Bibligrafia: Dieta wegańska Rastafarianizm

2005-2006

1. Chung, Carolyn S.; King, Janet C. Zinc. Encyclopedia of Dietary Supplements (2005), 791-800.

Abstract

A review. Zinc is the most abundant intracellular trace element, and is present in every living cell in the body and has many diverse biol. functions. Because zinc is a component of many enzymes involved in the synthesis and degrdn. of carbohydrates, lipids, proteins, nucleic acids, and gene expression, as well as in the metab. of other nutrients. Groups at risk of zinc deficiency include those with high zinc needs such as preterm infants, growing children and adolescents, and pregnant and lactating women. Dietary zinc intakes in the United States are adequate for most groups, with the exception of vegans, who may not consume fortified cereals, and possibly the elderly. Supplemental zinc has been used to treat a variety of diseases; however, not all disease outcomes are improved. The biochem. and physiol. functions, metab., indications, usage, and adverse interactions of zinc are discussed.

Indexing -- Section 18-0 (Animal Nutrition)

Section cross-reference(s): 1, 13

Dietary supplements

Disease, animal

Human

Metabolism, animal

Nutrition, animal

(biochem., physiol. functions, metab., indications, usage, and adverse interactions of zinc)

7440-66-6, Zinc, biological studies

Role: BSU (Biological study, unclassified); PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(biochem., physiol. functions, metab., indications, usage, and adverse interactions of zinc)

Supplementary Terms

review zinc diet supplement metab disease nutrition

Citations

1) Iznc Group; Food Nutr Bull 2004, 2(1 Suppl 2), S91

2) Prasad, A; Am J Med 1961, 31, 532

3) Da Silva, J; The Biological Chemistry of the Elements:The Inorganic Chemistry of Life 1991, 1

4) Cousins, R; Annu Rev Nutr 1994, 14, 449

5) Vallee, B; Physiol Rev 1993, 73, 79

6) Cousins, R; Present Knowledge in Nutrition 1996, 293

7) Klug, A; Tr Biochem Sci 1987, 12, 464

8) Cousins, R; J Infect Dis 2000, 182(Suppl 1), S81

9) Cui, L; J Nutr 2003, 133, 51

10) Powell, S; J Nutr 2000, 130(5), 1447S

11) Cousins, R; J Nutr 2003, 133(5 Suppl 1), 1521S

12) Thompson, C; Science 1995, 267, 1456

13) Thornalley, P; Biochim Biophys Acta 1985, 827, 36

14) Lichtlen, P; Nucleic Acids Res 2001, 29(7), 1514

15) Jiang, H; J Biol Chem 2003, 278(32), 30394

16) Otsuka, F; Biochim Biophys Acta (BBA)-Gene Struct Expr 2000, 1492(2-3), 330

17) Cousins, R; Proc Natl Acad Sci U S A 2003, 100(12), 6952

18) Huse, M; J Biol Chem 1998, 273(30), 18729

19) Maret, W; Proc Natl Acad Sci 2001, 98(22), 12325

20) Frederickson, C; J Nutr 2000, 130(5), 1471S

21) Rivera, J; J Nutr 1998, 128, 556

22) King, J; Modern Nutrition in Health and Disease 1999, 223

23) Truong-Tran, A; J Nutr 2000, 130(5), 1459S

24) Eide, D; Pflugers Arch Eur J Physiol 2004, 447, 796

25) Palmiter, R; Pflugers Arch Eur J Physiol 2004, 447, 744

26) Liuzzi, J; J Nutr 2003, 133(2), 342

27) Dufner-Beattie, J; J Biol Chem 2003, 278(50), 50142

28) McMahon, R; J Nutr 1998, 128, 667

29) Solomons, N; Absorption and Malabsorption of Mineral Nutrients 1984, 125

30) Lee, H; Am J Physiol 1989, 256, G87

31) Matseshe, J; Am J Clin Nutr 1980, 33, 1946

32) Institute Of Medicine; Dietary Reference Intakes:Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2002

33) Fung, E; Am J Clin Nutr 1997, 66, 80

34) Morgan, P; FASEB J 1990, 4, A648

35) Baer, M; Am J Clin Nutr 1984, 39, 556

36) Moser-Veillon, P; Analyst 1995, 120, 895

37) King, J; J Nutr 1990, 120, 1474

38) Gordon, P; Am J Clin Nutr 1982, 35, 113

39) Falchuck, K; N Engl J Med 1977, 296, 1129

40) Fell, G; Lancet 1973, 2, 280

41) King, J; J Nutr 1994, 124, 508

42) Cao, J; J Nutr 2000, 130(9), 2180

43) Jackson, M; J Clin Pathol 1977, 30, 284

44) Cousins, R; Zinc in Human Biology 1989, 79

45) Lowe, N; Am J Clin Nutr 1997, 65, 1810

46) Milne, D; Clin Chem 1985, 31, 65

47) Foster, D; Am J Physiol 1979, 237, R340

48) Wastney, M; Am J Physiol 1986, 251, R398

49) Dunn, M; Am J Physiol 1989, 256, E420

50) Miller, L; J Nutr 1994, 124, 268

51) Emmert, J; Poult Sci 1995, 74, 1011

52) Diaz-Gomez, N; Pediatrics 2003, 111(5), 1002

53) Morgan, P; FASEB J 1993, 5, A930

54) Hambidge, M; J Nutr 2000, 130, 1344S

55) Jackson, M; Br J Nutr 1984, 51, 199

56) Seal, C; J Nutr 1985, 115, 986

57) Victery, W; Am J Physiol 1981, 240, F299

58) Cousins, R; J Nutr 2000, 130(Suppl 5S), 1384S

59) Swanson, C; Am J Clin Nutr 1987, 46, 763

60) Michalczyk, A; Hum Genet 2003, 113, 202

61) Sandstead, H; Am J Dis Child 1991, 145(8), 853

62) Gibson, R; Nutr Res Rev 1994, 7, 151

63) Black, M; Am J Clin Nutr 1998, 68(Suppl), 464S

64) Subar, A; J Am Diet Assoc 1998, 98(5), 537

65) Ma, J; J Nutr 2000, 130(11), 2838

66) Sandstrom, B; Zinc in Human Biology 1989, 57

67) Wood, R; Am J Clin Nutr 1997, 65, 1803

68) Hunt, J; Am J Clin Nutr 1995, 62, 621

69) Sandstrom, B; Proc Nutr Soc 1992, 51, 211

70) World Health Organization; Trace Elements in Human Nutrition and Health 1996

71) Sandstrom, B; Dietary pattern and zinc supply Zinc in Human Biology 1989, 350

72) Briefel, R; J Nutr 2000, 130(5), 1367S

73) Ervin, R; J Nutr 2002, 132(11), 3422

74) Brown, K; Am J Cin Nutr 2002, 75, 1062

75) Bates, C; Br J Nutr 1993, 69, 243

76) Ruel, M; Pediatrics 1997, 99(6), 808

77) Sazawal, S; Am J Clin Nutr 1997, 66, 413

78) Sazawal, S; Pediatrics 1998, 102, 1

79) Shankar, A; Am J Trop Med Hyg 2000, 62(6), 663

80) World Health Organization; WHO/UNICEF Joint Statement:Clinical Management of Acute Diarrhoea 2004, 1

81) Anon; Nutr Rev 1997, 55, 82

82) Jackson, J; Arch Int Med 1997, 157, 2373

83) Garland, M; Ann Pharmacother 1998, 32, 63

84) Licastro, F; Biol Trace Elem Res 1996, 51, 55

85) Cuajungco, M; Brain Res Rev 1997, 23, 219

86) Zemel, B; Am J Clin Nutr 2002, 75(2), 300

87) Ferenci, P; Aliment Pharmacol Ther 2004, 19(2), 157

88) Turnlund, J; Modern Nutrition in Health and Disease 1994, 231

89) Arsenault, J; Am J Clin Nutr 2003, 78(5), 1011

90) Yadrick, M; Am J Clin Nutr 1989, 49(1), 145

91) Black, M; Am J Clin Nutr 1988, 47(6), 970

92) Hooper, P; J Am Med Assoc 1980, 244(17), 1960

93) Samman, S; Atherosclerosis 1988, 70(3), 247

94) Solomons, N; Am J Clin Nutr 1981, 34, 475

95) Solomons, N; J Nutr 1983, 113, 337

96) Solomons, N; J Lab Clin Med 1979, 94, 335

2. Larsson Christel L; Johansson Gunnar K Young Swedish vegans have different sources of nutrients than young omnivores. Journal of the American Dietetic Association (2005), 105(9), 1438-41.

Abstract

The aim of this study was to identify sources of nutrients in diets of young Swedish vegans and omnivores. Three months of dietary intakes were investigated by diet history interviews. Volunteers were recruited through advertising and visits to schools in the city of Umea, Sweden. Thirty vegans, 15 female and 15 male, aged 17.5+/-1.0 years, were compared with 30 sex-, age-, and height-matched omnivores. Vegans had different sources of nutrients than young omnivores and relied to a great extent on dietary supplements as a source of vitamin B-12, vitamin D, calcium, and selenium. Dietary intake of vegetables, fruits, and berries exceeded 500 g/day for 21 of the 30 vegans, whereas the same held true for only 1 of the 30 omnivores. Instead of animal products, young vegans rely on dietary supplements, legumes, vegetables, fruits, and berries as sources of nutrients.

