Within Europe large differences exist in mortality from coronary heart disease and stroke. These diseases show a clear West-East gradient with high rates in Eastern Europe. In spite the decreasing trend in age-adjusted cardiovascular disease mortality in Western European countries an increase in the number of cardiovascular patients is expected because of the ageing of the population. Consequently the health care cost for these diseases will increase.

Total and HDL cholesterol are major determinants of coronary heart disease. Saturated and trans fatty acids have a total and LDL cholesterol elevating effect and unsaturated fatty acids a lowering effect. N-3 polyunsaturated fatty acids seem to have a protective effect on coronary heart disease occurrence independent of their effect on cholesterol.

Dietary antioxidants could be of importance because they may prevent oxidation of the atherogenic cholesterol rich LDL lipoproteins. There is however no convincing evidence that either vitamin E, carotenoids or vitamin C protect against coronary heart disease. Observational research has shown that flavonols, polyphenols with strong antioxidant properties present in plant foods, may protect against coronary heart disease.

Blood pressure is a major determinant of coronary heart disease and stroke. Historically salt is viewed as the most important dietary determinant of blood pressure. Recent research shows that also a low-fat diet rich in potassium, calcium and magnesium lowers blood pressure substantially. This suggests a multifactorial influence of different nutrients on blood pressure.

It can be concluded that a diet low in saturated and trans fatty acids and rich in plant foods in combination with regular fish consumption is associated with a low risk of cardiovascular mortality.

For decades it has been postulated that the main environmental factor for coronary heart disease (CHD) was the intake of saturated fatty acids (SFA). Nevertheless, confirmation of the role of SFA in CHD through intervention trials has been disappointing. It was only when the diet was enriched in n-3 fatty acids that CHD was significantly prevented, especially cardiac death.

In addition to n-3 fatty acids, many other foodstuffs or nutrients such as fibers, antioxidants, folic acid, calcium and even alcohol contribute to prevent CHD. Thus the relationship between diet and CHD morbidity and mortality appears to be much more complex than formerly suspected considering as key factors only SFA, linoleic acid, cholesterol and atherosclerosis. Some of the mechanisms are briefly described, but many additional nutrients (or non nutrients) may also play an important role in the pathogenesis of CHD.

Finally, as a result of the most recent epidemiologic studies the ideal diet may comprise: 8% energy from SFA, 5% from polyunsaturated fatty acids with a ratio 5/1 of linoleic/alpha-linolenic acid+longer chains n-3, oleic acid as desired, large intake of cereals, vegetables, legumes and fruits, fish twice a week, cheese and yogurt as dairy products, rapeseed and olive oils as edible fat. Without side effects, such a diet can be highly palatable, easily enjoyed by many populations and may prevent effectively and rapidly (within a few weeks or months) CHD.

Over the past 20 years, a large number of epidemiological studies, particularly case-control and cohort studies, have been conducted to investigate the role of diet and the risk of developing different types of cancer. The most consistent finding so far is the association observed between consumption of vegetables and fruit and reduced risk of cancers of the digestive and respiratory tracts. More recently, evidence has accumulated indicating that high consumption of red meat (mainly beef, lamp and pork) and of preserved meat (‘charcuterie’) is specifically associated with a modest but significant increase in colorectal cancer risk. Finally, there is epidemiological evidence supporting an association between the risk of developing gastric cancer and the intake of salt and-preserved foods.

Cancer incidence and dietary habits vary substantially across Europe, and the expected benefit of dietary changes may be somewhat difference in different populations. Despite some uncertainly, it is generally agreed that an increase in the consumption of vegetables and fruits and a decrease in the intake of red meat, processed meat, alcoholic beverages, salt and salt-preserved foods should contribute to a reduction in the incidence of cancers of the digestive and respiratory tract.

