pp_alimentazione_benessere_vita_ES_NOTE

ALIMENTAZIONE E BENESSERE PER UNA VITA SANA NOTE E RIFERIMENTI BIBLIOGRAFICI

NOTE e RIFERIMENTI BIBLIOGRAFICI

un indicatore costruito in modo “artificiale” che non corrisponde esattamente al valore reale, ma che è adatto a confrontare i valori della mortalità tra periodi diversi per struttura di età.

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. Si tratta prevalentemente delle ore di assistenza ricevute dai pazienti affetti da malattie coronariche o cerebrovascolari da parte di persone non stipendiate.

CAPITOLO 1

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

1. Per un approfondimento specifico sulle grandi tendenze anagrafiche e demografiche in atto e sulle conseguenze in termini di salute, si veda il documento edito dal BCFN nel 2011, Longevità e benessere: il ruolo dell’alimentazione.

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

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6. “The future of Pensions and Healthcare in a Rapidity Ageing World, Conclusions, facts and projections”, World Economic Forum.

2. Italy in 2030: The Future Demographic, Euromonitor International, 2010.

3. Il numero di anni che in media un essere umano può aspirare a vivere.

4. Population Health Metrics, 2011.

5. “The future of Pensions and Healthcare in a Rapidity Ageing World”, World Economic Forum.

7. Un individuo risulta obeso se l’indice di massa corporea (IMC) è maggiore di 30.

8. Il tasso grezzo è il rapporto tra il numero di casi in cui si presenta la patologia oggetto di studio e la popolazione di riferimento, vale a dire il tasso senza ulteriori correzioni. Il tasso standardizzato è un sistema di aggiustamento di un tasso che permette di confrontare popolazioni che hanno distribuzioni diverse tra loro, come ad esempio quelle relative all’età.

9. American Diabetes Association, Economic Costs of Diabetes in the U.S. in 2007, in “Diabetes Care”, 31(3), March 2008.

25. Istat, Annuario statistico italiano 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 ma inferiore a 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.

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CAPITOLO 2 1. World Health Organization.

2. Healthy Living, WHO, 1999.

10. Fact Sheet n° 297, World Bank Organization, February 2009.

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.

11. Le forme tumorali che provocano il maggior numero di decessi a livello mondiale sono il tumore al polmone (1,3 milioni di morti all’anno), il tumore allo stomaco (803 mila morti all’anno), il tumore al colon-retto (639 mila morti all’anno), il tumore al fegato (610 mila morti all’anno) e il tumore al seno (519 mila morti all’anno).

4. Grundy S. M. e 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 e R. P. Mensink, Dietary oils, serum lipoproteins and coronary heart disease, in “American Journal of Clinical Nutrition”, 61(6), 1995, pp. 1368-73.

12. Rapporto Osservasalute 2008. Stato di salute e qualità dell’assistenza nelle regioni italiane, Università Cattolica del Sacro Cuore, 2008.

5. L’acido miristico è contenuto nella noce moscata, nell’olio di cocco e nel grasso dei prodotti caseari.

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. Ad esempio, infarto, ipertensione, trombosi, aneurisma, ictus ecc.

16. Causes of specific mortality, global burden disease, WHO. 17. Il tasso standardizzato consente di effettuare confronti tra periodi diversi, indipendentemente dalla diversa distribuzione per età della popolazione nei diversi periodi. Si tratta di

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

22. Rapporto mondiale Alzheimer, 2010.

6. L’acido palmitico è contenuto nell’olio di palma, nella carne e nei prodotti caseari.

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. Gli acidi grassi trans esistono in natura in quantità ridotte e si trovano all’interno delle carni e dei prodotti caseari, mentre la quasi totalità è generata nel processo d’idrogenazione.

Il cambiamento di struttura, dei grassi contenuti negli alimenti, che si ottiene con l’idrogenazione permette di prolungare la durata dei prodotti e di garantirne la freschezza riducendo i costi di produzione. Nella forma “trans” l’acido grasso non solo fa aumentare il livello delle

lipoproteine LDL, il cosiddetto “colesterolo cattivo”, ma fa anche diminuire quello “buono”, l’HDL, che protegge l’apparato cardiovascolare aiutando il corpo a eliminare il colesterolo.

