To briefly review the current understanding of the aetiology and prevention of chronic diseases using a life course approach, demonstrating the life-long influences on the development of disease.

A computer search of the relevant literature was done using Medline-‘life cycle’ and ‘nutrition’ and reviewing the articles for relevance in addressing the above objective. Articles from references dated before 1990 were followed up separately. A subsequent search using Clio updated the search and extended it by using ‘life cycle’, ‘nutrition’ and ‘noncommunicable disease’ (NCD), and ‘life course’. Several published and unpublished WHO reports were key in developing the background and arguments.

International and national public health and nutrition policy development in light of the global epidemic in chronic diseases, and the continuing nutrition, demographic and epidemiological transitions happening in an increasingly globalized world.

There is a global epidemic of increasing obesity, diabetes and other chronic NCDs, especially in developing and transitional economies, and in the less affluent within these, and in the developed countries. At the same time, there has been an increase in communities and households that have coincident under- and over-nutrition.

The epidemic will continue to increase and is due to a lifetime of exposures and influences. Genetic predisposition plays an unspecified role, and with programming during fetal life for adult disease contributing to an unknown degree. A global rise in obesity levels is contributing to a particular epidemic of type 2 diabetes as well as other NCDs. Prevention will be the most cost-effective and feasible approach for many countries and should involve three mutually reinforcing strategies throughout life, starting in the antenatal period.

To review the evidence on the diet and nutrition causes of obesity and to recommend strategies to reduce obesity prevalence.

The evidence for potential aetiological factors and strategies to reduce obesity prevalence was reviewed, and recommendations for public health action, population nutrition goals and further research were made.

Protective factors against obesity were considered to be: regular physical activity (convincing); a high intake of dietary non-starch polysaccharides (NSP)/fibre (convincing); supportive home and school environments for children (probable); and breastfeeding (probable). Risk factors for obesity were considered to be sedentary lifestyles (convincing); a high intake of energy-dense, micronutrient-poor foods (convincing); heavy marketing of energy-dense foods and fast food outlets (probable); sugar-sweetened soft drinks and fruit juices (probable); adverse social and economic conditions—developed countries, especially in women (probable).

A broad range of strategies were recommended to reduce obesity prevalence including: influencing the food supply to make healthy choices easier; reducing the marketing of energy dense foods and beverages to children; influencing urban environments and transport systems to promote physical activity; developing community-wide programmes in multiple settings; increased communications about healthy eating and physical activity; and improved health services to promote breastfeeding and manage currently overweight or obese people.

The increasing prevalence of obesity is a major health threat in both low- and high income countries. Comprehensive programmes will be needed to turn the epidemic around.

The overall objective of this study was to evaluate and provide evidence and recommendations on current published literature about diet and lifestyle in the prevention of type 2 diabetes.

Epidemiological and experimental studies, focusing on nutritional intervention in the prevention of type 2 diabetes are used to make disease-specific recommendations. Long-term cohort studies are given the most weight as to strength of evidence available.

Numerous clinical trials and cohort studies in low, middle and high income countries are evaluated regarding recommendations for dietary prevention of type 2 diabetes. These include, among others, the Finnish Diabetes Prevention Study, US Diabetes Prevention Program, Da Qing Study; Pima Indian Study; Iowa Women's Health Study; and the study of the US Male Physicians.

There is convincing evidence for a decreased risk of diabetes in adults who are physically active and maintain a normal body mass index (BMI) throughout adulthood, and in overweight adults with impaired glucose tolerance who lose weight voluntarily. An increased risk for developing type 2 diabetes is associated with overweight and obesity; abdominal obesity; physical inactivity; and maternal diabetes. It is probable that a high intake of saturated fats and intrauterine growth retardation also contribute to an increased risk, while non-starch polysaccharides are likely to be associated with a decreased risk. From existing evidence it is also possible that omega-3 fatty acids, low glycaemic index foods and exclusive breastfeeding may play a protective role, and that total fat intake and trans fatty acids may contribute to the risk. However, insufficient evidence is currently available to provide convincing proof.

Based on the strength of available evidence regarding diet and lifestyle in the prevention of type 2 diabetes, it is recommended that a normal weight status in the lower BMI range (BMI 21–23) and regular physical activity be maintained throughout adulthood; abdominal obesity be prevented; and saturated fat intake be less than 7% of the total energy intake.

To assess the epidemiological evidence on diet and cancer and make public health recommendations.

Review of published studies, concentrating on recent systematic reviews, meta-analyses and large prospective studies.

Overweight/obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colorectum, breast (postmenopausal), endometrium and kidney; body weight should be maintained in the body mass index range of 18.5–25?kg/m2, and weight gain in adulthood avoided. Alcohol causes cancers of the oral cavity, pharynx, oesophagus and liver, and a small increase in the risk for breast cancer; if consumed, alcohol intake should not exceed 2?units/d. Aflatoxin in foods causes liver cancer, although its importance in the absence of hepatitis virus infections is not clear; exposure to aflatoxin in foods should be minimised. Chinese-style salted fish increases the risk for nasopharyngeal cancer, particularly if eaten during childhood, and should be eaten only in moderation. Fruits and vegetables probably reduce the risk for cancers of the oral cavity, oesophagus, stomach and colorectum, and diets should include at least 400?g/d of total fruits and vegetables. Preserved meat and red meat probably increase the risk for colorectal cancer; if eaten, consumption of these foods should be moderate. Salt preserved foods and high salt intake probably increase the risk for stomach cancer; overall consumption of salt preserved foods and salt should be moderate. Very hot drinks and foods probably increase the risk for cancers of the oral cavity, pharynx and oesophagus; drinks and foods should not be consumed when they are scalding hot. Physical activity, the main determinant of energy expenditure, reduces the risk for colorectal cancer and probably reduces the risk for breast cancer; regular physical activity should be taken.

To review the evidence on diet and nutrition relating to osteoporosis and provide recommendations for preventing osteoporosis, in particular, osteopototic fracture.

Firstly, to review the definition, diagnosis and epidemiology of osteoporosis, to discuss the difficulties in using bone mineral density to define osteoporosis risk in a world-wide context and to propose that fragility fracture should be considered as the disease endpoint. Secondly, to provide an overview of the scientific data, the strengths and weaknesses of the evidence and the conceptual difficulties in interpreting studies linking diet, nutrition and osteoporosis. The following were considered: calcium, vitamin D, phosphorus, magnesium, protein and fluorine. Other potential dietary influences on bone health were also discussed, including vitamins, trace elements, electrolytes, acid–base balance, phyto-oestrogens, vegetarianism and lactose intolerance.

There is insufficient knowledge linking bone mineral status, growth rates or bone turnover in children and adolescents to long-term benefits in old age for these indices to be used as markers of osteoporotic disease risk. For adults, the evidence of a link between intakes of any dietary component and fracture risk is not sufficiently secure to make firm recommendations, with the exception of calcium and vitamin D. For other aspects of the diet, accumulating evidence suggests that current healthy-eating advice to decrease sodium intake, to increase potassium intake, and to consume more fresh fruits and vegetables is unlikely to be detrimental to bone health and may be beneficial.