Controlled Terms

Check Tags: Female; Male

Adolescent

*Adolescent Nutrition Physiology

Adult

Case-Control Studies

*Diet: ST, standards

*Diet, Vegetarian

Dietary Carbohydrates: AD, administration & dosage

Dietary Fats: AD, administration & dosage

Dietary Fiber: AD, administration & dosage

*Dietary Proteins: AD, administration & dosage

Dietary Supplements

Humans

*Minerals: AD, administration & dosage

Nutrition Assessment

Nutritive Value

Sweden

*Vitamins: AD, administration & dosage

Chemical Names

0 (Dietary Carbohydrates)

0 (Dietary Fats)

0 (Dietary Proteins)

0 (Minerals)

0 (Vitamins)

3. Skoldstam Lars; Brudin Lars; Hagfors Linda; Johansson Gunnar Weight reduction is not a major reason for improvement in rheumatoid arthritis from lacto-vegetarian, vegan or Mediterranean diets. Nutrition journal (2005), 4 15.

Abstract

OBJECTIVES: Several investigators have reported that clinical improvements of patients with rheumatoid arthritis (RA), from participating in therapeutic diet intervention studies, have been accompanied by loss of body weight. This has raised the question whether weight reduction per se can improve RA. In order to test this hypothesis, three previously conducted diet intervention studies, comprising 95 patients with RA, were pooled. Together with Age, Gender, and Disease Duration, change during the test period in body weight, characterised dichotomously as reduction or no reduction (dichoDeltaBody Weight), as well as Diet (dichotomously as ordinary diet or test diet), were the independent variables. Dependent variables were the difference (Delta) from baseline to conclusion of the study in five different disease outcome measures. DeltaESR and DeltaPain Score were both characterised numerically and dichotomously (improvement or no improvement). DeltaAcute Phase Response, DeltaPhysical Function, and DeltaTender Joint Count were characterised dichotomously only. Multiple logistic regression was used to analyse associations between the independent and the disease outcome variables. RESULTS: Statistically significant correlations were found between Diet and three disease outcome variables i.e. DeltaAcute-Phase Response, DeltaPain Score, and DeltaPhysical Function. Delta Body Weight was univariately only correlated to DeltaAcute-Phase Response but not significant when diet was taken into account. CONCLUSION: Body weight reduction did not significantly contribute to the improvement in rheumatoid arthritis when eating lacto-vegetarian, vegan or Mediterranean diets.

Controlled Terms

Check Tags: Female; Male

Activities of Daily Living

Acute-Phase Reaction

Analysis of Variance

*Arthritis, Rheumatoid: DT, drug therapy

Cross-Over Studies

*Diet, Mediterranean

*Diet, Vegetarian

Humans

Middle Aged

Pain Measurement

Prospective Studies

Questionnaires

Treatment Outcome

*Weight Loss

4. Allen, Lindsay H.; Jones, Katharine M. Vitamin B12. Encyclopedia of Dietary Supplements (2005), 735-744.

Abstract

A review. The article highlights several new aspects of the knowledge of vitamin B12. The more important issues include the much higher global prevalence of this deficiency than is generally recognized and the fact that higher risk of depletion. Deficiency also occurs more rapidly than was formerly believed, esp. in people whose stores are relatively depleted or who malabsorb the vitamin.

Indexing -- Section 18-0 (Animal Nutrition)

Section cross-reference(s): 14, 17

Development, mammalian postnatal

(child; methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Disease, animal

(deficiency; methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Diet

Food

Human

Newborn

Pregnancy

(dietary requirements and food sources of vitamin B12)

Aging, animal

(elderly; dietary requirements and food sources of vitamin B12)

Development, mammalian postnatal

(infant; dietary requirements and food sources of vitamin B12)

Anemia (disease)

(megaloblastic anemia; methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Biological transport

Nutrition, animal

(methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Coenzymes

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Nerve, disease

(neuropathy; methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

68-19-9, Vitamin B12

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(methods for evaluating vitamin B12 status, causes of deficiency, and consequences of deficiency)

Supplementary Terms

review vitamin B 12 vegan lacto vegetarian diet deficiency; nutrition food recommended intake anemia neuropathy immune system review

Citations

1) Institute of Medicine; Dietary Reference Intakes: Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline 2000

2) Schneider, R; J Clin Invest 1976, 57, 27

3) Meyers, P; Pediatrics 1984, 74, 866

4) Grasbeck, R; Clin Biochem 1984, 17, 99

5) Compher, C; J Parenter Enteral Nutr 2002, 26, 57

6) Alexander, D; Eur J Clin Nutr 1994, 48, 538

7) Helman, A; Am J Clin Nutr 1987, 45, 785

8) Herrmann, W; Am J Clin Nutr 2003, 78, 131

9) Hellegers, A; Am J Clin Nutr 1957, 5, 327

10) Shojania, A; Can Med Assoc J 1983, 126, 244

11) Pardo, J; Hum Reprod 2000, 15, 224

12) Stoll, C; Reprod Toxicol 1999, 13, 53

13) Frery, N; Eur J Obstet Gynecol Reprod Biol 1992, 45, 155

14) Vollset, S; Am J Clin Nutr 2000, 71, 962

15) Levine, R; Am J Obstet Gynecol 2002, 186, 1107

16) Bondevik, G; Eur J Clin Nutr 2001, 55, 856

17) Giugliani, E; Am J Clin Nutr 1985, 41, 330

18) Specker, B; Am J Clin Nutr 1988, 47, 89

19) Schneede, J; Pediatr Res 1994, 36, 194

20) Lindenbaum, J; Am J Clin Nutr 1994, 60, 2

21) Rogers, L; Am J Clin Nutr 2003, 77(2), 433

22) Holleland, G; Clin Chem 1999, 45, 189

23) Carmel, R; Arch Intern Med 1996, 156, 1097

24) Suter, P; Gastroenterology 1991, 101, 1039

25) Carmel, R; Dig Dis Sci 1994, 39, 309

26) Herrmann, W; Clin Chim Acta 2002, 326, 47

27) Refsum, H; Am J Clin Nutr 2001, 74, 233

28) Louwman, M; Am J Clin Nutr 2000, 72, 762

29) Healton, E; Medicine (Baltimore) 1991, 70, 229

30) Campbell, A; J Nutr in press

31) Allen, L; Adv Exp Med Biol 2002, 503, 57

32) Wighton, M; Med J Aust 1979, 2, 1

33) Graham, S; J Pediatr 1992, 121, 710

34) Dagnelie, P; Am J Clin Nutr 1994, 59, 1187S

35) Tamura, J; Clin Exp Immunol 1999, 116, 28

36) Haddad, E; Am J Clin Nutr 1999, 70, 586S

5. Goff, L. M.; Bell, J. D.; So, P-W.; Dornhorst, A.; Frost, G. S. Veganism and its relationship with insulin resistance and intramyocellular lipid. European Journal of Clinical Nutrition (2005), 59(2), 291-298.

Abstract

Objective: To test the hypothesis that dietary factors in the vegan diet lead to improved insulin sensitivity and lower intramyocellular lipid (IMCL) storage. Design: Case-control study. Setting: Imperial College School of Medicine, Hammersmith Hospital Campus, London, UK. Subjects: A total of 24 vegans and 25 omnivores participated in this study; three vegan subjects could not be matched therefore the matched results are shown for 21 vegans and 25 omnivores. The subjects were matched for gender, age and body mass index (BMI). Interventions: Full anthropometry, 7-day dietary assessment and phys. activity levels were obtained. Insulin sensitivity (%S) and beta-cell function (%B) were detd. using the homeostatic model assessment (HOMA). IMCL levels were detd. using in vivo proton magnetic resonance spectroscopy; total body fat content was assessed by bioelec. impedance. Results: There was no difference between the groups in sex, age, BMI, waist measurement, percentage body fat, activity levels and energy intake. Vegans had a significantly lower systolic blood pressure (-11.0 mmHg, CI -20.6 to -1.3, P=0.027) and higher dietary intake of carbohydrate (10.7%, CI 6.8-14.5, P<0.001), nonstarch polysaccharides (20.7 g, CI 15.8-25.6, P<0.001) and polyunsatd. fat (2.8%, CI 1.0-4.6, P=0.003), with a significantly lower glycemic index (-3.7, CI -6.7 to -0.7, P=0.01). Also, vegans had lower fasting plasma triacylglycerol (-0.7 mmol/l, CI -0.9 to -0.4, P<0.001) and glucose (-0.4 mmol/l, CI -0.7 to -0.09, P=0.05) concns. There was no significant difference in HOMA %S but there was with HOMA %B (32.1%, CI 10.3-53.9, P=0.005), while IMCL levels were significantly lower in the soleus muscle (-9.7, CI -16.2 to -3.3, P=0.01). Conclusion: Vegans have a food intake and a biochem. profile that will be expected to be cardioprotective, with lower IMCL accumulation and beta-cell protective. Sponsorship: MRC PhD studentship.

