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Nutrition & Well-Being for healthy living Notes and bibliographic references


Notes and bibliographic references

structed “artificially” so that it does not correspond exactly to the actual value, but is suitable for comparing the values of mortality among different age periods. 18. Foot D. et al., Demographics and cardiology, 1950–2050, in “Journal of the American College of Cardiology,” 35(5), 2000. 19. European cardiovascular disease statistics 2008, British Heart Foundation; Health Promotion Research Group, Department of Public Health, University of Oxford; Health Economics Research Centre, Department of Public Health, University of Oxford, 2009. 20. European cardiovascular disease statistics 2008, British Heart Foundation; Health Promotion Research Group, Department of Public Health, University of Oxford; Health Economics Research Centre, Department of Public Health, University of Oxford, 2009. 21. It consists mostly of hours of care received by patients with coronary artery disease or cerebrovascular by unpaid persons.

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chapter 1

23. Consensus Development Conference. Diagnosis, prophylaxis, and treatment of osteoporosis, in “American Journal of Medicine,” 1993.

1. For further details on major registry and demographic trends underway and the consequences in terms of health, see the document published by the BCFN in 2011, Longevity and Well-being: the role of diet.

24. Prevention and Management of Osteoporosis, WHO, 2003.

2. Italy in 2030: The Future Demographic, Euromonitor International, 2010. 3. The number of years of the average life expectancy of a human being. 4. Population Health Metrics, 2011. 5. “The future of Pensions and Healthcare in a Rapidity Ageing World,” World Economic Forum. 6. “The future of Pensions and Healthcare in a Rapidity Ageing World, Conclusions, facts and projections,” World Economic Forum. 7. An individual is obese if their body mass index (BMI) is more than 30. 8. The rough rate is the ratio between the number of cases in which the disease under study is present and the reference population, namely the rate without any further corrections. The standardized rate is a system of adjustment of a rate that allows to compare populations that have different distributions within them, such as those relating to age. 9. American Diabetes Association, Economic Costs of Diabetes in the U.S. in 2007, in “Diabetes Care,” 31(3), March 2008. 10. Fact Sheet n° 297, World Bank Organization, February 2009. 11. The kinds of cancer that cause the greatest number of deaths worldwide are lung cancer (1.3 million deaths per year), stomach cancer (803 thousand deaths per year), colorectal cancer (639 thousand deaths per year), liver cancer (610 thousand deaths per year) and breast cancer (519,000 deaths per year). 12. Health Watch Report 2008. Health status and quality of care in the Italian regions, Catholic University of Sacred Heart, 2008. 13. Cancer Facts&Figures 2009, American Cancer Society, 2009. 14. ISDOC, Actual and preferred place of death of cancer patients. Results from the Italian survey of the dying of cancer (ISDOC), in “Journal of Epidemiology and Community Health,” 2006. 15. For example, heart attck, hypertension, thrombosis, aneurysm, stroke, etc. 16. Causes of specific mortality, global burden disease, WHO. 17. The standardized rate allows for comparisons between different periods, independently of the different age distribution of the population in different periods. It is an indicator con-

25. Istat, Italian Statistical Annual, 2010. 26. Ström O. et al., The Burden of Fractures in France, Germany, Italy, Spain, Sweden, and the UK, in “Osteoporosis International,” 2011. 27. BMI>24 but less than 30. 28. Olshansky S. J., A Potential Decline in Life Expectancy in the United States in the 21st Century, in “The New England Journal of Medicine,” 2005.

Nutrition & Well-Being for healthy living

Nutrition & Well-Being for healthy living

22. World Alzheimer Report, 2010.

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chapter 2 1. World Health Organization. 2. Healthy Living, WHO, 1999. 3. Kris-Etherton P., Summary of the scientific conference on dietary fatty acids and cardiovascular health: conference summary from the nutrition committee of the American Heart Association, in “Circulation,” 103, 2001, pp. 1034-39. 4. Grundy S. M. and G. L. Vega, Plasma cholesterol responsiveness to saturated fatty acids, in “American Journal of Clinical Nutrition,” 47, 1988, pp. 822-24; Katan M. J., P. L. Zock and R. P. Mensink, Dietary oils, serum lipoproteins and coronary heart disease, in “American Journal of Clinical Nutrition,” 61(6), 1995, pp. 1368-73. 5. Myristic acid is contained in nutmeg, coconut oil and the fat of dairy products. 6. Palmitic acid is contained in palm oil, meat and dairy products. 7. Hu F. B. et al., Dietary fat intake and the risk of coronary heart disease in women, in “The New England Journal of Medicine,” 337, 1997, pp. 1491-99; Xu, J. et al., Dietary fat intake and risk of coronary heart disease: the Strong Heart Study, in “American Journal of Clinical Nutrition,” 84(4), 2006, pp. 894-902. 8. Trans fatty acids occur naturally in small quantities and are found in meat and dairy products, while nearly all are generated in the process of hydrogenation. The change in structure of the fats contained in food, which is obtained with the hydrogenation, can prolong the life of the products and ensure their freshness by reducing production costs. In the “trans” for, fatty acid not only increases the level of LDL, the so-called “bad cholesterol,” but it also decreases


the “good” HDL, which protects the cardiovascular system by helping the body eliminate cholesterol.