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. e M. B. Katan, Effect of dietary trans fatty acids on high-density and lowdensity 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. e 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. L’acido eicosapentaenoico (EPA) e l’acido docosaesaenoico (DHA) sono acidi grassi polinsaturi appartenenti alla famiglia degli omega 3. Contrariamente ad altri acidi grassi omega 3, l’EPA e il DHA non sono acidi grassi essenziali, ma si ritiene svolgano un ruolo molto importante nella salute dell’individuo, essendo dei modulatori positivi della sintesi degli eicosanoidi buoni. L’EPA e il DHA sono presenti in particolar modo nel grasso di pesce (100 g di salmone, trota, sardine, sgombro, aringhe o tonno contengono una quantità che varia da 1,5 a 3 g di omega 3). Malgrado non siano acidi grassi essenziali, è stato dimostrato come siano nutrienti fondamentali per il corretto sviluppo e per il mantenimento di un buono stato di salute, riducendo il rischio cardiovascolare e diminuendo i livelli di trigliceridi.

20. Mori T. A. e 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. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico, GISSI-Prevenzione 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.

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

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

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 e 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 e 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 e N. J. Wald, By how much does salt reduction lower blood pressure? IIIAnalysis of data from trials of salt reduction, in “British Medical Journal”, 302, 1991, pp. 819-24.

39. Cutler J. A., D. Follmann e 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.

44. Khaw K. T. ed E. Barrett-Connor, Dietary potassium and stroke-associated mortality. A12year prospective population study, in “NewEngland Journal of Medicine”, 316, 1987, pp. 235-40.

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

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.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

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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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. e 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.

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

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

54. Hu F. B.e 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 e 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.

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

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

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.

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.

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.

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.

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-insulindependent 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.

80. A tal riguardo si veda il position statement pubblicato nel gennaio 2008 dall’ADA, Nutrition recommendations and interventions for diabetes.

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.

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.

82. La “dieta a scambio” si basa sulla necessità di avere un’alimentazione variata mantenendo un costante apporto dei vari nutrienti. I cibi vengono quindi divisi in gruppi di alimenti simili per contenuto di principi nutritivi e si stabilisce, poi, una dieta bilanciata di base sulla quale vengono fatte le sostituzioni all’interno delle liste di scambio (i gruppi di alimenti). Ad esempio, se sono previsti tot. grammi di pane (carboidrati) questi possono essere sostituiti da una corrispondente quantità di un altro degli alimenti della stessa lista (patate, pasta, riso, polenta, grissini ecc.). (Fonte: Progetto Diabete).

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.

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.

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.

84. Lean M. E. J., T. S. Han e C. E. Morrison, Waist circumference as a measure for indicating need for weight management, in “British Medical Journal”, 311, 1995, p. 158.

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.

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).

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.

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

62. St-Onge M. P., I. Janssen e S. B. Heymsfield, Metabolic syndrome in normal-weight Americans, in “Diabetes Care”, 27, 2004, p. 2222.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

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.

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.

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87. Si veda a tal riguardo il position statement pubblicato nel gennaio 2002 dall’ADA, Evidencebased nutrition principles and recommendations for the treatment and prevention of diabetes and related complications.

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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.

89. Willett W.C., J. Manson e S. Liu, Glycemic index, glycemic load, and risk of type 2 diabetes, in “American Journal of Clinical Nutrition”, 76, 2001, p. 274S.

108. Toeller M. et al. e l’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.

90. Frost G., J. Wilding e J. Beecham, Dietary advice based on the glycaemic index improves dietary profile and metabolic control in type 2 diabetic patients, in “Diabetic Medicine”, 11, 1994, p. 397.

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.

91. Brand J. et al., Low-glycemic index foods improve long-term glycemic control in NIDDM, in “Diabetes Care”, 14, 1991, p. 95.