Indexing -- Section 18-4 (Animal Nutrition)

Section cross-reference(s): 14

Carbohydrates, biological studies

Fats and Glyceridic oils, biological studies

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(dietary; veganism and its relationship with insulin resistance and intramyocellular lipid)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(monounsatd., dietary; veganism and its relationship with insulin resistance and intramyocellular lipid)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., dietary; veganism and its relationship with insulin resistance and intramyocellular lipid)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(satd., dietary; veganism and its relationship with insulin resistance and intramyocellular lipid)

Dietary energy

Human

Muscle

(veganism and its relationship with insulin resistance and intramyocellular lipid)

Glycerides, biological studies

High-density lipoproteins

Low-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(veganism and its relationship with insulin resistance and intramyocellular lipid)

Diet

(vegetarian; veganism and its relationship with insulin resistance and intramyocellular lipid)

Pancreatic islet of Langerhans

(-cell; veganism and its relationship with insulin resistance and intramyocellular lipid)

50-99-7, D-Glucose, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(glycemia; veganism and its relationship with insulin resistance and intramyocellular lipid)

9004-10-8, Insulin, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(resistance; veganism and its relationship with insulin resistance and intramyocellular lipid)

57-88-5, Cholesterol, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(veganism and its relationship with insulin resistance and intramyocellular lipid)

Supplementary Terms

vegan diet insulin sensitivity muscle lipid

Citations

Albano, J; Acta Endocrinol 1972, 70, 487

Appleby, P; Am J Clin Nutr 1999, 70, 525S

Baecke, J; Am J Clin Nutr 1982, 36, 936

Brechtel, K; Mag Res Med 2001, 45, 179

Burr, M; Am J Clin Nutr 1982, 36, 873

Coulston, A; Metabolism 1985, 34, 962

Department of Health; Report of the Panel on Dietary Reference Values of the Committee on Medical Aspects of Food Policy 1991

Dwyer, J; Am J Clin Nutr 1988, 48, 712

Falholt, K; Diabet Med 1988, 5, 27

Feskens, E; Diabet Care 1995, 18, 1104

Forouhi, N; Diabetologia 1999, 42, 932

Foster, P; Am J Clin Nutr 1995, 62, 871S

Frentzel-Beyme, R; Nutr Cancer 1988, 11, 117

Friedwald, W; Clin Chem 1972, 18, 499

Frost, G; Metabolism 1996, 45, 669

Hermans, M; Diabetologia 1999, 42, 678

Jacob, S; Diabetes 1999, 48, 1113

Key, T; Proc Nutr Soc 1999, 58, 271

Key, T; Am J Clin Nutr 1999, 70, 516S

Krssak, M; Diabetologia 1999, 42, 113

Krssak, M; Proc Int Soc Mag Reson Med 2000, 8

Marshall, J; Diabet Care 1994, 17, 50

McGarry, J; Diabetologia 1999, 42, 128

McGarry, J; Diabetes 2002, 51, 7

Nelson, M; A Photographic Atlas of Food Portion Sizes 1997

Nicholson, A; Prev Med 1999, 29, 87

Pan, D; Diabetes 1997, 46, 983

Phillips, D; Metabolism 1996, 45, 947

Randle, P; Lancet 1963, 1, 785

Reiser, S; Am J Clin Nutr 1979, 32, 2206

Reiser, S; Am J Clin Nutr 1981, 34, 2348

Rico-Sanz, J; J Physiol 1998, 510, 615

Salmeron, J; Diabet Care 1997, 20, 545

Salmeron, J; JAMA 1997, 277, 472

Sinha, R; Diabetes 2002, 51, 1022

Snowdon, D; Am J Clin Nutr 1988, 48, 739

Szczepaniak, L; Am J Physiol 1999, 276, E977

Thorogood, M; BMJ 1987, 295, 351

Thorogood, M; Community Med 1989, 11, 230

Thorogood, M; BMJ 1990, 300, 1297

Thomas, E; Abstracts of Original Communications 2000, C30

van den Boogaart, A; Proceedings of the ESMRMB (13th Annual Meeting of the ESMRMB) 1996, 318

van Haeften, T; Mol Cell Endocrinol 2002, 197, 197

Vessby, B; Diabetologia 2001, 44, 312

Weiss, R; J Clin Endocrinol Metab 2003, 88, 2014

Wolever, T; Am J Clin Nutr 1986, 43, 167

Wolever, T; Diabet Med 1992, 9, 451

Zimmet, P; Nature 2001, 414, 782

6. Herrmann, Wolfgang; Obeid, Rima; Schorr, Heike; Geisel, Juergen. The usefulness of holotranscobalamin in predicting vitamin B12 status in different clinical settings. Current Drug Metabolism (2005), 6(1), 47-53.

Abstract

Blood serum concns. of homocysteine (Hcy) and methylmalonic acid (MMA) are increased in vitamin B12-deficient subjects and are considered specific markers of vitamin B12 deficiency. Serum levels of holotranscobalamin (holoTC) become decreased before the development of the metabolic dysfunction. We investigated the usefulness of holoTC in diagnosing vitamin B12 deficiency in some clin. settings. Serum concns. of holoTC, MMA, Hcy and total vitamin B12 were measured in omnivores, vegetarians, elderly people, and hemodialysis patients. The incidence of holoTC <35 pmol/L was highest in the vegans (76%). Low holoTC and elevated MMA levels were detected in 64% vegans and 43% lacto- and lacto-ovovegetarians. Elevated MMA and low holoTC levels were found in subjects with total serum vitamin B12 levels as high as 300 pmol/L. The distribution of holoTC in elderly people was similar to that in younger adults (median holoTC 55 pmol/L in both groups). Low holoTC and elevated MMA levels were found in 16% elderly subjects. Elevated MMA and normal holoTC levels were found in 20% elderly subjects with relatively high median serum concns. of creatinine (106.1 mol/L). Serum concns. of holoTC in dialysis patients were considerably higher than in all other groups (median 100 pmol/L). This was also assocd. with severely increased serum levels of MMA (median 987 nmol/L). Thus, blood serum concn. of holoTC is a much better predictor of vitamin B12 status than total vitamin B12 level. This was particularly evident in dietary B12 deficiency. Serum concns. of holoTC and MMA can be affected by renal dysfunction. Elevated MMA and normal holoTC in patients with renal insufficiency may not exclude vitamin B12 deficiency. HoloTC seems not to be a promising marker in evaluating vitamin B12 status in renal patients.

Indexing -- Section 18-2 (Animal Nutrition)

Section cross-reference(s): 14

Blood serum

Disease, animal

Human

Nutrition, animal

(blood serum holotranscobalamin usefulness in predicting vitamin B12 nutritional status in patients in different clin. settings)

Diet

(vegetarian; blood serum holotranscobalamin usefulness in predicting vitamin B12 nutritional status in patients in different clin. settings)

59-30-3, Folic acid, biological studies

60-27-5, Creatinine

6027-13-0, Homocysteine

8059-24-3, Vitamin B6

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood serum holotranscobalamin usefulness in predicting vitamin B nutritional status in patients in different clin. settings)

516-05-2, Methylmalonic acid

708211-52-3, Holo-transcobalamin

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood serum holotranscobalamin usefulness in predicting vitamin B12 nutritional status in patients in different clin. settings)

68-19-9, Vitamin B12

Role: BSU (Biological study, unclassified); FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(blood serum holotranscobalamin usefulness in predicting vitamin B12 nutritional status in patients in different clin. settings)

Supplementary Terms

nutrition vitamin B12 blood holotranscobalamin methylmalonate homocysteine disease

Citations

1) Carmel, R; Annu Rev Med 2000, 51, 357

2) Carmel, R; Am J Hematol 1990, 34, 108

3) Joosten, E; Am J Clin Nutr 1993, 58, 468

4) Henning, B; Res Exp Med 2001, 200, 155

5) Hoffer, L; Clin Invest Med 2004, 27, 10

6) Herrmann, W; Am J Clin Nutr 2003, 78, 131

7) Herrmann, W; Eur J Clin Invest 2000, 30, 1083

8) Lesho, E; Arch Intern Med 1999, 159, 407

9) Obeid, R; Clin Chem 2002, 48, 2064

10) Herrmann, W; Clin Chem Lab Med 2003, 41, 1478

11) Clarke, R; Kidney Int 2003, 84, S131

12) Lindgren, A; Scand J Clin Lab Invest 2002, 62, 15

13) Ulleland, M; Clin Chem 2002, 48, 526

14) Lloyd-Wright, Z; Clin Chem 2003, 49, 2076

15) Nexo, E; Clin Chem 2002, 48, 1768

16) Hvas, A; Clin Chem Lab Med 2003, 41, 1489

17) Allen, R; Metabolism 1993, 42, 978

18) Stabler, S; Blood 1993, 81, 3404

19) Moestrup, S; Proc Natl Acad Sci USA 1996, 93, 8612

20) Herbert, V; Am J Clin Nutr 1988, 48(3 Suppl), 852

21) Herbert, V; Am J Clin Nutr 1994, 59(5 Suppl), 1213S

22) Herrmann, W; Clin Chem 2001, 47, 1094

23) Naurath, H; Lancet 1995, 346, 85

24) Vakur, B; Clin Chem 2004, 50, 1043

25) Lindenbaum, J; Am J Clin Nutr 1994, 60, 2

26) Sipponen, P; Scand J Gastroenterol 2003, 38, 1209

27) Morris, M; J Nutr 2002, 132, 2799

28) Vasan, R; J Am Med Assoc 2003, 289, 1251

29) Ravaglia, G; Am J Clin Nutr 2003, 77, 668

30) Johnson, M; Am J Clin Nutr 2003, 77, 211

31) Miller, J; Am J Clin Nutr 2003, 78, 441

32) Howard, J; Eur J Clin Nutr 1998, 52, 582

33) Obeid, R; Clin Chem 2004, 50, 238

34) Rajan, S; J Am Geriatr Soc 2002, 50, 1789

35) Andres, E; Am J Med 2001, 111, 126

7. McCarty, Mark F. The low-AGE content of low-fat vegan diets could benefit diabetics - though concurrent taurine supplementation may be needed to minimize endogenous AGE production. Medical Hypotheses (2005), 64(2), 394-398.