26. Rimm E. B., Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men, in “Journal of the American Medical Association,” 275, 1996, pp. 447-51.

9. Mensink, R. P. and M. B. Katan, Effect of dietary trans fatty acids on high-density and low-density lipoprotein cholesterol levels in healthy subjects, in “The New England Journal of Medicine,” 323, 1990, pp. 439-45.

27. www.chd-taskforce.de

10. Sundram, K. et al., Trans (elaidic) fatty acids adversely impact lipoprotein profiles relative to specific saturated fatty acids in humans, in “Journal of Nutrition,” 127, 1997, pp. 514S-20S; Wood, R. et al., Effect of butter, mono- and polyunsaturated fatty acid-enriched butter, trans fatty acid margarine and zero trans fatty acid margarine on serum lipids and lipoproteins in healthy men, in “Journal of Lipid Research,” 34, 1993, pp. 1-11. 11. www.nasonline.org.

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13. Willett, W. C. et al., Intake of trans fatty acids and risk of coronary heart disease among women, in “Lancet,” 341, 1993, pp. 581-85. 14. Ascherio, A. et al., Trans fatty acids intake and risk of myocardial infarction, in “Circulation,” 89, 1994, pp. 94-101. 15. Koletzko, B. and T. Decsi, Metabolic aspects of trans fatty acids, in “Clinical Nutrition,” 16, 1997, pp. 229-37. 16. Oomen C. M. et al., Association between trans fatty acid intake and 10-year risk of coronary heart disease in the Zutphen Elderly Study: a prospective population based study, in “Lancet,” 357, 2001, pp. 746-51. 17. Willett W. C., Intake of trans fatty acids and risk of coronary heart disease among women, in “Lancet,” 341, 1993, pp. 581-85. 18. Katan M. B., Trans fatty acids and plasma lipoproteins, in “Nutrition Reviews,” 58, 2000, pp. 188-91. 19. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are polyunsaturated fatty acids belonging to the family of omega 3. Contrary to other omega 3 fatty acids, EPA and DHA are essential fatty acids, but are believed to play an important role in the health of the individual, as positive modulators of the synthesis of the good eicosanoids. EPA and DHA are found especially in fatty fish (100 grams of salmon, trout, sardines, mackerel, herring or tuna contain an amount ranging from 1.5 to 3 grams of omega 3). Even though they are not essential fatty acids, it has been shown that as nutrients, they are essential for the proper development and for the maintenance of good health, reducing cardiovascular risk and lowering triglyceride levels. 20. Mori T. A. and L. J. Beilin, Long-chain omega 3 fatty acids, blood lipids and cardiovascular risk reduction, in “Current Opinion in Lipidology,” 12, 2001, pp. 11-17. 21. Italian Group for the Study of Heart-attack Survival, GISSI-Prevention investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial, in “Lancet,” 354, 1999, pp. 447-55, (www. gissi.org). 22. Hu F. B., Fish and omega-3 fatty acid intake and risk of coronary heart disease in women, in “American Journal of Clinical Nutrition,” 69, 1999, pp. 890-97. 23. Ascherio A. et al., Dietary fat and risk of coronary heart disease in men: cohort follow-up study in the United States, in “British Medical Journal,” 313, 1996, pp. 84-90.

29. Heart Protection Study Collaborative Group, MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20536 high-risk individuals: a randomized placebo-controlled trial, in “Lancet,” 306, 2002, pp. 23-33. 30. Brouwer I. A., Low dose folic acid supplementation decreases plasmahomocysteine concentrations: a randomized trial, in “American Journal of Clinical Nutrition,” 69, 1999, pp. 99-104. 31. Ueland P. M. et al., The controversy over homocysteine and cardiovascular risk, in “American Journal of Clinical Nutrition,” 72, 2000, pp. 324-32; Nygard O. et al., Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study, in “Journal of the American Medical Association,” 274, 1995, pp. 1526-33. 32. www.channing.harvard.edu 33. Rimm E. B. et al., Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women, in “Journal of the American Medical Association,” 279, 1998, pp. 359-64. 34. Wald D. S., M. Law and J. K. Morris, Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis, in “British Medical Journal,” 325, 2002, pp. 1202-08. 35. Keli S. O., Dietary flavonoids, antioxidant vitamins, and incidence of stroke: the Zutphen study, in “Archives of Internal Medicine,” 156, 1996, pp. 637-42. 36. Hertog M. G. L., Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study, in “Lancet,” 342, 1993, pp. 1007-11. 37. Gibbs C. R., G. Y. Lip and D. G. Beevers, Salt and cardiovascular disease: clinical and epidemiological evidence, in “Journal of Cardiovascular Risk,” 7, 2000, pp. 9-13. 38. Law M. R., C. D. Frost and N. J. Wald, By how much does salt reduction lower blood pressure? III-Analysis of data from trials of salt reduction, in “British Medical Journal,” 302, 1991, pp. 819-24. 39. Cutler J. A., D. Follmann and P. S. Allender, Randomized trials of sodium reduction: an overview, in “American Journal of Clinical Nutrition,” 65, 1997, pp. 643-51. 40. Midgley J. P., Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials, in “Journal of the American Medical Association,” 275, 1996, pp. 1590-97. 41. Sacks F. M., Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet, in “The New England Journal of Medicine,” 344, 2001, pp. 3-10. 42. Whelton P. K., Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials, in “Journal of the American Medical Association,” 277, 1997, pp. 1624-32. 43. Ascherio A., Intake of potassium, magnesium, and fiber and risk of stroke among US men, in “Circulation,” 98, 1998, pp. 1198-204.