At least six types of gene–environment interactions (GEI) have been proposed (Kouhry and Wagener, 1993) In the first type, neither the environmental exposure (EE) nor the genetic risk factor (GRF) have any effect by themselves, but interaction between them causes disease. This is the case of phenylalanine exposure and the phenylketonuria genotype. Type 2 is a situation in which the GRF has no effect on disease in the absence of exposure, but exacerbates the effects of the latter. This is the most important type of GEI in relation to metabolic susceptibility genes and human carcinogenesis. The third type is the converse of the second (EE is ineffective per se, but enhances the effect of GRF). Type 4 occurs when both EE and GRF increase the risk for disease, but the combination is interactive or synergistic: an example is the interaction between Xeroderma Pigmentosum and UV radiation. Types 5 and 6, according to the classification proposed by Kouhry, refer to cases in which the GRF is protective.

The model of GEI that is emerging as the most important in chemical carcinogenesis refers to metabolic susceptibility genes. The general population can be divided into subgroups depending on their susceptibility to the action of carcinogens, based on their ability to metabolize such compounds to electrophilic, reactive metabolites (which form adducts with DNA), or, respectively, electrophobic metabolites that are excreted. The present contribution is a short review of the relevant literature, with particular emphasis on some polymorphisms involved in dietary exposures. In addition, the practical implications of genetic testing in this field are discussed.

Homocysteine is an emerging new risk factor for cardiovascular disease. It is a thiol compound derived from methionine and involved in two main metabolic pathways: the cycle of activated methyl groups, requiring folate and vitamin B12 as cofactors, and the transsulfuration pathway to cystathionine and cysteine requiring vitamin B6 as cofactor. The homocysteine metabolism represents an interesting model of gene-environment interaction. Elevations in homocysteine may be caused by genetic defects in enzymes involved in its metabolism or by deficiencies in cofactor levels. A common polymorphism in the gene coding for the 5, 10-methylene tetrahydrofolate reductase (MTHFR) (C677T, Ala → Val) is associated with a decreased activity of the enzyme due to thermolability. In case of homozygosity for the Val allele, a relative deficiency in the remethylation process of homocysteine into methionine leads to a mild-to-moderate hyperhomocysteinemia, a condition recognized as an independent risk factor for atherosclerosis. The genetic influence of the MTHFR polymorphism on homocysteine levels is attenuated in females in premenopausal age and is not significant in subjects who exhibit serum levels of folate and/or vitamin B12 above the 50th percentile of distribution in the general population. The prevalence of the Val/Val genotype varies among different ethnic groups. It is very low in African populations, whereas in Europe and North America it ranges between 5% and 15%. In Italy an even higher prevalence has been reported in some regions. The question whether the MTHFR polymorphism might be per se an independent contributor to cardiovascular risk is debated. The interaction between this or other genetic factors and environmental/nutritional conditions (i.e. intake of vitamins such as folate) is a key determinant for homocysteine concentrations in healthy conditions as well as in some disease (i.e. in renal disorders). Another example of gene/environment interaction in the field of atherosclerosis is given by the apolipoprotein E polymorphism and its influence in response to diet. The presence of a high prevalence of risk-related allelic variants of such candidate genes within a certain population could serve to locally reinforce the recommendations concerning nutrient intake.

The prevalence of obesity is increasing rapidly in all age groups in most EU-countries and is one of the fastest growing epidemics, now affecting 10–40% of the adult population. Obesity increases the risk of serious co-morbidities such as type 2 diabetes, cardiovascular disease, certain cancers and reduced life expectancy, and these complications may account for 5–10% of all health costs in EU countries. The risk of diabetes is particularly increased by obesity, and 80–95% of the increase in diabetes can be attributed to obesity and overweight with abdominal fat distribution. There is robust evidence from cross-sectional and longitudinal studies to support that an energy-dense, high fat diet and physical inactivity are independent risk factors for weight gain and obesity. Furthermore, interaction between dietary fat and physical fitness determine fat balance, so that the obesity promoting effect of a high fat diet is enhanced in susceptible subjects, particularly in sedentary individuals with a genetic predisposition to obesity.