Abstract

A review. Increased endogenous generation of advanced glycation end-products (AGEs) contributes importantly to the vascular complications of diabetes, in part owing to activation of the pro-inflammatory RAGE receptor. However, AGE-altered oligopeptides with RAGE-activating potential can also be absorbed from the diet, and indeed make a significant contribution to the plasma and tissue pool of AGEs; this contribution is esp. prominent when compromised renal function impairs renal clearance of AGEs. Perhaps surprisingly, foods rich in both protein and fat, and cooked at high heat, tend to be the richest dietary sources of AGEs, whereas low-fat carbohydrate-rich foods tend to be relatively low in AGEs. Conceivably, this reflects the fact that the so-called "AGEs" in the diet are generated primarily, not by glycation reactions, but by interactions between oxidized lipids and protein; such reactions are known to give rise to certain prominent AGEs, such as N-carboxymethyl-lysine and methylglyoxal. Although roasted nuts and fried or broiled tofu are relatively high in AGEs, low-fat plant-derived foods, including boiled or baked beans, typically are low in AGEs. Thus, a low-AGE content may contribute to the many benefits conferred to diabetics by a genuinely low-fat vegan diet. Nonetheless, the plasma AGE content of healthy vegetarians has been reported to be higher than that of omnivores - suggesting that something about vegetarian diets may promote endogenous AGE prodn. Some researchers have proposed that the relatively high-fructose content of vegetarian diets may explain this phenomenon, but there so far is no clin. evidence that normal intakes of fructose have an important impact on AGE prodn. An alternative or addnl. possibility is that the relatively poor taurine status of vegetarians up-regulates the physiol. role of myeloperoxidase-derived oxidants in the generation of AGEs - in which case, taurine supplementation might be expected to suppress elevated AGE prodn. in vegetarians.

Thus, a taurine supplemented low-fat vegan diet may be recommended as a strategy for minimizing AGE-mediated complications in diabetics and in patients with renal failure.

Indexing -- Section 18-0 (Animal Nutrition)

Section cross-reference(s): 14

Glycoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(AGE (advanced glycosylation end product); low-AGE content of low-fat vegan diets could benefit diabetics although concurrent taurine supplementation may be needed to minimize endogenous AGE prodn.)

Diabetes mellitus

Dietary supplements

Human

Nutrition, animal

(low-AGE content of low-fat vegan diets could benefit diabetics although concurrent taurine supplementation may be needed to minimize endogenous AGE prodn.)

Fats and Glyceridic oils, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-AGE content of low-fat vegan diets could benefit diabetics although concurrent taurine supplementation may be needed to minimize endogenous AGE prodn.)

Diet

(vegetarian; low-AGE content of low-fat vegan diets could benefit diabetics although concurrent taurine supplementation may be needed to minimize endogenous AGE prodn.)

107-35-7, Taurine

Role: BSU (Biological study, unclassified); FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(low-AGE content of low-fat vegan diets could benefit diabetics although concurrent taurine supplementation may be needed to minimize endogenous AGE prodn.)

Supplementary Terms

review AGE fat vegan diet diabetes taurine supplementation nutrition

Citations

1) Yamamoto, Y; Ann NY Acad Sci 2000, 902, 163

2) Vlassara, H; J Intern Med 2002, 251, 87

3) Stitt, A; Diabetes 2002, 51, 2826

4) Metz, T; Arch Biochem Biophys 2003, 419, 41

5) Schmidt, A; Trends Endocrinol Metab 2000, 11, 368

6) Yamamoto, Y; Ann NY Acad Sci 2000, 902, 163

7) Wautier, M; Am J Physiol Endocrinol Metab 2001, 280, E685

8) Basta, G; Circulation 2002, 105, 816

9) Wendt, T; Am J Pathol 2003, 162, 1123

10) Wendt, T; J Am Soc Nephrol 2003, 14, 1383

11) Bucala, R; J Clin Invest 1991, 87, 432

12) Hogan, M; J Clin Invest 1992, 90, 1110

13) Wolffenbuttel, B; Proc Natl Acad Sci USA 1998, 95, 4630

14) Aronson, D; J Hypertens 2003, 21, 3

15) Thornalley, P; Arch Biochem Biophys 2003, 419, 31

16) Khalifah, R; Biochem Biophys Res Commun 1999, 257, 251

17) Metz, T; Arch Biochem Biophys 2003, 419, 41

18) Koschinsky, T; Proc Natl Acad Sci USA 1997, 94, 6474

19) Lin, R; Atherosclerosis 2002, 163, 303

20) Zheng, F; Diabetes Metab Res Rev 2002, 18, 224

21) Vlassara, H; Proc Natl Acad Sci USA 2002, 99, 15596

22) Uribarri, J; J Am Soc Nephrol 2003, 14, 728

23) Lin, R; Atherosclerosis 2003, 168, 213

24) Uribarri, J; Am J Kidney Dis 2003, 42, 532

25) Koschinsky, T; Proc Natl Acad Sci USA 1997, 94, 6474

26) Uribarri, J; J Am Soc Nephrol 2003, 14, 728

27) Uribarri, J; Am J Kidney Dis 2003, 42, 532

28) Wendt, T; Am J Pathol 2003, 162, 1123

29) Wendt, T; J Am Soc Nephrol 2003, 14, 1383

30) Zheng, F; Diabetes Metab Res Rev 2002, 18, 224

31) Lin, R; Atherosclerosis 2003, 168, 213

32) Vlassara, H; Proc Natl Acad Sci USA 2002, 99, 15596

33) Kislinger, T; J Biol Chem 1999, 274, 31740

34) Uribarri, J; J Am Soc Nephrol 2003, 14, 728

35) Uribarri, J; J Am Soc Nephrol 2003, 14, 728

36) Teresia, G; Personal communication 2004

37) Vlassara, H; Proc Natl Acad Sci USA 2002, 99, 15596

38) Teresia, G; Personal communication 2004

39) Fu, M; J Biol Chem 1996, 271, 9982

40) Miyata, T; FEBS Lett 1998, 437, 24

41) Alderson, N; Kidney Int 2003, 63, 2123

42) Onorato, J; J Biol Chem 2000, 275, 21177

43) Li, J; J Biol Chem 1997, 272, 16498

44) Tanaka, N; J Biol Chem 2000, 275, 25781

45) Koschinsky, T; Proc Natl Acad Sci USA 1997, 94, 6474

46) Nicholson, A; Prev Med 1999, 29, 87

47) Barnard, R; Diabetes Care 1994, 17, 1469

48) Jenkins, D; Am J Clin Nutr 2003, 78, 610S

49) Sacks, F; Am J Epidemiol 1974, 100, 390

50) Sacks, F; New Engl J Med 1975, 292, 1148

51) Barnard, R; Am J Cardiol 1992, 69, 440

52) Fukagawa, N; Am J Clin Nutr 1990, 52, 524

53) Barsotti, G; Am J Nephrol 1991, 11, 380

54) Barsotti, G; Nephron 1996, 74, 390

55) Nenonen, M; Brit J Rheumatol 1998, 37, 274

56) Donaldson, M; BMC Complement Altern Med 2001, 1, 1

57) Sebekova, K; Eur J Nutr 2001, 40, 275

58) Krajcovicova-Kudlackova, M; Physiol Res 2002, 51, 313

59) Sakai, M; Kobe J Med Sci 2002, 48, 125

60) Levi, B; J Nutr 1998, 128, 1442

61) Lingelbach, L; J Nutr 2000, 130, 1247

62) Anderson, M; J Clin Invest 1997, 99, 424

63) Anderson, M; J Clin Invest 1999, 104, 103

64) Nagai, R; J Biol Chem 2002, 277, 48905

65) Wright, C; Prog Clin Biol Res 1985, 179, 137

66) Laidlaw, S; Am J Clin Nutr 1988, 47, 660

67) Trachtman, H; Am J Physiol 1995, 269, F429

8. Barnard, Neal D.; Scialli, Anthony R.; Turner-McGrievy, Gabrielle; Lanou, Amy J.; Glass, Jolie. The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity. American Journal of Medicine (2005), 118(9), 991-997.

Abstract

This study investigated the effect of a low-fat, plant-based diet on body wt., metab., and insulin sensitivity, while controlling for exercise in free-living individuals. In an outpatient setting, 64 overweight, postmenopausal women were randomly assigned to a low-fat, vegan diet or a control diet based on National Cholesterol Education Program guidelines, without energy intake limits, and were asked to maintain exercise unchanged. Dietary intake, body wt. and compn., resting metabolic rate, thermic effect of food, and insulin sensitivity were measured at baseline and 14 wk. Mean  std. deviation intervention-group body wt. decreased 5.83.2 kg, compared with 3.82.8 kg in the control group (P =.012). In a regression model of predictors of wt. change, including diet group and changes in energy intake, thermic effect of food, resting metabolic rate, and reported energy expenditure, significant effects were found for diet group (P <.05), thermic effect of food (P <.05), and resting metabolic rate (P <.001). An index of insulin sensitivity increased from 4.62.9 to 5.73.9 (P =.017) in the intervention group, but the difference between groups was not significant (P =.17). Adoption of a low-fat, vegan diet was assocd. with significant wt. loss in overweight postmenopausal women, despite the absence of prescribed limits on portion size or energy intake.