24. Anderson J. W. and T. J. Hanna, Impact of non-digestible carbohydrates on serum lipoproteins and risk for cardiovascular disease, in “Journal of Nutrition,” 129, 1999, pp. 1457-66.

44. Khaw K. T. and E. Barrett-Connor, Dietary potassium and stroke-associated mortality. A12-year prospective population study, in “NewEngland Journal of Medicine,” 316, 1987, pp. 235-40.

25. Truswell A. S., Cereal grains and coronary heart disease, in “European Journal of Clinical Nutrition,” 56, 2002, pp. 1-14.

45. Ness A. R. and J. W. Powles, Fruit and vegetables, and cardiovascular disease: a review, in “International Journal of Epidemiology,” 26, 1997, pp. 1-13.

Nutrition & Well-Being for healthy living

Nutrition & Well-Being for healthy living

12. Institute of Medicine, “Letter report on dietary reference intakes for trans fatty acids,” National Academy of Sciences (USA), July 2002.

28. Yusuf S. et al., Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators, in “The New England Journal of Medicine,” 342, 2000, pp. 154-60.

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67. Chan J. M. et al., Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men, in “Diabetes Care,” 17, 1994, pp. 961-69.

47. Joshipura K. J., Fruit and vegetable intake in relation to risk of ischemic stroke, in “Journal of the American Medical Association,” 282, 1999, pp. 1233-39.

68. Boyko E. J. et al., Visceral adiposity and risk of type 2 diabetes: a prospective study among Japanese Americans, in “Diabetes Care,” 23, 2000, pp. 465-71.

48. Gilman M. W. et al., Protective effect of fruits and vegetables on development of stroke in men, in “Journal of the American Medical Association,” 273, 1995, pp. 1113-17.

69. Despres J. P., Health consequences of visceral obesity, in “Annals of Medicine,” 33, 2001, pp. 534-41.

49. Appel L. J. et al., A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group, in “The New England Journal of Medicine,” 336, 1998, pp. 1117-24.

70. Franz M. J. et al., Evidence- based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications, in “Diabetes Care,” 25, 2002, pp. 148-98.

50. Marckmann P. and M. Gronbaek, Fish consumption and coronary heart disease mortality. A systematic review of prospective cohort studies, in “European Journal of Clinical Nutrition,” 53, 1999, pp. 585-90.

71. Tuomilehto J. et al., Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, in “The New England Journal of Medicine,” 344, 2001, pp. 1343-50.

51. Burr M. L. et al., Effects of changes in fat, fish and fibre intakes on death and myocardial re-infarction: diet and re-infarction trial (DART), in “Lancet,” 2, 1989, pp. 757-61.

72. Knowler W. C. et al., Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin, in “The New England Journal of Medicine,” 346, 2002, pp. 393-403.

52. Zhang J., Fish consumption and mortality from all causes, ischemic heart disease, and stroke: an ecological study, in “Preventive Medicine,” 28, 1999, pp. 520-29.

73. Hu F.B. et al., Diet, lifestyle and the risk of type 2 diabetes mellitus in women, in “The New England Journal of Medicine,” 345, 2001, pp. 790-97.

53. Kris-Etherton P. M., The effects of nuts on coronary heart disease risk, in “Nutrition Reviews,” 59, 2001, pp. 103-11.

74. Pan X. R. et al., Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study, in “Diabetes Care,” 20, 1997, pp. 537-44.

54. Hu F. B. and M. J. Stampfer, Nut consumption and risk of coronary heart disease: a review of epidemiologic evidence, in “Current Atherosclerosis Reports,” 1, 1999, pp. 204-09. 55. Crouse J. R., Randomized trial comparing the effect of case in with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins, in “Archives of Internal Medicine,” 159, 1999, pp. 2070-76. 56. Third International Symposium on the Role of Soy in Preventing and Treating Chronic Disease, in “Journal of Nutrition,” 130(suppl.), 2000, pp. 653-711. 57. Anderson J. W., B. M. Smith and C. S. Washnok, Cardiovascular and renal benefits of dry bean and soybean intake, in “American Journal of Clinical Nutrition,” 70, 1999, pp. 464-74. 58. Rimm E. B., Moderate alcohol intake and lower risk of coronary heart disease: metaanalysis of effects on lipids and haemostatic factors, in “British Medical Journal,” 319, 1999, pp. 1523-28.

75. Ramachandran A. et al., The Indian Diabetes Prevention shows that lifestyle modification and metformin prevent type 2 diabetes in Asian Indian with Impaired Glucose Tolerance (IDPP-1), in “Diabetologia,” 49, 2006, pp. 289-97. 76. Manson J. E. et al., A prospective study of exercise and incidence of diabetes among US male physicians, in “Journal of the American Medical Association,” 268, 1992, pp. 63-67. 77. Kriska A. M. et al., The association of physical activity with obesity, fat distribution and glucose intolerance in Pima Indians, in “Diabetologia,” 36, 1993, pp. 863-69. 78. Helmrich S. P. et al., Physical activity and reduced occurrence of non-insulin dependent diabetes mellitus, in “The New England Journal of Medicine,” 325, 1991, pp. 147-52. 79. McAuley K. A. et al., Intensive lifestyle changes are necessary to improve insulin sensitivity: A randomised controlled trial, in “Diabetes Care,” 25, 2002, p. 445.