Ad libitum consumption of diets low in fat and high in protein and complex carbohydrates, with a low glycaemic index, contributes to the prevention of weight gain in normal weight subjects. It also causes a spontaneous weight loss of 3–4 kg in overweight subjects, and has beneficial effects on risk factors for diabetes and CVD. To prevent obesity and diabetes there are grounds for recommending the combination of increasing daily physical activity level to a PAL-value of at least 1.8 and reducing dietary fat content to 20–25 energy-% in sedentary subjects, and to 25–35% in more physically active individuals.

Regular physical activity causes numerous and substantial performance-improving And health-enhancing effects. Most of them are highly predictable, dose-dependent and generalizable to a wide range of population groups. Many of the biological effects of regular, moderate physical activity translate into substantially reduced risk of coronary heart disease, cerebrovascular disease, hypertension, maturity onset diabetes, overweight and obesity, and osteoporosis. These effects also substantially reduce the risk of deterioration of functional capacity. In the genesis of these conditions, alack of physical activity and inadequate nutrition act synergistically and in part additively, and they operate largely through the same pathways. It is conceivable to suggest that the prevalence of, e.g, the above mentioned metabolic diseases is so high in Europe largely because of the high prevalence of sedentariness and inadequate nutrition. Thus, both physical activity and nutrition have to be given strong emphasis in policies, strategies and programmes that will be developed and implemented for improving the health of Europeans.

Iodine deficiency disorders (IDD) are related to the degree of iodine deficiency. In european countries, characterized by mild to moderate iodine deficiency, neurological deficits or minor neuropsychological impairments have been described. Urinary iodine excretion (UIE) ranged from 30 to 170 mcg/L, 141 millions of people were at risk of IDD, 97 millions were affected by goiter and 0.9 millions had an impaired mental development.

Iodine prophylaxis is devoid of adverse reactions with the exception of sporadic cases of transitory hyperthyroidism, associated to the severity of iodine deficiency before the prophylaxis. The International Council for Control of IDD recommends an universal iodine prophylaxis, instituted gradually in severe iodine deficient countries. The total cost of universal iodine prophylaxis is very cheap compared to the social cost of goiter and cretinism.

In conclusion, most european countries are still characterized by mild to moderate iodine deficiency. Iodine prophylaxis programs are already operating, its cost is irrelevant with respect to the undebatable beneficial impact on the health. Adverse effects are not observed except in severe iodine deficient areas where iodine intake was abruptly increased.

In Europe, iron deficiency is considered to be one of the main nutritional deficiency disorders affecting large fractions of the population, particularly such physiological groups as children, menstruating women and pregnant women. Some factors such as type of contraception in women, blood donation or minor pathological blood loss (haemorrhoids, gynaecological bleeding,..) considerably increase the difficulty of covering iron needs. Moreover, women, especially adolescents consuming lowenergy diets, vegetarians and vegans are at high risk of iron deficiency.

Although there is no evidence that an anbsence of iron stores has any adverse consequences, it does indicate that iron nutrition is borderline, since any further reduction in body iron is associated with a decrease in the level of functional compounds such as haemoglobin.

The prevalence of iron-deficient anaemia has slightly decreased in infants and menstruating women. Some positive factors may have contributed to reducing the prevalence of iron-deficiency anaemia in some groups of population: the use of iron-frotified formulas and iron-fortified cereals; the use of oral contraceptives and increased enrichment of iron in several countries; and the use of iron supplements during pregnancy in some European countries.

It is possible to prevent and control iron deficiency by counseling individuals and families about sound iron nutrition during infancy and beyond, and about iron supplementation during pregnancy, by screening persons on the basis of their risk for iron deficiency, and by treating and following up persons with presumptive iron deficiency. This may help to reduce manifestations of iron deficiency and thus improve public health. Evidence linking iron status with risk of cardiovascular disease or cancer is unconvincing and does not justify changes in food fortification or medical practice, particularly because the benefits of assuring adequate iron intake during growth and development are well established. But stronger evidence is needed before rejecting the hypothesis that greater iron stores increase the incidence of CVD or cancer. At present, currently available data do not support radical changes in dietary recommendations. They include all means for increasing the content of dietary factors enhancing iron absorption or reducing the content of factors inhibiting iron absorption. Increased knowledge and increased information about factors may be important tools in the prevention of iron deficiency in Europe.