110. Mann J., Dietary fibre and diabetes revisited, in “European Journal of Clinical Nutrition”, 55, 2001, pp. 919-21.

92. Fontvieille A. et al., The use of low glycaemic index foods improve metabolic control of diabetic patients over five weeks, in “Diabetic Medicine”, 9, 1992, p. 444.

111. Mann J., Lines to legumes: changing concepts of diabetic diets, in “Diabetic Medicine”, 1, 1984, pp. 191-98.

93. Wolever T. et al., Beneficial effect of a low glycaemic index diet in type 2 diabetes, in “Diabetic Medicine”, 9, 1992, p. 451.

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.

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.

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.

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.

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 noninsulindependent diabetes mellitus in women, in “Journal of the American Medical Association”, 277, 1997, pp. 472-77.

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. e l’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 e R. Giacco, Glycemic index of local foods and diets: the Mediterranean experience, in “Nutrition Reviews”, 61, 2003, p. S56.

99. Si vedano a riguardo, tra gli altri, Foster et al. (2003) e Samaha et al. (2003); tale assenza di efficacia è dovuta probabilmente anche al fatto che diete a basso contenuto di carboidrati risultano essere normalmente ricche di grassi, con un conseguente potenziale effetto negativo sul mantenimento di un ottimale peso corporeo nel lungo periodo e sulla sensibilità insulinica: si vedano al riguardo anche Vessby et al. (2001); Toeller et al. (2001) e 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. A tal riguardo si veda il recente position statement pubblicato nel gennaio 2008 dall’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 noninsulindependent 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.

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. La sindrome metabolica è identificata come la presenza contemporanea di tre o più dei seguenti elementi: obesità addominale (circonferenza addominale superiore a 102 cm per gli uomini, superiore a 88 cm per le donne), alti livelli di trigliceridi nel sangue (pari o superiori a 150 mg/dl), bassi livelli di colesterolo HDL (meno di 40 mg/dl per gli uomini, meno di 50 mg/dl per le donne), pressione alta (pari o superiore a 130/85 mmHg) e alti livelli di glucosio nel sangue a digiuno (pari o superiori a 100 mg/dl). (Fonte: American Heart Association).

120. Poppitt S.D. et al., Long term effects of ad libitum low-fat highcarbohydrate 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.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

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.

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.

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

279. Kelley J. R. e J. M. Duggan, Gastric cancer epidemiology and risk factors, in “Journal of Clinical Epidemiology”, 56, 2003, pp. 1-9.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

246. Michels K. B., Prospective study of fruit and vegetable consumption and incidence of colon and rectal cancers, in “Journal of the National Cancer Institute”, 92, 2000, pp. 1740-52.

264. Giovannucci E., The epidemiology of vitamin D and colorectal cancer: recent findings, in “Current Opinion in Gastroenterology”, 22, 2006, pp. 24-29; Giovannucci E., Y. Liu ed E. B. Rimm, Prospective study of predictors of vitamin D status and cancer incidence and mortality in men, in “Journal of the National Cancer Institute”, 98, 2006, pp. 451-59.

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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 e 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.

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286. Il beta-amiloide è il maggior costituente delle placche senili, formazioni extracellulari che rappresentano una delle caratteristiche microscopiche principali del morbo di Alzheimer, in quanto una produzione anomala di beta-amiloide è la causa di molte malattie neurodegenerative.

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.

295. Misonou H., M. Morishima-Kawashima e Y. Ihara, Oxidative stress induces intracellular accumulation of amyloid B-protein (AB) in human neuroblastoma Cells, in “Biochemistry”, 39, 2000, pp. 6951-59.

296. Ortega R. M. et al., Dietary intake and cognitive function in a group of elderly People, in “American Journal of Clinical Nutrition”, 66, 1997, pp. 803-09.

297. The 9th International Conference on “Alzheimer’s Disease and Related Disorders” in Philadelphia, July 17-22, 2004; Kang J., Fruit and Vegetable Consumption and Cognitive Decline in Women, pp. 2-283.