59. Eriksson K. F. and F. Lindgarde, Prevention of type 2 (non insulin dependent) diabetes mellitus by diet and physical exercise, in “Diabetologia,” 34, 1991, p. 891.

80. In this regard, see the position statement published in January 2008 by the ADA, Nutrition recommendations and interventions for diabetes.

60. Goldstein D. J., Beneficial health effects of modest weight loss, in “International Journal of Obesity,” 16, 1992, pp. 397-415.

81. Ryan D. H. et al., Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes, in “Controlled Clinical Trials,” 24, 2003, pp. 610-28.

61. Brage S. et al., The European Youth Heart Study (EYHS): Features of the metabolic syndrome are associated with objectively measured physical activity and fitness in Danish children, in “Diabetes Care,” 27, 2004, p. 2141. 62. St-Onge M. P., I. Janssen and S. B. Heymsfield, Metabolic syndrome in normal-weight Americans, in “Diabetes Care,” 27, 2004, p. 2222. 63. Tuomilehto J. et al., Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, in “The New England Journal of Medicine,” 344, 2002, pp. 1343-50. 64. Knowler W. C. et al., Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin, in “The New England Journal of Medicine,” 346, 2002, pp. 393-403. 65. Colditz G. A. et al., Weight as a risk factor for clinical diabetes in women, in “American Journal of Epidemiology,” 132, 1990, pp. 501-13. 66. Despres J. P. et al., Treatment of obesity: need to focus on high-risk abdominally obese patients, in “British Medical Journal,” 322, 2001, pp. 716-20.

82. The “exchange diet” is based on the need for a varied diet while maintaining a constant intake of various nutrients. The foods are divided into groups of foods that are similar as to nutrient content and then, a balanced diet is established based on which substitutions are made within the exchange lists (the food groups). For example, if a certain amount of grams of bread are needed (carbohydrates), these may be replaced by a corresponding amount from another of the food on the same list (potatoes, pasta, rice, polenta, bread sticks, etc.). (Source: Diabetes Project). 83. Van Gaal L. et al., Relationship of body fat distribution pattern to atherogenic risk factors in NIDDM, in “Diabetes Care,” 11, 1988, p. 103. 84. Lean M. E. J., T. S. Han and C. E. Morrison, Waist circumference as a measure for indicating need for weight management, in “British Medical Journal,” 311, 1995, p. 158. 85. SIGN, Obesity in children and young people, in “Scottish Intercollegiate Guidelines Network Guidelines,” 69, 2003 (www.show.scot.nhs.uk/guidelines/fulltext/69.html).

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46. Liu S., Fruit and vegetable intake and risk of cardiovascular disease: the Women’s Health Study, in “American Journal of Clinical Nutrition,” 72, 2000, pp. 922-28.

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86. World Health Organization, Diet, nutrition and the prevention of chronic diseases. Report of a Joint FAO/WHO Expert Consultation, in “WHO Technical Report Series,” 916, Geneva 2003.

106. Knowler W. C. et al., Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin, in “The New England Journal of Medicine,” 346, 2002, pp. 393-403.

87. With regard to this, see the position statement published in January, 2002 by the ADA, Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications.

107. Appleby P. N. et al., Low body mass index in non-meat eaters: the possible roles of animal fat, dietary fibre and alcohol, in “International Journal of Obesity,” 22, 1998, p. 454.

88. Jenkins D. J. et al., Glycemic index of foods: a physiological basis for carbohydrate exchange, in “American Journal of Clinical Nutrition,” 34, 1981, pp. 362-66. 89. Willett W. C., J. Manson and S. Liu, Glycemic index, glycemic load, and risk of type 2 diabetes, in “American Journal of Clinical Nutrition,” 76, 2001, p. 274S. 90. Frost G., J. Wilding and J. Beecham, Dietary advice based on the glycemic index improves dietary profile and metabolic control in type 2 diabetic patients, in “Diabetic Medicine,” 11, 1994, p. 397.