Osteoporosis, a systemic skeletal disease characterized by a low bone mass, is a major public health problem in EC member states because of the high incidence of fragility fractures, especially hip and vertebral fracture. In EC member states the high incidence of osteoporotic fractures leads to considerable mortality, morbidity, reduced mobility and decreased quality of life. In 1995 the number of hip fractures in 15 countries of EC has been 382.000 and the estimated total care cost of about 9 billion of ECUs. Given the magnitude of the problem public health measures are important for preventive intervention.

Skeletal bone mass is determined by a combination of endogenous (genetic, hormonal) and exogenous (nutritional, physical activity) factors. Nutrition plays an important role in bone health. The two nutrients essential for bone health are calcium and vitamin D. Reduced supplies of calcium are associated with a reduced bone mass and osteoporosis, whereas a chronic and severe vitamin D deficiency leads to osteomalacia, a metabolic bone disease characterized by a decreased mineralization of bone. Vitamin D insufficiency, the preclinical phase of vitamin D deficiency, is most commonly found in the elderly. The major causes of vitamin D deficiency and insufficiency are decreased renal hydroxylation of vitamin D, poor nutrition, scarce exposition to sunlight and a decline in the synthesis of vitamin D in the skin.

The daily average calcium intake in Europe has been evaluated in the SENECA study concerning the diet of elderly people from 19 towns of 10 European countries. In about one third of subjects the dietary calcium intake results were very low, between 300 and 600 mg/day in women, and 350 and 700 mg/day in men. Calcium supplements reduce the rate of bone loss in osteoporotic patients. Some recent studies have reported a significant positive effect of calcium treatment not only on bone mass but also on fracture incidence. The SENECA study, has also shown that vitamin D insufficiency is frequent in elderly populations in Europe. There are a number of studies on the effects of vitamin D supplementation on bone loss in the elderly, showing that supplementations with daily doses of 400–800 IU of vitamin D, given alone or in combination with calcium, are able to reverse vitamin D insufficiency, to prevent bone loss and to improve bone density in the elderly.

In recent years, there has been much uncertainty about the intake of calcium for various ages and physiological states. In 1998, the expert committee of the European Community in the Report on Osteoporosis-Action on prevention, has given the recommended daily dietary allowances (RDA) for calcium at all stage of life. For the elderly population, above age 65 the RDA is 700–800 mg/day. The main source of calcium in the diet are dairy products (milk, yoghurts and cheese) fish (sardines with bones), few vegetables and fruits. The optimal way to achieve adequate calcium intake is through the diet. However, when dietary sources are scarce or not well tolerated, calcium supplementation may be used. Calcium is generally well tolerated and reports of significant side-effects are rare.

Adequate sunlight exposure may prevent and cure vitamin D insufficiency. However, the sunlight exposure or the ultraviolet irradiation are limited by concern about skin cancer and skin disease. The most rational approach to reducing vitamin D insufficiency is supplementation. In Europe, the RDA is 400–800 IU (10–20 μg) daily for people aged 65 years or over. This dose is safe and free of side effects.

In conclusion, in Europe a low calcium intake and a suboptimal vitamin D status are very common in the elderly. Evidence supports routine supplementation for these people at risk of osteoporosis, by providing a daily intake of 700–800 mg of calcium and 400–800 IU of vitamin D. This is an effective, safe and cheap means of preventing osteoporotic fractures.

Dental caries is a highly prevalent chronic disease and its consequences cause a lot of pain and suffering. Sugars, particularly sucrose, are the most important dietary aetiological cause of caries. Both the frequency of consumption and total amount of sugars is important in the aetiology of caries. ‘The evidence establishing sugars as an aetiological factor in dental caries is overwhelming. The foundation of this lies in thenmultiplicity of studies rather than the power of any one.’1. That statement by the British Nutrition Foundation's Task Force on Oral Health, Diet and Other Factors, sums up the relationship between sugars and caries in Europe. There is no evidence that sugars naturally incorporated in the cellular structure of foods (intrinsic sugars) or lactose in milk or milk products (milk sugars) have adverse effects on health. Foods rich in starch, without the addition of sugars, play a small role in coronal dental caries.

