Table 1 Age Adjusted Mortality in CHD(1985) (rate/ person/year) Fig. 1 The Cause of Death. (K. Uemura, Z. Pisa)

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1 The Forefront of Lipid Nutrition Kazuo KONDO and Tamami IWAMOTO The National Institute of Health and Nutrition (1-23-1, Toyama, Shinjyuku-ku Tokyo, 162) Abstract : The mortality of heart disease in Japan remains very low compared with that in the United States, France and the United Kingdom. Genetic factors presumably play a large part in this difference but lifestyle, together with recent efforts in understanding dietary contributions through clinical nutrition research also plays an important role. Many studies have confirmed that while saturated fatty acids increase serum cholesterol levels, polyunsaturated fatty acids, especially n-6 fatty acids decrease serum cholesterol levels. However, the biological down-side of increasing n-6 fatty acid levels is an increase in susceptibility of LDL to oxidation : when associated with oxidative changes to PUFA-rich LDL, the result is that an increased atherogenesity of this lipoprotein intake is an increased susceptibility of LDL to oxidation. With this in mind, an analysis of the current Japanese fat intake suggests that the present levels of consumption regarding both quantity and quality of fat are ideal for preventing the current low levels of atherosclerosis in this country. Key word : clinical nutrition, atherosclerosis, fatty acid, fat intake, LDL oxidation

2 Table 1 Age Adjusted Mortality in CHD(1985) (rate/ person/year) Fig. 1 The Cause of Death. (K. Uemura, Z. Pisa)

3 Fig. 2 The Percent Distribution of Nutrients Consumed in Japan. Fig. 3 Ten-year Coronary Death Rates of the Cohorts Plotted against the Percentage of Dietary Calories Supplied by Saturated Fatty Acids. B, Belgrade ; C, Crevalcore ; D, Dalmatia ; E, east Finland ; G, Corfu ; J, Ushibuka ; K, Crete ; M, Montegiorgia ; N, Zutphen ; R, Rome railroad ; S, Slavonia ; T, Tanushimaru ; U, American railroad ; V, Velika Krsna ; W, west Finland ; Z, Zrenjanin. [From Keys (1980), with permision.] Fig. 4 Fat Intake in United Kingdom and Japan.

4 Fig. 5 The Relationship between Fat Consumption and Life Expectancy. Fig. 6 Fatty Acid Structure.

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6 Fig. 7 The Mechanism of Arteriosclerosis. Fig. 8 The Mechanism of Arteriosclerosis.

7 Fig. 11 The Mechanism of Arteriosclerosis. Fig. 9 Metabolism of LDL Fig. 10 Hypothesis of Modified LDL-Scavenger Receptor.

8 Fig. 14 Flavonoid Intake and CHD Risk. Fig. 12 CHD Mortality and Butterfat Consumption. (Renaud, S. : Lancet 339 : , 1992) Fig. 13 LDL Oxidation in Volunteers with Red Wine Intake Values are Means (SE). *paired t test.

9 1) H.B. Brown, J. Am. Diet. Assor., 58, 303 (1971). 2) S. Rinzler, Bull. N.Y. Acad. Med., 44, 936 (1968). 3) S. Dayton, Circulation, 40 (Suppl II), II-1 (1969). 4) O. Turpeinen et al., Am. J. Clin. Nutr., 21, 255 (1968). 5) M. Miettinen et al., Lancet ii, 835 (1972). 6) A. Keys, J.T. Anderson, F. Grande, Lancet i, 66 (1957). 7) D.M. Hegsted, R.B. Mc Gandy, M.I. Myers et al., Am. J. Clin. Nutr., 17, 281 (1965). 8) D.K. Spady, J.M. Dietschy, Proc. Natl. Acad. Sci. USA, 82, 4526 (1985). 9) R.J. Nicolosi, A.F. Stucchi, M.C. Kowala et al., Arteriosclerosis, 10, 119 (1990). 10) J.C. Fox, H.C. McGill, Jr. K.D. Carey et al., J. Biol. Chem., 262, 7014 (1987). 11) M. Sorci-Thomas, M.D. Wilson, F.L. Johnson et al., J. Biol. Chem., 264, 9039 (1989). 12) A. Bonanome, S.M. Grundy, J. Nutr., 119, 1556 (1989). 13) J. Dyerberg et al., Am. J. Clin. Nutr., 28, 958 (1975). 14) P.J. Nestel, W.E. Connor, M.F. Reardon et al., J. Clin. Invest., 74, 82 (1984). 15) R.A. Failor, M.T. Childs E.L. Bierman, Metabolism, 37, 1021 (1988). 16) K. Kondo et al., Lancet, 344, 1152 (1994) 17) M.G.L. Hertog et al., Lancet, 342, 1007 (1993). 18) M.G.L. Hertog et al., Arch Intern. Med., 155, 381 (1995). 19) P. Kenkt et al., British Med. J., 312, 478 (1996).

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