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92. Fontvieille A. et al., The use of low glycemic index foods improve metabolic control of diabetic patients over five weeks, in “Diabetic Medicine,” 9, 1992, p. 444. 93. Wolever T. et al., Beneficial effect of a low glycemic index diet in type 2 diabetes, in “Diabetic Medicine,” 9, 1992, p. 451. 94. Jensinks D. et al., Effect of a Low Glycemic Index or a High Cereal Fiber Diet on Type 2 Diabetes: A Randomized Trial, in “Journal of the American Medical Association,” 300(23), 2008. 95. Liese A. D. et al., Dietary glycemic index and glycemic load, carbohydrate and fiber intake, and measures of insulin sensitivity, secretion, and adiposity in the Insulin Resistance Atherosclerosis Study, in “Diabetes Care,” 28, 2005, pp. 2832-38. 96. Sheard N. F. et al., Dietary carbohydrate (amount and type) in the prevention and management of diabetes: a statement of the American Diabetes Association, in “Diabetes Care,” 27, 2001, pp. 2266-71. 97. Buyken A. E. et al. and the EURODIAB IDDM Complications Study Group, Glycemic index in the diet of European outpatients with type 1 diabetes: relations to HbA1c and serum lipids, in “American Journal of Clinical Nutrition,” 73, 2001, p. 574. 98. Riccardi G., G. Clemente and R. Giacco, Glycemic index of local foods and diets: the Mediterranean experience, in “Nutrition Reviews,” 61, 2003, p. S56. 99. In this regard see, among others, Foster et al. (2003) and Samaha et al. (2003); such lack of effectiveness is probably due to the fact that low-carbohydrate diets are normally high in fat, resulting in a potential negative effect on the maintenance of optimum body weight in the long term and on insulin sensitivity: in this regard, also see Vessby et al. (2001); Toeller et al. (2001) and Shah et al. (1996). 100. Garg A., High-monounsaturated fat diets for patients with diabetes mellitus: a metaanalysis, “American Journal of Clinical Nutrition,” 67(suppl.), 1998, p. 577S. 101. In this regard, see the recent position statement published in January, 2008 by the ADA, Nutrition recommendations and interventions for diabetes. 102. Salmeron J. et al., Dietary fiber, glycemic load and risk of NIDDM in men, in “Diabetes Care,” 20, 1997, pp. 545-50; Salmeron J. et al., Dietary fiber, glycemic load, and risk of noninsulin-dependent diabetes mellitus in women, in “Journal of the American Medical Association,” 277, 1997, pp. 472-77. 103. Meyer K. et al., Carbohydrates, dietary fiber, and incident type 2 diabetes in older women, in “American Journal of Clinical Nutrition,” 71, 2000, pp. 921-30. 104. Mann J., Dietary fibre and diabetes revisited, in “European Journal of Clinical Nutrition,” 55, 2001, pp. 919-21. 105. Tuomilehto J. et al., Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance, in “The New England Journal of Medicine,” 344, 2002, pp. 1343-50.

109. McKeown N. M. et al., Carbohydrate nutrition, insulin resistance, and the prevalence of the Metabolic Syndrome in the Framingham Offspring Cohort, in “Diabetes Care,” 27, 2004, p. 538, 2004. 110. Mann J., Dietary fibre and diabetes revisited, in “European Journal of Clinical Nutrition,” 55, 2001, pp. 919-21. 111. Mann J., Lines to legumes: changing concepts of diabetic diets, in “Diabetic Medicine,” 1, 1984, pp. 191-98. 112. Simpson H. R. C. et al., A high carbohydrate leguminous fibre diet improves all aspects of diabetic control, in “Lancet,” 1, 1981, pp. 1-5. 113. Chandalia M. et al., Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus, in “The New England Journal of Medicine,” 342, 2000, pp. 1392-98. 114. Salmeron J. et al., Dietary fiber, glycemic load and risk of NIDDM in men, in “Diabetes Care,” 20, 1997, pp. 545-50; Salmeron J. et al., Dietary fiber, glycemic load, and risk of noninsulin-dependent diabetes mellitus in women, in “Journal of the American Medical Association,” 277, 1997, pp. 472-77. 115. Lousely S. E. et al., High carbohydrate high fibre diets in poorly controlled diabetes, in “Diabetic Medicine,” 1, 184, p. 21. 116. Simpson R. W. et al., High-carbohydrate diets and insulin dependent diabetics, in “British Medical Journal,” 2, 1979, p. 523. 117. Simpson H. C. R. et al., Digestible carbohydrate – an independent effect on diabetic control in type II (non-insulin dependent) diabetic patients?, in “Diabetologia,” 23, 1982, p. 235. 118. Perrotti N. et al., Effect of digestible carbohydrates on glucose control in insulin dependent patients with diabetes, in “Diabetes Care,” 7, 1984, p. 354. 119. The metabolic syndrome is identified as the simultaneous presence of three or more of the following: abdominal obesity (waist circumference greater than 102 cm for men, greater than 88 cm for women) high levels of blood triglycerides (greater than or equal to 150 mg/ dl), low levels of HDL cholesterol (less than 40 mg/dl for men, less than 50 mg/dl for women), high blood pressure (greater than or equal to 130/85 mmHg) and high levels of glucose in the blood when fasting (greater than or equal to 100 mg/dl). (Source: American Heart Association). 120. Poppitt S. D. et al., Long term effects of ad libitum low-fat high carbohydrate diets on body weight and serum lipids in overweight subjects with metabolic syndrome, in “American Journal of Clinical Nutrition,” 75, 2002, p. 11. 121. Raben A. et al., Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects, in “American Journal of Clinical Nutrition,” 76, 2002, p. 721. 122. Franz M. J. et al., Evidence- based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications, in “Diabetes Care,” 25, 2002, pp.148-98. 123. Bantle J. et al., Effects of dietary fructose on plasma lipids in healthy subjects, in “American Journal of Clinical Nutrition,” 72, 2000, p. 1128.

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108. Toeller M. et al. and the EURODIAB IDDM Complications Study Group, Nutrient intakes as predictors of body weight in European people with type 1 diabetes, in “International Journal of Obesity,” 25, 2001, p. 1815.