The intake of extrinsic sugars beyond four times a day leads to an increase risk of dental caries. The current dose-response relationship between caries and extrinsic sugars suggests that the sugars levels above 60 g/person/day for teenagers and adults increases the rate of caries. For pre-school and young children the intakes should be proportional to those for teenagers; about 30 g/person/day for pre-school children.

Fluoride, particularly in toothpastes, is a very important preventive agent against dental caries. Toothbrushing without fluorides has little effect on caries. As additional fluoride to that currently available in toothpaste does not appear to be benefiting the teeth of the majority of people, the main strategy to further reduce the levels of caries, is reducing the frequency of sugars intakes in the diet.

Dental erosion rates are considered to be increasing. The aetiology is acids in foodsand drinks and to a much lesser extent from regurgitation.

Selenium is of fundamental importance to human health. It is an essential component of several major metabolic pathways, including thyroid hormone metabolism, antioxidant defence systems, and immune function. The decline in blood selenium concentration in the UK and other European Union countries has therefore several potential public health implications, particularly in relation to the chronic disease prevalence of the Western world such as cancer and cardiovascular disease. Ten years have elapsed since recommended dietary intakes of selenium were introduced on the basis of blood glutathione peroxidase activity. Since then 30 new selenoproteins have been identified, of which 15 have been purified to allow characterisation of their biological function. The long term health implications in relation to declining selenium intakes have not yet been thoroughly examined, yet the implicit importance of selenium to human health is recognised universally.

Selenium is incorporated as selenocysteine at the active site of a wide range of selenoproteins. The four glutathione peroxidase enzymes (classical GP×1, gastrointestinal GP×2, plasma GP×3, phospholipid hydroperoxide GP×4)) which represent a major class of functionally important selenoproteins, were the first to be characterised.

Thioredoxin reductase (TR) is a recently identified seleno-cysteine containing enzyme which catalyzes the NADPH dependent reduction of thioredoxin and therefore plays a regulatory role in its metabolic activity.

Approximately 60% of Se in plasma is incorporated in selenoprotein P which contains 10 Se atoms per molecule as selenocysteine, and may serve as a transport protein for Se. However, selenoprotein-P is also expressed in many tissues which suggests that although it may facilitate whole body Se distribution, this may not be its sole function.

A second major class of selenoproteins are the iodothyronine deiodinase enzymes which catalyse the 5′5-mono-deiodination of the prohormone thyroxine (T4) to the active thyroid hormone 3,3′5-triiodothyronine (T3).

Sperm capsule selenoprotein is localised in the mid-peice portion of spermatozoa where it stabilises the integrity of the sperm flagella.

Se intake effects tissue concentrations of selenoprotein W which is reported to be necessary for muscle metabolism.

It is of great concern that the health implications of the decline in Se status in the UK over the past two decades have not been systematically investigated. It is well recognised that dietary selenium is important for a healthy immune response. There is also evidence that Se has a protective effect against some forms of cancer; that it may enhance male fertility; decrease cardiovascular disease mortality, and regulate the inflammatory mediators in asthma. The potential influence of Se on these chronic diseases within the European population are important considerations when assessing Se requirement.

Research in the past decade has established that low or inadequate folate status may contribute to congenital malformations and the development of chronic disease in later life. Using an evidence based approach, there are clear guidelines for recommending folic acid supplementation or fortification in certain disease conditions but further proof of its efficacy is required in other circumstances.

There is conclusive evidence that maternal periconceptional supplementation with folic acid prevents the majority of NTDs, probably by overcoming one or more genetically inherited metabolic blocks in folate dependent enzymes. Public health efforts to advise women to increase their folate intake have not been successful. As a result, the U.S. government passed legislation to have all flour fortified with folic acid. This intervention has had a dramatic effect on folate status in the U.S. To date, countries of the EU have not adopted mandatory fortification policies.