Indexing -- Section 18-5 (Animal Nutrition)

Section cross-reference(s): 13

Energy metabolism

Human

Obesity

(low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

Fats and Glyceridic oils, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

Menopause

(postmenopause; low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

Diet

(vegetarian; low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

50-99-7, D-Glucose, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

9004-10-8, Insulin, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat, plant-based dietary intervention effect on body wt., metab., and insulin sensitivity)

Supplementary Terms

vegan diet postmenopause woman energy metab insulin obesity

Citations

1) Kennedy, E; J Am Diet Assoc 2001, 101, 411

2) Appleby, P; Int J Obes Relat Metab Disord 1998, 22, 454

3) Barnard, N; Obstet Gynecol 2000, 95, 245

4) Ornish, D; JAMA 1998, 280, 2001

5) Nicholson, A; Prev Med 1999, 29, 87

6) Barnard, N; J Cardiopulm Rehabil 2004, 24, 229

7) Turner-McGrievy, G; Nutrition 2004, 20, 738

8) Henry, C; Br J Nutr 2003, 89, 811

9) National Cholesterol Education Program; JAMA 1993, 269, 3015

10) Anon; Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) 2002

11) Thompson, F; J Nutr 1994, 124(suppl), 2245S

12) Schaefer, E; Am J Clin Nutr 2000, 71, 746

13) Bouchard, C; Am J Clin Nutr 1983, 37, 461

14) Dempster, P; Med Sci Sports Exerc 1995, 27, 1692

15) Siri, W; Techniques for Measuring Body Composition 1961, 223

16) Kushi, L; Am J Epidemiol 1988, 128, 740

17) Tai, M; Diabetes Care 1994, 17, 152

18) Matsuda, M; Diabetes Care 1999, 22, 1462

19) Barthelmai, W; Klinische Wochenshrift 1962, 40, 585

20) Wadden, T; Ann Intern Med 1993, 119, 688

21) Howarth, N; Nutr Rev 2001, 59, 129

22) Bell, E; Am J Clin Nutr 2001, 73, 1010

23) Duncan, K; Am J Clin Nutr 1983, 37, 763

24) Ravussin, E; J Clin Invest 1985, 76, 1268

25) Lovejoy, J; Metabolism 1998, 47, 1520

26) Hua, N; Br J Nutr 2001, 86, 515

27) McKeown, N; Am J Clin Nutr 2002, 76, 390

28) Swinburn, G; Diabetes Care 2001, 24, 619

29) Chandalia, M; N Engl J Med 2000, 342, 1392

30) Lichtenstein, A; Atherosclerosis 2000, 150, 227

31) Bonora, E; Int J Obes Relat Metab Disord 2000, 24, 32S

32) de Jonge, L; Obesity Res 1997, 5, 622

33) Houde-Nadeau, M; J Am Coll Nutr 1993, 12, 511

34) Snowdon, D; Am J Public Health 1985, 75, 507

35) American Dietetic Association; J Am Diet Assoc 1997, 97, 1317

36) Johansson, G; Public Health Nutr 2001, 4(4), 919

9. Marcus E L; Fassberg C Wasserstein; Namestnik J; Guedj D; Caine Y Strict vegan , low-calorie diet administered by caregiving daughter to elderly mother--is this elder abuse?. Medicine and law (2005), 24(2), 279-96.

Abstract

We present a case in which a 40 year old woman, who was the primary care-giver of her 78 year-old mother, provided a strict vegan diet which caused the mother severe malnutrition. The mother was hospitalized with severe functional deterioration and, while eating a proper diet during hospitalization, gained weight and her condition improved. The case was reported to the Welfare Officer and the mother was released under the supervision of the Welfare Officer. Cases of severe malnutrition and even death of infants who were fed a strict vegan diet have been reported. This case raises some ethical and legal issues. Should a guardian or a caregiver be allowed to make decisions regarding the way of life and medical treatment of the person in his/her charge which are likely to endanger that person's health and when is it appropriate for society to intervene in individual freedom? The paper includes a review of some reported cases of child and elder abuse or neglect which illustrate these issues.

Controlled Terms

Check Tags: Female

*Adult Children

*Caregivers

*Diet, Vegetarian

*Elder Abuse: LJ, legislation & jurisprudence

*Energy Intake

Humans

Israel

Mother-Child Relations

Supplementary Terms

health care and public health; legal approach

10. Fokkema, M. Rebecca; van Rieke, H. M.; Bauermann, O. J.; Smit, E. N.; Muskiet, F. A. J. Short-term carnitine supplementation does not augment LCP 3 status of vegans and lacto-ovo-vegetarians. Journal of the American College of Nutrition (2005), 24(1), 58-64.

Abstract

Objective: Long-chain polyunsatd. omega-3 fatty acids (LCP3) synthesis, notably that of docosahexaenoic acid (DHA), from the precursor alpha-linolenic acid (ALA) proceeds with difficulty. The authors investigated whether carnitine supplementation augments the LCP3 status of apparently healthy vegans and lacto-ovo-vegetarians, who are expected to have low carnitine status. Methods: Group A (n = 11) took 990 mg/day 1-carnitine from weeks 1-4, and 990 mg/day 1-carnitine + 4 mL/day linseed oil from weeks 5-8. Group B (n = 9) took 4 mL/day linseed oil from weeks 1-4, and 4 mL/day linseed oil + 990 mg/day 1-carnitine from weeks 5-8. Fatty acid compns. of red blood cells, platelets, plasma cholesterol esters and plasma triglycerides were measured in the fasting state at baseline, and after 4 and 8 wk. Results: Carnitine supplementation increased plasma free and total carnitine concns. with 30 and 25%, resp., but did not affect eicosapentaenoic acid (EPA) and DHA contents of any of the investigated compartments. EPA and DHA changes were neg. related to initial carnitine status. Conclusions: The authors' results suggest that carnitine is not an important limiting factor, if any, for LCP3 synthesis in vegans and lacto-ovo-vegetarians. This conclusion is also likely to apply to omnivores. The most efficient means to augment EPA and particularly DHA status remains consumption of LCP3 from e.g. fish or supplements.

Indexing -- Section 18-5 (Animal Nutrition)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-3; short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

Blood plasma

Dietary supplements

Erythrocyte

Human

Platelet (blood)

(short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

Linseed oil

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

Diet

(vegetarian, lacto-ovo-; short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

Diet

(vegetarian; short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

57-88-5, Cholesterol, biological studies

57-88-5D, Cholesterol, esters

463-40-1, -Linolenic acid

541-15-1, L-Carnitine

6217-54-5, Docosahexaenoic acid

10417-94-4, Eicosapentaenoic acid

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(short-term carnitine supplementation does not augment LCP3 status of vegans and lacto-ovo-vegetarians)

Supplementary Terms

carnitine supplement blood n3 fatty acid vegan lactoovovegetarian diet

Citations

1) Simopoulos, A; Biomed Pharmacother 2002, 56, 365

2) Freeman, M; Ann Clin Psychiatry 2000, 12, 159

3) Sanderson, P; Br J Nutr 2002, 88, 573

4) Infante, J; Mol Genet Metab 2002, 75, 108

5) Brenna, J; Curr Opin Clin Nutr Metab Care 2002, 5, 127

6) Fu, Z; Pediatr Res 2000, 47, 414

7) Fokkema, M; Prostaglandins Leukot Essent Fatty Acids 2000, 63, 287

8) Voss, A; J Biol Chem 1991, 266, 19995

9) Infante, J; Mol Cell Biochem 1997, 168, 101

10) Infante, J; FEBS Lett 1998, 431, 1

11) Lombard, K; Am J Clin Nutr 1989, 50, 301

12) Vreken, P; J Inherit Metab Dis 1999, 22, 302

13) Hoving, E; J Chromatogr 1988, 434, 395

14) Ahmad, S; Kidney Int Suppl 1989, 27, S243

15) Ferdinandusse, S; J Lipid Res 2001, 42, 1987

16) Ramsay, R; Am J Med Sci 1999, 318, 28

17) Rebouche, C; Am J Clin Nutr 1993, 58, 660

18) Broquist, H; Modern Nutrition in Health and Disease 1994, 459

19) Brouwer, D; Prostaglandins Leukot Essent Fatty Acids 1998, 59, 329

20) Pawlosky, R; J Lipid Res 2001, 42, 1257

21) Hoffman, D; J Lipid Res 2001, 42, 1395

22) Willett, W; Am J Clin Nutr 1999, 70, 434S

23) Mezzano, D; Thromb Res 2000, 100, 153

24) Jump, D; J Biol Chem 2002, 277, 8755

25) Renaud, S; Am J Clin Nutr 2002, 76, 903

11. Baatenburg de Jong Rianne; Bekhof Jolita; Roorda Ruurdjan; Zwart Pieter Severe nutritional vitamin deficiency in a breast-fed infant of a vegan mother. European journal of pediatrics (2005), 164(4), 259-60.