298. Weinreb O. et al., Neurological mechanisms of green tea polyphenols in Alzheimer’s and Parkinson’s diseases, in Eve Topf and US National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research and Department of Pharmacology, “Rappaport Family Research Institute”, Technion-Faculty of Medicine, Haifa, 2004.

299. L’omocisteina è un amminoacido contenente zolfo che si forma in seguito alla trasformazione enzimatica della metionina, un altro aminoacido solforato presente negli alimenti proteici (latticini, carne, legumi, uova). Se presente in eccesso nel circolo sanguigno (iperomocisteinemia) l’omocisteina causa danni addirittura superiori rispetto a quelli causati dal

300. Leblhuber F. et al., Hyperhomocysteinemia in dementia, in “Journal of Neural Transmission”, 2000.

301. Per un approfondimento, si rimanda al paragrafo 5.2 del presente position paper, riguardante il tema della “restrizione calorica e longevità”.

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, Ginevra 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. Raccomandazioni del Ministero della Salute sul corretto utilizzo degli integratori alimentari, Ministero della Salute del governo Italiano, 2005.

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 e 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, Ginevra.

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.

317. Kitchin B. e 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.

318. Miggiano G. A. e L. Gagliardi, Diet, nutrition and bone health, Centro di Ricerche in Nutrizione Umana, Istituto di Biochimica e Biochimica Clinica, Facoltà di Medicina e Chirurgia, Università Cattolica S. Cuore, Roma 2005.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

285. Behl C. e F. Holsboer, Oxidative stress in the pathogenesis of Alzheimer’s and antioxidant neuroprotection, in “Fortschr Neurologie-Psychiatrie”, 66, 1998, pp. 113-21.

colesterolo. Per questo essa viene considerata un fattore di rischio indipendente, poiché da sola è in grado di aumentare l’incidenza di malattie cardiovascolari indipendentemente dalla presenza di altri fattori predisponenti. Già valori superiori a 10-12 μmoli per litro si correlano a un aumentato rischio di aterosclerosi, ictus e infarto del miocardio, nonché di molte altre patologie sia del sistema cardiocircolatorio (trombosi venosa, embolia polmonare) che non (malformazioni fetali, decadimento mentale, Alzheimer, fratture spontanee).

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CAPITOLO 3 1. Per un’approfondita analisi in merito a questo tema, si veda il documento Crescita sana e nutrizione nei bambini, pubblicato dal BCFN nel 2010.

2. WHO, Food and Nutrition Board, Società Italiana di Nutrizione Umana.

3. Per un’approfondita analisi in merito a questo tema, si veda il documento Longevità e benessere: il ruolo dell’alimentazione, pubblicato dal BCFN nel 2011.

4. “National Vital Statistics Reports”, 56(10), 2008 5. Sears B. e C. Ricordi, Anti-infiammatory nutrition as a Pharmacological Approach to treat Obesity, in “Journal of obesity”, 2011.

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7. A tal riguardo, si vedano anche: Fontana L., Obesità viscerale, restrizione calorica ed invecchiamento, in “Giornale di Gerontologia”, 54, 2006, pp. 131-33; Weindruch R. e 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.

8. Albanes D., Cancer Research, 1987.

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.

CAPITOLO 4 1. Per l’Italia si vedano le Linee Guida per una sana alimentazione italiana, identificate nel 2003 dall’Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN).

2. Agriculture Fact Book, Profiling Food Consumption in America, 2002.

3. National Nutrition Survey, The Japan Dietetic Association, 2001.

4. Cucina Mediterranea. Ingredienti, principi dietetici e ricette al sapore di sole, Mondadori, Milano 1993.

5. Ancel Benjamin Keys (1904-2004), medico e fisiologo statunitense, è conosciuto per essere stato uno dei principali sostenitori dei benefici della dieta mediterranea per contrastare molte patologie diffuse soprattutto in Occidente, in particolare le malattie cardiovascolari.

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 e 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. e A. Menotti, The Seven Countries Study: A Scientific Adventure in Cardiovascular Disease Epidemiology, Brouwer, Utrecht 1994.