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125. Lovejoy J. and M. Di Girolamo, Habitual dietary intake and insulin sensitivity in lean and obese adults, in “American Journal of Clinical Nutrition,” 55, 1992, pp. 1174-79.

144. Katan M. B., P. L. Zock and M. P. Mensink, Dietary oils, serum lipoproteins, and coronary heart disease, in “American Journal of Clinical Nutrition,” 61, 1995, p. 1368S.

126. Feskens E. J. M. et al., Dietary factors determining diabetes and impaired glucose tolerance. A 20-year follow-up of the Finnish and Dutch cohorts of the Seven Countries Study, in “Diabetes Care,” 18, 1995, pp. 1104-12.

145. Howell W. H. et al., Plasma lipid and lipoprotein responses to dietary fat and cholesterol: meta analysis, in “American Journal of Clinical Nutrition,” 65, 1997, p. 1747.

127. Marshall J. A. et al., Dietary fat predicts conversion from impaired glucose tolerance to NIDDM. The San Luis Valley Diabetes Study, in “Diabetes Care,” 17, 1994, pp. 50-56.

146. Mensink R. P. et al., Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL-cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, in “American Journal of Clinical Nutrition,” 77, 2003, p. 1146.

128. Feskens E. J. M. et al., Dietary factors determining diabetes and impaired glucose intolerance. A 20-year follow-up of the Finnish and Dutch cohorts of the Seven Countries Study, in “Diabetes Care,” 18, 1995, p. 1104.

147. Vessby B. et al., Substituting polyunsaturated for saturated fat as a single change in a Swedish diet: effects on serum lipoprotein metabolism and glucose tolerance in patients with hyperlipoproteinaemia, in “European Journal of Clinical Investigation,” 10, 1980, p. 193.

129. Bo S. et al., Dietary fat and gestational hyperglycemia, in “Diabetologia,” 44, 2001, pp. 972-78.

148. Vessby B. et al., Substituting dietary saturated fat with monounsaturated fat impairs insulin sensitivity in healthy men and women: the KANWU Study, in “Diabetologia,” 44, 2001, p. 312.

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279. Kelley J. R. and J. M. Duggan, Gastric cancer epidemiology and risk factors, in “Journal of Clinical Epidemiology,” 56, 2003, pp. 1-9. 280. Sharp L., Risk factors for squamous cell carcinoma of the oesophagus in women: a casecontrol study, in “British Journal of Cancer,” 85, 2001, pp. 1667-70. 281. International Agency for Research on Cancer, Weight control and physical activity, in “IARC Handbooks of Cancer Prevention,” 6, 2002. 282. Martinez M. E., E. Giovannucci and D. Spiegelman, Leisure-time physical activity, body size, and colon cancer in women. Nurses’ Health Study Research Group, in “Journal of National Cancer Institute,” 89, 1997, pp. 948-55. 283. Hardman A. E., Physical activity and cancer risk, in “Proceedings of the Nutrition Society,” 60, 2001, pp. 107-13. 284. Jeandel C. et al., Lipid peroxidation and free radical scavengers in Alzheimer’s disease, in “Gerontology,” 35, 1989, pp. 257-82. 285. Behl C. and F. Holsboer, Oxidative stress in the pathogenesis of Alzheimer’s and antioxidant neuro-protection, in “Fortschr Neurologie-Psychiatrie,” 66, 1998, pp. 113-21. 286. The beta-amyloid is the major constituent of senile plaques, extracellular formations which represent one of the main microscopic features of Alzheimer’s disease, in that an anomalous production of beta-amyloid is the cause of many neurodegenerative diseases. 287. De Rich M. C. et al., Dietary antioxidants and Parkinson’s disease. The Rotterdam Study, in “Archives of Neurology,” 54, 1997, pp. 762-65. 288. De Rijk M. et al. Dietary antioxidants and Parkinson disease, in “The Rotterdam Study. Archives of Neurology,” 1997. 289. Ahlskog J. E. et al., Guamanian neurodegenerative disease: investigation of the calcium metabolism/heavy metal hypothesis, in “Neurology,” 45, 1995, pp. 1340-44. 290. Glick J. L., Dementias: the role of magnesium deficiency and an hypothesis concerning the pathogenesis of Alzheimer’s disease, in “Medical Hypotheses,” 31, 1990, pp. 211-25. 291. Simons M. et al., Cholesterol and Alzheimer’s disease. Is there a link?, in “Neurology,” 57, 2001, pp. 1089-93. 292. Kalmijn S. et al., Dietary fat intake and the risk of incident dementia, in “The Rotterdam Study. Annals of Neurology,” 42, 1997, pp. 776-82. 293. Diet and Alzheimer’s Disease, Physicians Committee for Responsible Medicine, August 1 2004. 294. Morris M. C. et al., Dietary fats and the risk of incident Alzheimer disease, in “Archives of Neurology,” 60, 2003, pp. 194-200.