Controlled Terms

Check Tags: Male

Anemia: CO, complications

Anemia: DT, drug therapy

*Anemia: ET, etiology

*Breast Feeding: AE, adverse effects

*Diet, Vegetarian: AE, adverse effects

Failure to Thrive: CO, complications

Failure to Thrive: DT, drug therapy

*Failure to Thrive: ET, etiology

Humans

Infant

Infant Nutrition Physiology

Vitamin B 12: TU, therapeutic use

Vitamin B 12 Deficiency: DT, drug therapy

*Vitamin B 12 Deficiency: ET, etiology

Vitamin B 12 Deficiency: PP, physiopathology

Vitamin D: TU, therapeutic use

Registry Numbers

1406-16-2 (Vitamin D)

68-19-9 (Vitamin B 12)

12. Newby, P. K.; Tucker, Katherine L.; Wolk, Alicja. Risk of overweight and obesity among semivegetarian, lactovegetarian, and vegan women. American Journal of Clinical Nutrition (2005), 81(6), 1267-1274.

Abstract

Background: Observational studies suggest that a plant-based diet is inversely related to body mass index (BMI), overweight, and obesity. Objective: Our objective was to examine the BMI (kg/m2) and risk of overweight and obesity of self-defined semivegetarian, lactovegetarian, and vegan women. Design: Data analyzed in this cross-sectional study were from 55 459 healthy women participating in the Swedish Mammog. Cohort. Women were asked whether they considered themselves to be omnivores (n = 54 257), semivegetarians (n = 960), lactovegetarians (n = 159), or vegans (n = 83), and this question was the main exposure variable in this study. In secondary analyses, we reclassified women as lactovegetarians on the basis of food intakes reported on the food-frequency questionnaire. Results: The prevalence of overweight or obesity (BMI ≥ 25) was 40% among omnivores, 29% among both semivegetarians and vegans, and 25% among lactovegetarians. In multivariate, adjusted logistic regression analyses, self-identified vegans had a significantly lower risk of overweight or obesity [odds ratio (OR) = 0.35; 95% CI: 0.18, 0.69] than did omnivores, as did lactovegetarians (OR = 0.54; 95% CI: 0.35, 0.85) and semivegetarians (OR = 0.52; 95% CI: 0.43, 0.62). Risk of overweight or obesity remained significantly lower among lactovegetarians classified on the basis of the food-frequency questionnaire (OR = 0.48; 95% CI: 0.30, 0.78). Conclusions: Even if vegetarians consume some animal products, our results suggest that self-identified semivegetarian, lactovegetarian, and vegan women have a lower risk of overweight and obesity than do omnivorous women. The advice to consume more plant foods and less animal products may help individuals control their wt.

Citations

1) Seidell, J; Acta Paediatrica Suppl 1999, 88, 46

2) Newby, P; Nutr Rev 2004, 62, 177

3) Togo, P; Int J Obes Relat Metab Disord 2001, 25, 1741

4) Steffen, L; Am J Epidemiol 2003, 158, 243

5) Liu, S; Am J Clin Nutr 2003, 78, 920

6) Koh-Banerjee, P; Proc Nutr Soc 2003, 62, 25

7) Newby, P; Am J Clin Nutr 2003, 77, 1417

8) Zemel, M; Obes Res 2004, 12, 582

9) Zemel, M; Am J Clin Nutr 2004, 79(suppl), 907S

10) Rouse, I; J Hypertens 1983, 1, 65

11) Appleby, P; Public Health Nutr 2002, 5, 645

12) Reddy, S; Atherosclerosis 1992, 95, 223

13) Krajcovicova-Kudlackova, M; Ann Nutr Metab 1994, 38, 331

14) Toohey, M; J Am Coll Nutr 1998, 17, 425

15) Key, T; Public Health Nutr 1998, 1, 33

16) Appleby, P; Am J Clin Nutr 1999, 70(suppl), 525S

17) Lin, C; Atherosclerosis 2001, 158, 247

18) Fraser, G; Am J Clin Nutr 1999, 70(suppl), 532S

19) Key, T; Am J Clin Nutr 1999, 70(suppl), 516S

20) Appleby, P; Public Health Nutr 2002, 5, 29

21) Phillips, F; J Hum Nutr Diet 2004, 17, 249

22) Spencer, E; Int J Obes Relat Metab Disord 2003, 27, 728

23) Key, T; BMJ 1996, 313, 816

24) Appleby, P; Int J Obes Relat Metab Disord 1998, 22, 454

25) Brathwaite, N; Ethn Dis 2003, 13, 34

26) Key, T; Proc Nutr Soc 1999, 58, 271

27) Dwyer, J; Am J Clin Nutr 1988, 48, 712

28) Kennedy, E; J Am Diet Assoc 2001, 101, 411

29) Barr, S; J Am Coll Nutr 2000, 19, 781

30) Michels, K; Ann Epidemiol 2002, 12, 21

31) Kuskowska-Wolk, A; Int J Obes 1989, 13, 441

32) James, P; Obes Res 2001, 9(suppl), 228S

33) Haddad, E; Am J Clin Nutr 2003, 78(suppl), 626S

34) Levin, N; J Clin Gastroenterol 1986, 8, 451

35) Stubbs, R; Ann N Y Acad Sci 1997, 819, 44

36) Willett, W; Nutritional epidemiology. 2nd ed 1998

37) Livingstone, M; J Nutr 2003, 133(suppl), 895S

13. Mann, Neil J. Omega-3 fatty acids from red meat in the Australian diet. Lipid Technology (2005), 17(4), 79-82.

Abstract

A recent study has shown that red meat in the diet of Australians is an important source of long-chain omega-3 fatty acids such as eicosapentaenoic acid. The capacity for red meat to deliver measurable quantities of these beneficial fatty acids is detd. by the feeding practices used in Australia, with pasture feeding being predominant and yielding the highest tissue omega-3 fatty acid content relative to grain feeding regimes. Australian people who eat meat were shown to consume on av. 140 mg of long-chain omega-3 fatty acids per day, much of this coming from red meat; in contrast, vegans (strict vegetarians) consumed no long-chain omega-3 fatty acids and exhibited lower plasma levels and a higher plasma omega-6: omega-3 ratio than those who eat meat.

Indexing -- Section 18-5 (Animal Nutrition)

Meat

(beef; -3 fatty acids from red meat in the Australian diet)

Carbohydrates, biological studies

Fats and Glyceridic oils, biological studies

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(dietary; -3 fatty acids from red meat in the Australian diet)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-3; -3 fatty acids from red meat in the Australian diet)

Diet

(vegetarian, lacto-ovo-; -3 fatty acids from red meat in the Australian diet)

Diet

(vegetarian; -3 fatty acids from red meat in the Australian diet)

Blood serum

Diet

Dietary energy

Human

(-3 fatty acids from red meat in the Australian diet)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(-3 fatty acids from red meat in the Australian diet)

463-40-1, C18:3n-3

506-32-1

6217-54-5, C22:6n-3

10417-94-4, C20:5n-3

24880-45-3, C22:5n-3

121250-47-3, Conjugated linoleic acid

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(-3 fatty acids from red meat in the Australian diet)

Supplementary Terms

nutrition diet meat n3 fatty acid

Citations

1) Simopoulos, A; World Rev Nutr and Dietetics 1998, 83, 1

2) Kris-Etherton, P; Circulation 2002, 106, 2747

3) Aro, A; Nutrition and Cancer 2000, 38, 151

4) Meyer, B; Lipids 2003, 38, 391

5) Gunstone, F; The Lipid Handbook 1994

6) Mann, N; Nutrition & Dietetics 2003, 60(1), 42

14. McCarty, Mark F. Nutritional modulation of parathyroid hormone secretion may influence risk for left ventricular hypertrophy. Medical Hypotheses (2005), 64(5), 1015-1021.

Abstract

A review. Recent studies demonstrate low serum levels of 25-hydroxyvitamin D in patients with congestive heart failure (CHF). Although this may in part reflect reduced capacity for outdoor exercise, the possibility that poor vitamin D status increases risk for left ventricular hypertrophy (LVH), and its common sequel CHF, merits consideration. In cardiomyocytes, hormones which activate protein kinase C (PKC) - including norepinephrine, angiotensin II, and endostatin, implicated in the pathogenesis of LVH - induce a hypertrophic response analogous to that seen in LVH. Transgenic mice overexpressing PKC-2 or its upstream activator Gq in cardiac myofibers develop a syndrome similar to LVH. Parathyroid hormone (PTH) also activates Gq and PKC in cardiomyocytes, and provokes the expected hypertrophic response. Both primary and secondary hyperparathyroidism are assocd. with high risk for LVH. Moreover, in uncomplicated essential hypertension, left ventricular mass index has been shown to correlate very tightly with serum PTH levels, independent of blood pressure. This latter finding suggests that variations of PTH within the normal range can influence induction of LVH in at-risk subjects. If so, nutritional and lifestyle measures which modulate PTH secretion may have an impact on LVH risk. PTH secretion should be down-regulated by good vitamin D status - achieved through supplementation or regular uv exposure - and by vegan diets moderately low in bioavailable phosphate. Although high calcium intakes can likewise suppress PTH, they also boost renin secretion, which could have a countervailing effect on risk for LVH. Whether these nutritional measures do indeed influence LVH risk could be examd. in prospective studies targeting patients at high risk, such as hypertensives.