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 ofall-cause mortality in a U.S. population: results from the NIH-AARP Diet and Health Study, in “Archives of Internal Medicine”, 2007.

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.

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

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.

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

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

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.

CAPITOLO 5 1. Ad esempio, l’Agenzia per i Servizi Sanitari Regionali (ASSR).

2. La scelta dei Paesi è stata dettata dalla disponibilità di serie statistiche ampie, complete e omogenee; per l’Italia questo requisito non è presente in quanto non è disponibile una serie storica sufficientemente ampia.

3. Il modello ha preso in considerazione due componenti la cui evoluzione e interazione determinerà la dinamica della spesa sanitaria pubblica nei prossimi anni. La prima è di tipo demografico, ovvero connessa al numero e alla struttura per sesso e per età della popolazione.

La seconda è di tipo economico, imputabile a una propensione, riscontrabile in tutte le società avanzate, verso una crescita della spesa sanitaria complessiva (pubblica e privata) più che proporzionale rispetto alla crescita del PIL. Per una descrizione dettagliata della metodologia e dei risultati del modello di previsione della spesa sanitaria si veda: The European HouseAmbrosetti, Meridiano Sanità – Le coordinate della salute, Rapporto Finale, novembre 2011.

4. L’ipotesi che il beneficio della prevenzione si manifesti come diminuzione delle spese per una qualsiasi altra tipologia di prestazioni definita nell’ambito del modello previsionale non impatta sul valore totale del beneficio, ma sulla ripartizione della spesa sanitaria tra tipologie di prestazioni.

9. Willett W. C., F. Sacks e A. Trichopoulou, Mediterranean diet pyramid: a cultural model for healthy eating, in “American Journal of Clinical Nutrition”, 1995.

5. L’assunto può essere ritenuto ragionevole se si considera il contenuto livello dell’investimento in prevenzione e la sua bassa incidenza sulla spesa sanitaria pubblica. Per valori più consistenti dell’investimento in prevenzione e/o della sua incidenza sulla spesa sanitaria pubblica è plausibile ritenere che il trend del beneficio manifesti un andamento decrescente al crescere del valore dell’investimento.

10. Panagiotakosa D., C. Pitsavosd e 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.

6. Lewington S. et al., Age-specific relevance of usual blood pressure to vascular mortality: a metaanalysis of individual data for one million adults in 61 prospective studies, in “Lancet”, 360, 2002, pp. 1903-13.

Alimentazione e benessere per una vita sana

Alimentazione e benessere per una vita sana

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

11. La scala utilizzata nello studio è compresa tra 0 e 55, quindi un incremento di 10 punti sulla scala di adeguatezza mediterranea equivale a un incremento del 20% circa.

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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.

Alimentazione e benessere per una vita sana

CAPITOLO 6

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1. Il BCFN ha analizzato a fondo le valenze sociali e culturali del cibo e le dinamiche in atto all’interno del rapporto dialettico fra l’uomo e il cibo. Per approfondire questo tema, sempre più centrale, si rimanda a tre documenti che il BCFN ha prodotto nel corso degli ultimi ventiquattro mesi: La dimensione culturale del cibo (2009), Il valore della Mediterraneità (2010) e il fascicolo Food for Culture del presente rapporto.

2. Questo stile alimentare, peraltro – e questa è un’ulteriore evidenza emersa nel corso dei confronti interdisciplinari condotti dal BCFN – non solo costituisce un’efficace tutela per le persone dal punto di vista medico, ma è altresì “amico dell’ambiente”. Le evidenze scientifiche in ambito di water management e climate change (si vedano i position paper Water Management e Cambiamento Climatico, Agricoltura e Alimentazione) dimostrano come le implicazioni per l’ambiente delle scelte produttive legate agli stili dietetici siano molto rilevanti, sia in positivo che in negativo. Nel secondo position paper citato abbiamo, infatti, potuto costruire la piramide ambientale associata alla nota piramide alimentare, dimostrando come una dieta sana ed equilibrata si caratterizzi per il suo basso impatto ambientale, misurato in termini di footprint complessivo.