299. Homocysteine is a sulfur-containing amino acid that is formed after the enzymatic transformation of methionine, another sulfur amino acid present in protein foods (dairy, meat, vegetables, eggs). If present in excess in the bloodstream (hyperhomocysteinemia) homocysteine causes damage even greater than that caused by cholesterol. For this reason it is considered an independent risk factor, because it alone is able to increase the incidence of cardiovascular disease irrespective of the presence of other predisposing factors. Already higher values at 10-12 μmoli per liter correlate with an increased risk of atherosclerosis, stroke and myocardial infarction, as well as many other diseases of the cardiovascular system (venous thrombosis, pulmonary embolism) or not (birth defects, mental decline, Alzheimer’s, spontaneous fractures). 300. Leblhuber F. et al., Hyperhomocysteinemia in dementia, in “Journal of Neural Transmission,” 2000. 301. For more details, please refer to section 5.2 of this position paper, on the topic of “caloric restriction and longevity.” 302. Mattson M. P., Will Caloric Restriction and folate protect against AD and PD?, in “Neurology,” 2003. 303. Luchsinger J. A. et al., Caloric intake and the risk of Alzheimer disease, in “Archives of Neurology,” 2002. 304. Keep fit for life. Meeting the nutritional needs of older persons, World Health Organization, Geneva 2002. 305. Tucker K. L., Dietary intake and bone status with aging, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, 2003. 306. Abrahamsen B., Patient level pooled analysis of 68.500 patients from seven major vitamin D fracture trials in US and Europe, Department of Internal Medicine and Endocrinology, Copenhagen University Hospital Gentofte, 2010. 307. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine, Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride, National Academy Press, Washington DC 1999. 308. NIH Consensus Development Panel on Optimal Calcium Intake, Optimal calcium intake. NIH Consensus conference, in “Journal of the American Medical Association,” 1994. 309. World Health Organization, “Interim report and recommendations of the World Health Organization Task-Force for osteoporosis, in “Osteoporosis International,” 1999. 310. Prevention and Management of osteoporosis, World Health Organization, 2003. 311. Dietary Reference Intakes for Calcium and Vitamin D, Food and Nutrition Board, Institute of Medicine, 2010. 312. Recommendations of the Ministry of Health on the proper use of food supplements, Ministry of Health of the Italian Government, 2005.

Nutrition & Well-Being for healthy living

Nutrition & Well-Being for healthy living

278. Palli D., Epidemiology of gastric cancer: an evaluation of available evidence, in “Journal of Gastroenterology,” 35(12), 2000, pp. S84-89.

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313. Lee W. T. K. et al., Relationship between long-term calcium intake and bone mineral content of children aged from birth to 5 years, in “British Journal of Nutrition,” 1993. 314. Malabanan A., I. E. Veronikis and M. F. Holick, Redefining vitamin D insufficiency, in “Lancet,” 1998. 315. Vitamin and mineral requirements in human nutrition, Report of the Joint FAO/ WHO Expert Consultation, World Health Organization, Geneva. 316. Chevalley T. et al., Effects of calcium supplements on femoral bone mineral density and vertebral fracture rate in vitamin-D-replete elderly patients, in “Osteoporosis International,” 1994.

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318. Miggiano G. A. and L. Gagliardi, Diet, nutrition and bone health, Center for Research in Human Nutrition, Institute of Biochemistry and Clinical Biochemistry, Faculty of Medicine, Sacred Heart Catholic University, Rome, 2005.

chapter 3 1. For a thorough analysis on this topic, see the document Healthy growth and nutrition in children, published by the BCFN in 2010. 2. WHO, Food and Nutrition Board, Italian Society of Human Nutrition 3. For further detail in this regard, see the paper Longevity and Well-Being: the role of diet, published by the BCFN in 2011.

6. Keys A. et al., A Multivariate Analysis of Death and Coronary Heart Disease, Harvard University Press, Cambridge (MA)- London 1980, pp. 1-381; Toshima H., Y. Koga and H. Blackburn, Lessons for Science from the Seven Countries Study, Springer Verlag, Tokyo 1995. 7. Keys A. et al., Epidemiologic studies related to coronary heart disease: characteristics of men aged 40-59 in seven countries, in “Acta Med Scand,” 460(suppl.), 1967, pp. 1-392. 8. Keys A., Coronary heart disease in seven countries, in “Circulation,” 41(suppl.), 1970, pp. 1-211; Kromhout D. and A. Menotti, The Seven Countries Study: A Scientific Adventure in Cardiovascular Disease Epidemiology, Brouwer, Utrecht 1994. 9. Willett W. C., F. Sacks and A. Trichopoulou, Mediterranean diet pyramid: a cultural model for healthy eating, in “American Journal of Clinical Nutrition,” 1995. 10. Panagiotakosa D., C. Pitsavosd and F. Arvanitic, Adherence to the Mediterranean food pattern predicts the prevalence of hypertension, hypercholesterolemia, diabetes and obesity, among healthy adults; the accuracy of the MedDietScore, in “Preventive Medicine,” 44(4), April 2007. 11. The scale used in the study is between 0 and 55, so an increase of 10 points on the scale of adequacy Mediterranean is equivalent to an increase of about 20%. 12. Trichopoulou A. et al., Adherence to a Mediterranean Diet and Survival in a Greek Population, in “The New England Journal of Medicine,” 348(26), 2003. 13. Mitrou P. N. et al., Mediterranean dietary pattern and prediction of all-cause mortality in a U.S. population: results from the NIH-AARP Diet and Health Study, in “Archives of Internal Medicine,” 2007.