Indexing -- Section 14-0 (Mammalian Pathological Biochemistry)

Hypertension

(essential; regulating parathyroid secretion by high vitamin D, vegan diet moderately low in bioavailable phosphate and high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

Heart, disease

(left ventricle, hypertrophy; regulating parathyroid secretion by high vitamin D, vegan diet moderately low in bioavailable phosphate and high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

Hypertrophy

(left ventricular; regulating parathyroid secretion by high vitamin D, vegan diet moderately low in bioavailable phosphate and high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

Risk assessment

(nutritional modulation of parathyroid hormone secretion may influence risk for left ventricular hypertrophy)

Blood pressure

Heart

Human

(regulating parathyroid secretion by high vitamin D, vegan diet moderately low in bioavailable phosphate and high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

Diet

(vegetarian; regulating parathyroid secretion by vegan diet moderately low in bioavailable phosphate can reduce risk of left ventricular hypertrophy in hypertensive patient)

7440-70-2, Calcium, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(regulating parathyroid secretion by high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

64719-49-9, 25-Hydroxyvitamin D

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); BIOL (Biological study)

(regulating parathyroid secretion by high vitamin D can reduce risk of left ventricular hypertrophy in hypertensive patient)

9002-64-6, Parathyroid hormone

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); BIOL (Biological study)

(regulating parathyroid secretion by high vitamin D, vegan diet moderately low in bioavailable phosphate and high calcium intake can reduce risk of left ventricular hypertrophy in hypertensive patient)

Supplementary Terms

review parathyroid hormone left ventricular hypertrophy risk assessment

Citations

1) Shane, E; Am J Med 1997, 103, 197

2) Zittermann, A; J Am Coll Cardiol 2003, 41, 105

3) Nishio, K; J Intern Med 2003, 253, 439

4) Christ, E; Schweiz Med Wochenschr 1996, 126, 1553

5) Schmid, C; Am J Med 1998, 104, 508

6) Kelm, M; J Hypertens 1996, 14, 1357

7) White, M; Can J Cardiol 1999, 15(Suppl F), 10F

8) Ehmke, H; Hypertension 1999, 33, 954

9) Hua, L; Hypertens Res 2000, 23, 377

10) Wolf, S; J Cardiovasc Pharmacol 2000, 36, S348

11) Knowlton, K; J Biol Chem 1993, 268, 15374

12) Long, C; J Cardiovasc Pharmacol 1991, 17(Suppl 2), S20

13) Sadoshima, J; Cell 1993, 75, 977

14) Shubeita, H; J Biol Chem 1990, 265, 20555

15) Bowling, N; Circulation 1999, 99, 384

16) Simpson, P; Circulation 1999, 99, 334

17) Kariya, K; J Biol Chem 1994, 269, 3775

18) Karns, L; J Biol Chem 1995, 270, 410

19) Wakasaki, H; Proc Natl Acad Sci USA 1997, 94, 9320

20) MacLellan, W; Circulation 1998, 97, 1433

21) D'Angelo, D; Proc Natl Acad Sci USA 1997, 94, 8121

22) Adams, J; Proc Natl Acad Sci USA 1998, 95, 10140

23) Mende, U; Proc Natl Acad Sci USA 1998, 95, 13893

24) Feuerstein, G; Circ Res 2000, 87, 1085

25) Akhter, S; Science 1998, 280, 574

26) Wettschureck, N; Nat Med 2001, 7, 1236

27) Takeishi, Y; J Clin Invest 1998, 102, 72

28) Schluter, K; Am J Physiol 1992, 263, H1739

29) Schluter, K; Biochem J 1995, 310(Pt 2), 439

30) Schluter, K; Cardiovasc Res 1998, 37, 34

31) McGonigle, R; Nephron 1984, 36, 94

32) London, G; Kidney Int 1987, 32, 900

33) Meggs, L; J Assoc Acad Minor Phys 1994, 5, 59

34) Hara, S; Miner Electrolyte Metab 1995, 21, 72

35) Park, C; Am J Kidney Dis 1999, 33, 73

36) Strozecki, P; Ren Fail 2001, 23, 115

37) Symons, C; Brit Heart J 1985, 54, 539

38) Dominiczak, A; Clin Sci (Lond) 1990, 78, 127

39) Sato, S; Miner Electrolyte Metab 1995, 21, 67

40) Stefenelli, T; Surgery 1997, 121, 157

41) Piovesan, A; Clin Endocrinol (Oxf) 1999, 50, 321

42) Bauwens, F; Am J Cardiol 1991, 68, 925

43) Hui, Y; Chin Med J (Engl) 1996, 109, 885

44) Li, Y; J Clin Invest 2002, 110, 229

45) Sigmund, C; J Clin Invest 2002, 110, 155

46) Petrov, V; Am J Hypertens 1999, 12, 1217

47) McCarty, M; Med Hypotheses [in press] 2004

48) Vieth, R; Am J Clin Nutr 1999, 69, 842

49) Vieth, R; Am J Clin Nutr 2001, 73, 288

50) Portale, A; J Clin Invest 1989, 83, 1494

51) Zhang, M; Endocrinology 2002, 143, 587

52) Rodriguez, M; Curr Opin Nephrol Hypertens 1996, 5, 321

53) Barsotti, G; Nephron 1996, 74, 390

54) Soroka, N; Nephron 1998, 79, 173

55) Kempson, S; Am J Physiol 1995, 268, F784

56) Holick, M; J Cell Biochem 2003, 88, 296

57) Zittermann, A; Brit J Nutr 2003, 89, 552

58) Levy, D; New Engl J Med 1990, 322, 1561

59) Koren, M; Ann Intern Med 1991, 114, 345

60) Ghali, J; Ann Intern Med 1992, 117, 831

61) Schmieder, R; Adv Exp Med Biol 1997, 432, 191

62) Sharp, A; J Renin Angiotensin Aldosterone Syst 2002, 3, 141

63) Beil, A; Cardiovasc Drugs Ther 1994, 8, 425

64) Schmieder, R; Circulation 1996, 94, 1304

65) Heimann, J; J Cardiovasc Pharmacol 1991, 17(Suppl 2), S122

66) Jula, A; Circulation 1994, 89, 1023

67) Denton, D; Nat Med 1995, 1, 1009

68) MacGregor, G; Salt, diet and health: Neptune's poisoned chalice: the origins of high blood pressure 1998

69) de Wardener, H; Curr Opin Cardiol 2002, 17, 360

70) Militante, J; Amino Acids 2002, 23, 381

71) Fujita, T; Circulation 1987, 75, 525

72) Sato, Y; Jpn Circ J 1991, 55, 500

73) Azuma, J; Clin Cardiol 1985, 8, 276

74) Azuma, J; Adv Exp Med Biol 1994, 359, 425

75) Digiesi, V; Mol Aspects Med 1994, 15(Suppl 1), s257

76) Burke, B; South Med J 2001, 94, 1112

77) Baggio, E; Mol Aspects Med 1994, 15(Suppl 1), s287

78) Soja, A; Mol Aspects Med 1997, 18(Suppl 1), S159

79) Sasson, Z; Circulation 1993, 88, 1431

80) Lind, L; J Hypertens 1995, 13, 433

81) Kamide, K; Am J Hypertens 1996, 9, 1165

82) Watanabe, K; J Hypertens 1999, 17, 1153

83) Facchini, F; Am J Hypertens 1996, 9, 1013

84) Watanabe, K; J Hypertens 1999, 17, 1161

85) Barnard, R; Am J Cardiol 1992, 69, 440

86) Turner, M; J Gerontol A: Biol Sci Med Sci 2000, 55, M245

87) Hulter, H; J Clin Hypertens 1986, 2, 360

88) Fliser, D; Nephrol Dial Transplant 1997, 12, 933

89) Lind, L; Am J Hypertens 1988, 1, 397

90) Raine, A; Kidney Int 1993, 43, 700

91) Rostand, S; Hypertension 1997, 30, 150

92) Rostand, S; New Engl J Med 1999, 340, 965

93) Krause, R; Lancet 1998, 352, 709

94) Sacks, F; Am J Epidemiol 1974, 100, 390

95) Beilin, L; Am J Clin Nutr 1988, 48, 806

15. Dunn-Emke, Stacey R.; Weidner, Gerdi; Pettengill, Elaine B.; Marlin, Ruth O.; Chi, Christine; Ornish, Dean M. Nutrient adequacy of a very low-fat vegan diet. Journal of the American Dietetic Association (2005), 105(9), 1442-1446.

Abstract

This study assessed the nutrient adequacy of a very low-fat vegan diet. Thirty-nine men (mean age = 65 years) with early stage prostate cancer who chose the "watchful waiting" approach to disease management, were instructed by a registered dietitian and a chef on following a very low-fat (10%) vegan diet with the addn. of a fortified soy protein powd. beverage. Three-day food diaries, excluding vitamin and mineral supplements, were analyzed and nutrient values were compared against Dietary Ref. Intakes (DRI). Mean dietary intake met the recommended DRIs. On the basis of the Adequate Intake std., a less than adequate intake was obsd. for vitamin D. This demonstrates that a very low-fat vegan diet with comprehensive nutrition education emphasizing nutrient-fortified plant foods is nutritionally adequate, with the exception of vitamin D. Vitamin D supplementation, esp. for those with limited sun exposure, can help assure nutritional adequacy.