The amino acid homocysteine is an essential intermediate in folate metabolism. Substantial evidence indicates that elevated plasma homocysteine is an independent risk factor for heart disease and stroke. Plasma homocysteine levels can be reduced by folic acid supplements. A food fortification policy would probably be an effective population strategy to reduce plasma homocysteine. However, many experts believe that this would be premature without first showing that such reduction would cause a decrease in the prevalence of cardiovascular disease.

The contribution of folate to cancer risk is not well defined although there is reasonable evidence to implicate low folate status in the specific case of colorectal cancer. In particular, long-term folic acid supplementation may reduce risk of colorectal cancer substantially.

Various mental disorders including Alzheimer's Disease have been associated with low folate status or elevated plasma homocysteine. While it is hard to determine if this is cause or effect, there is little doubt that if it were true then low dose folic acid intervention would be highly effective.

Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of ‘programming’, whereby a stimulus or insult at a critical, sensitive period of early life has permanent effects on structure, physiology and metabolism. Programming of the fetus may result from adaptations invoked when the materno-placental nutrient supply fails to match the fetal nutrient demand. Although the influences that impair fetal development and programme adult cardiovascular disease remain to be defined, there are strong pointers to the importance of maternal body composition and dietary balance during pregnancy.

In a successful pregnancy maternal health is maintained, a healthy baby is delivered and the mother is able to nurture her newborn adequately. Despite continued interest in the role and importance of maternal diet in this process, we do not have a clear understanding of how the nutritional status of the mother influences fetal growth and development. Recent epidemiological evidence of an association between poor fetal growth and adult disease highlights the need to reconsider the influences which act on the fetus, and the role maternal nutrition may play.

Nutrient needs are increased in pregnancy. For the mother to be solely dependent upon her dietary intake to meet these demands, would represent a very high risk strategy. Hence adequate reserves are important for a successful outcome. Whilst there are numerous observational studies of diet during pregnancy, there are only limited data from well-controlled, randomised supplementation studies. A recent systematic review showed only dietary supplements balanced in energy and protein content to result consistently in improved fetal growth. There is no strong evidence that nutrient supplements confer benefit in women without overt deficiency.

To interpret future dietary studies in pregnancy we need to consider metabolic differences between women which may influence their ability to meet fetal nutrient demand, to allow for nutrient–nutrient interactions, and to take account of differences in timing in gestation. Consideration of these factors in studies of pregnancy, will lead to a clearer understanding of the links between maternal diet and fetal growth and development. Until we have this understanding, it is reasonable to expect that women entering pregnancy are provided with a diet which is adequate, based upon our normal understanding of requirements, and it is not acceptable for women to be expected to carry a pregnancy with an obvious or overt nutritional deficiency.

Recommendations suggest exclusive breastfeeding for at least the first 4 to 6 months after birth. Paradoxically, an overwhelming proportion of breastfeeding (BF) data in Europe refers to all BF, i.e. not only exclusive but also partial BF (including formula, juices, water, sweetened water etc). This makes it difficult to estimate to what extent the recommendations are met. There is currently strong evidence for recommending exclusive breastfeeding for at least 6 months.

Exclusive BF has progressively gained scientific support. Prevention of infections, allergies and chronic diseases and a favourable cognitive development are highlighted in the recent scientific literature. Further long-term studies on the effects of BF on prevention of chronic disease in the adult are needed.

Great differences exist in BF prevalence and duration both within and between European countries. Trends point towards higher prevalence and duration, with some exceptions. Young mothers breastfeed less than older mothers; single and/or less educated mothers breastfeed less than married mothers with more education. However, inefficient and unreliable monitoring systems prevail, and the data are scarce, not only on exclusive BF but also on demographic, socio-economic, psychosocial and medical determinants of BF patterns. National BF co-ordinators have not been appointed in many countries, and only every second country has promotion of BF incorporated into their national plan of action for nutrition.