4. “National Vital Statistics Reports,” 56(10), 2008

14. De Lorgeril M. et al., Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study, in “Circulation,” 1999.

5. Sears B. and C. Ricordi, Anti-infiammatory nutrition as a Pharmacological Approach to treat Obesity, in “Journal of obesity,” 2011.

15. Lorgeli M. and P. Salen, Mediterranean diet in secondary prevention of HCD, in “Public Health Nutrition,” August 2011.

6. Fontana L. et al., Extending Healthy Lifespan—From Yeast to Humans, in “Science”, 2010

16. Fung T. T. et al., Diet-quality scores and plasma concentrations of markers of inflammation and endothelial dysfunction, in “American Journal of Clinical Nutrition,” 2005.

7. In this regard, also see: Fontana L., “Visceral obesity, calorie restriction and ageing” in the “Journal of Gerontology,” 54, 2006, pp. 131-33; Weindruch R. and R. S. Sohal, Caloric intake and aging, in “The New England Journal of Medicine,” 377, 1997, pp. 986-94; Masoro E. J., Overview of caloric restriction and ageing, in “Mechanisms of Ageing and Development,” 126, 2005, pp. 913-22.

17. Sofi F. et al., Adherence to Mediterranean diet and health Adherence to Mediterranean diet and health, in “British Medical Journal,” July 2008.

8. Albanes D., Cancer Research, 1987.

18. Tognon G. and E. Rothenberg, Does the Mediterranean diet predict longevity in the elderly?, in “Public Health Epidemiology,” University of Gothenburg, 2010.

9. Shimokawa I. et al., Diet and the suitability of the male Fischer 344 rat as a model for aging research, in “Journal of Gerontology of Biological Science,” 48, 1993, pp. B27-32.

19. Baldini M. et al., Is the Mediterranean lifestyle still a reality? Evaluation of food consumption and energy expenditure in Italian and Spanish university students, in “Public Health Nutrition,” 2008.

chapter 4

chapter 5

1. For Italy, see the Italian Guidelines for healthy eating, identified in 2003 by the National Research Institute for Food and Nutrition (INRAN).

1. For example, the Regional Sanitary Services Agency (ASSR).

2. Agriculture Fact Book, Profiling Food Consumption in America, 2002. 3. National Nutrition Survey, The Japan Dietetic Association, 2001. 4. Mediterranean cuisine. Ingredients, dietary principles and recipes with the flavor of sun, Mondadori, Milan 1993.

2. The choice of countries was dictated by the availability of large, complete and consistent sets of statistics; for Italy, this requirement is not present because there is not a sufficiently large time series. 3. The model has taken into account two components which will determine the dynamic evolution and interaction of public health spending in the coming years. The first is demographic,

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

317. Kitchin B. and S. L. Morgan, Not just calcium and vitamin D: other nutritional considerations in osteoporosis, School of Health Professions and UAB Osteoporosis Prevention and Treatment Clinic, The University of Alabama, 2007.

5. Ancel Benjamin Keys (1904-2004), American physician and physiologist, was known for being a leading advocate of the benefits of the Mediterranean diet to combat many diseases prevalent in the West, particularly cardiovascular disease.

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or related to the number and structure by sex and by age of the population. The second is economic, due to a tendency, found in all advanced societies, toward an increase in the total health expenditure (public and private) more than in proportion to the GDP growth. For a detailed description of the methodology and results of the prediction model of health expenditure, see: The European House-Ambrosetti, Health Meridian - The coordinates of Health, Final Report, November 2011.

Alimentazione e benessere per una vita sana

4. The hypothesis that the benefit of prevention is manifested as decreased of the expenditure for any other type of performance defined in the prediction model has no impact on the total value of the benefit, but on the distribution of health spending among the types of performance. 5. The assumption may be considered reasonable if one considers the low level of investment in prevention and its low impact on public health expenditure. For larger values of the investment in prevention and/or its impact on public health expenditure is plausible to consider that the trend of a benefit would manifest a declining trend of the growth in the value of the investment. 6. Lewington S. et al., Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies, in “Lancet,” 360, 2002, pp. 1903-13. 7. Chobanian A. et al., Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, in “Journal of the American Medical Association,” 2003. 8. European cardiovascular disease statistics 2008, British Heart Foundation; Health Promotion Research Group, Department of Public Health, University of Oxford; Health Economics Research Centre, Department of Public Health, University of Oxford, 2009.

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chapter 6 1. The BCFN has thoroughly analyzed the social and cultural meanings of food and the dynamics involved in the dialectical relationship between man and food. To pursue this increasingly vital issue, please refer to three documents that the BCFN has produced over the last twenty-four months: The cultural dimension of food (2009), The value of the Mediterranean Character (2010) and the treatise Food for Culture of the present report. 2. This style of food, however - and this is further evidence that emerged in the course of the interdisciplinary comparisons conducted by the BCFN – not only provides effective protection for people from the medical point of view, but is also “environmentally friendly.” The scientific evidence concerning water management and climate change (see the position paper on Water Management and Climate Change, Agriculture and Food) shows that the environmental implications of production decisions related to dietary models are very important, both positively and negatively. In the second position paper, as mentioned, we have actually created the environmental pyramid in association with the known food pyramid, demonstrating how a healthy and balanced diet is characterized by its low environmental impact, measured in terms of its global footprint.


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