels (2,24,36,55).
With one exception (6), the dietary trials support the role for aggressive dietary therapy in the secondary prevention of CHD. However, despite intensive dietary measures, the reduction in cholesterol concentrations frequently is insufficient. In these cases, an additional drug therapy is necessary to achieve the desired very low cholesterol levels. Impressive examples for the efficacy of intensive lipid-lowering measures are the Scandinavian Simvastatin Survival Study (4S) (45) and the CARE Study (43). They both documented that the significant reduction in total and LDL cholesterol due to a therapy with diet and drugs (HMG-CoA-reductase inhibitor) was associated with a highly significant reduction in non fatal myocardial infarction and CHD mortality in patients after myocardial infarction or CHD.
Until now, only one study has been conducted to investigate the particular effects of a Mediterranean type diet for secondary prevention of CHD (9,40). In the Lyon Diet Heart Study a Mediterranean diet resembling that of Crete in the 1960s was compared to the prudent diet usually recommended in France in 605 patients recovering from myocardial infarction. The experimental group received more bread, more root vegetables and green vegetables, more fish, less meat (beef, lamb and pork to be replaced with poultry), no day without fruit, and butter and cream were replaced with a special, rapeseed oil-based margarine. The oils recommended for salads and food preparation were rapeseed and olive oils exclusively whereas sunflower oil was consumed in the control group. Moderate alcohol consumption in the form of wine was allowed at meals. In terms of nutrients the experimental groups showed a lower intake of SFA, cholesterol, and linoleic acid, but a higher intake of oleic acid, -linolenic acid, and vitamin C as compared to the control group.
Throughout the follow-up period, serum total, LDL, and HDL cholesterol, serum triglycerides, body weight, and blood pressure were similar in both groups. After a mean follow-up period of 27 months, there were 16 cardiac deaths in the control and 3 in the experimental group; 17 non-fatal myocardial infarction in the control and 5 in the experimental group. Overall mortality was 20 in the control and 8 in the experimental group.
The protective effects of the Mediterranean diet which were caused by several factors were largely independent of serum lipids and blood pressure since these risk factors did not differ between the groups. The Mediterranean diet contained a larger proportion of -linolenic acid (18:3n-3) which was provided to a large extent by the rapeseed oil and the rapeseed oil-based margarine. As described above (see olive oil and thrombogenic risk factors) n-3 fatty acids have been shown to have favourable effects on bleeding time and platelet aggregation, thus reducing the risk of thrombosis. Furthermore, the intake of oleic acid was higher in the experimental than in the control group due to the intake of olive and rapeseed oils. The control group consumed sunflower oil, and therefore had a higher intake of linoleic acid. Because the cholesterol-lowering effects of both fatty acids were similar in this study, one can suggest that the high oleic acid content has yielded beneficial effects by reducing the oxidation of LDL-cholesterol which is assumed to play an important role in the pathogenesis of atherosclerosis6 . In addition, the increase in natural antioxidants also probably played a protective role by further reducing the susceptibility to lipid peroxidation.
In conclusion, the Lyon Diet Heart
Study constitutes the first demonstration that the Cretan Mediterranean diet,
even when adapted to a Western population, protects against CHD much more
efficiently than a prudent diet, rich in linoleic acid. The specific factors
that contribute to the protective effects of this diet need further
examination, but the low intake of SFA, the high concentrations of oleic acid,
a ratio of 18:3n-3 to 18:2n-6 fatty acids of 1:5, and the high content of
natural antioxidants seem to be the most reasonable candidates.
The Seven Countries Study gave the best scientific proof for the association between a diet low in animal products and saturated fat and low mean population levels of serum cholesterol with low incidence and mortality from CHD. It also documented a negative correlation between the intake of monounsaturated fat and the MUFA to SFA ratio on the one hand and CHD on the other hand. All-cause and CHD death rates were low in cohorts with the MUFA-rich olive oil as the main fat, underlining the favourable role of olive oil. There is a body of indirect evidence from interventional studies that the traditional Mediterranean diet with its abundance in plant foods, preferential and regular intake of olive oil, and low to moderate consumption of animal foods efficiently protects against CHD.
Recent findings indicate that olive
oil and the Mediterranean diet yield their benefits not only through their
effects on established CHD risk factors such as hyperlipidaemia, hypertension,
diabetes, and obesity, but also through directly protective effects,
particularly their antioxidative properties. In addition, it has been
documented that a Mediterranean diet adapted from the Cretan diet is efficient
in the secondary prevention of coronary events and death.
1. The whole topic of
antioxidants will be dealt with in detail in a further fact sheet.