Indexing -- Section 18-2 (Animal Nutrition)

Section cross-reference(s): 13

Nutrients

(macronutrients; nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Nutrients

(micronutrients; nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Human

Nutrition, animal

Prostate gland, neoplasm

(nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Mineral elements, biological studies

Vitamins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Proteins

Role: BSU (Biological study, unclassified); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(soybean; nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Diet

(vegetarian, low-fat; nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

1406-16-2, Vitamin D

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(nutrient, but not vitamin D, adequacy of a very low-fat vegan diet plus a fortified soy protein powd. beverage in patients with early stage prostate cancer)

Supplementary Terms

vegan diet fat soy protein vitamin D prostate cancer

Citations

1) Haddad, E; Am J Clin Nutr 1999, 70(suppl), S586

2) Fraser, G; Am J Clin Nutr 1999, 70(suppl), S532

3) Key, T; Proc Nutr Soc 1999, 58, 271

4) Appleby, P; Am J Clin Nutr 1999, 70(suppl 3), S525

5) Key, T; Am J Clin Nutr 1999, 70(suppl 3), S516

6) Singh, P; Am J Clin Nutr 2003, 78(suppl 3), S526

7) Barnard, N; Am J Cardiol 2000, 85, 969

8) Ornish, D; JAMA 1998, 280, 2001

9) Mills, P; Am J Clin Nutr 1994, 59(suppl 5), S1136

10) White, R; West J Med 1994, 160, 465

11) Key, T; Lancet 2002, 360, 861

12) Jenkins, D; Am J Clin Nutr 2003, 78(suppl 3), S610

13) Sanders, T; Proc Nutr Soc 1999, 58, 265

14) Scherwitz, L; Homeostasis 1994, 35, 198

15) Abdulla, M; Am J Clin Nutr 1984, 40, 325

16) Laidlaw, S; Am J Clin Nutr 1988, 47, 660

17) Bar-Sella, P; Isr J Med Sci 1990, 26, 309

18) Abdulla, M; Am J Clin Nutr 1981, 34, 2464

19) Herrmann, W; Am J Clin Nutr 2003, 78, 131

20) Ball, M; Am J Clin Nutr 1999, 70, 353

21) Messina, V; J Am Diet Assoc 1997, 97, 1317

22) Gibson, R; Am J Clin Nutr 1994, 59(suppl), S1223

23) Craig, W; Am J Clin Nutr 1994, 59(suppl 5), S1233

24) Lichtenstein, A; Circulation 1998, 98, 935

25) Dwyer, J; Am J Clin Nutr 1999, 70(suppl 3), S620

26) Sabate, J; Am J Clin Nutr 2003, 78(suppl 3), S502

27) Anon; J Am Diet Assoc 2003, 103, 748

28) Ornish, D; Urology 2001, 57, 200

29) Messina, M; Nutr Rev 2003, 61, 117

30) Zhou, J; J Nutr 1999, 129, 1628

31) Geller, J; Prostate 1998, 34, 75

32) Santibanez, J; Anticancer Res 1997, 17, 1199

33) Lee, M; Cancer Epidemiol Biomarkers Prev 2003, 12, 665

34) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride 2002

35) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients) 2002

36) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2000

37) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline 1998

38) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids 2000

39) Food and Nutrition Board Institute of Medicine; Dietary Reference Intakes: Applications in Dietary Assessment 2000

40) Hunt, J; Am J Clin Nutr 2003, 78(suppl), S633

41) Hokin, B; Am J Clin Nutr 1999, 70(suppl 3), S576

42) Freedman, M; Obes Res 2001, 9(suppl 1), S1

43) Ornish, D; Eat More, Weigh Less 1993

44) Antony, A; Am J Clin Nutr 2003, 78, 3

45) Vieth, R; Am J Clin Nutr 1999, 69, 842

46) Naglak, M; J Am Diet Assoc 2000, 100, 1385

47) Fairfield, K; JAMA 2002, 287, 3116

48) Peregrin, T; J Am Diet Assoc 2002, 102, 1214

16. Borak Jonathan Neonatal hypothyroidism due to maternal vegan diet. Journal of pediatric endocrinology & metabolism : JPEM (2005), 18(6), 621.

Controlled Terms

Check Tags: Female

Adult

*Diet, Vegetarian: AE, adverse effects

Humans

*Hypothyroidism: ET, etiology

Infant, Newborn

Iodide Peroxidase: AI, antagonists & inhibitors

Iodine: DF, deficiency

Isoflavones: AE, adverse effects

Pregnancy

Soybeans: CH, chemistry

Registry Numbers

7553-56-2 (Iodine)

Chemical Names

0 (Isoflavones)

EC 1.11.1.8 (Iodide Peroxidase)

17. McCarty Mark F; Block Keith I Multifocal angiostatic therapy: an update. Integrative cancer therapies (2005), 4(4), 301-14.

Abstract

Multifocal angiostatic therapy (MAT) is a strategy that seeks to impede cancer-induced angiogenesis by addressing multiple targets that regulate the angiogenic capacity of a cancer and/or the angiogenic responsiveness of endothelial cells, using measures that are preferentially, but not exclusively, nutraceutical. A prototype of such a regimen has been proposed previously, composed of green tea polyphenols, fish oil, selenium, and high-dose glycine, complementing a low-fat vegan diet, exercise training, and the copper-sequestering drug tetrathiomolybdate (TM). A review of more recent evidence suggests additional agents that could appropriately be included in this regimen and clarifies to some extent the mechanisms of action of its constituents. Diindolylmethane, a widely available crucifera-derived nutraceutical, has inhibited cancer growth in several mouse xenograft models; this effect may be largely attributable to an angiostatic action, as concentrations as low as 5 to 10 muM inhibit proliferation, migration, and tube-forming capacity of human endothelial cells in vitro, and a parenteral dose of 5 mg/kg markedly impairs matrigel angiogenesis in mice. Silymarin/silbinin, which has slowed the growth of human xenografts in a number of studies, suppresses the proliferation, migration, and tube-forming capacity of endothelial cells and inhibits vascular endothelial growth factor (VEGF) secretion by a range of human cancer cell lines, in concentrations that should be clinically feasible. The angiostatic activity of orally administered green tea now appears likely to reflect inhibition of the kinase activity of VEGFR-2. Glycine's angiostatic activity may be attributable to a hyperpolarizing effect on endothelial cells that decreases the activity of NADPH oxidase, now known to promote tyrosine kinase signaling in endothelial cells. The ability of TM to suppress cancer cell production of a range of angiogenic factors results at least in part from a down regulation of NF-kappaB activation.

Dual-purpose molecular targets, whose inhibition could be expected to decrease the aggressiveness and chemoresistance of cancer cells while simultaneously impeding angiogenesis, include NF-kappaB, cox-2, c-Src, Stat3, and hsp90; drugs that can address these targets are now in development, and salicylates are notable for the fact that they can simultaneously inhibit NF-kappaB and cox-2. The potential complementary of the components of MAT should be assessed in nude mouse xenograft models.

Controlled Terms

Angiogenesis Inhibitors: PD, pharmacology

*Angiogenesis Inhibitors: TU, therapeutic use

Complementary Therapies: MT, methods

Humans

Neoplasms: BS, blood supply

*Neoplasms: DT, drug therapy

*Neovascularization, Pathologic: DT, drug therapy

Chemical Names

0 (Angiogenesis Inhibitors)

18. Fox Michael W More on vegetarian/ vegan cat foods. Journal of the American Veterinary Medical Association (2005), 226(7), 1047; author reply 1047-8.

Controlled Terms

*Animal Feed: AN, analysis

*Animal Nutrition Physiology

Animals

Cats

*Diet, Vegetarian

Evidence-Based Medicine

Nutritional Requirements

19. Wang, Jui-Line; Shaw, Ning-Sing; Yeh, Hsiang-Yu; Kao, Mei-Ding. Magnesium status and association with diabetes in the Taiwanese elderly. Asia Pacific Journal of Clinical Nutrition (2005), 14(3), 263-269.

Abstract

The av. dietary intake of magnesium is below recommended dietary allowances in many affluent Western countries. Prolonged low magnesium intake tends to result in hypomagnesemia which might increase the risk of chronic diseases in elderly people. A national population-based cross-sectional nutrition survey, the Elderly Nutrition and Health Survey in Taiwan (1999-2000), was used to investigate the magnesium status and assocn. with diabetes in the Taiwanese elderly. Dietary magnesium intake was based on 24-h dietary recalls. Blood biochem. parameters including plasma magnesium and blood glucose were also measured. Av. magnesium intake was 250mg in men and 216mg in women, which is equiv. to 68-70% of relevant Taiwanese Dietary Ref. Intakes. The mean plasma magnesium concn. was 0.903 mmol/L in men and 0.906 mmol/L in women. The prevalence of a plasma magnesium level of <0.7 mmol/L was 0.7 - 0.9% in the elderly, and that of <0.8 mmol/L was 8.0-9.1%. Elderly vegans had a significantly lower magnesium intake than ovo-lacto vegetarians and non-vegetarians. Diabetic men and women had significantly higher blood glucose levels than non-diabetics. The risk of diabetes was elevated 3.25 times at plasma magnesium levels <0.863mmol/L. There was an inverse assocn. between plasma magnesium concn. and the prevalence of diabetes. However, no assocn. was found between diabetes and low dietary magnesium. Taiwanese elderly persons had suboptimal levels of dietary magnesium intake, which although may be sufficient to avoid overt magnesium deficiency, may not be sufficient to reduce the risk of diabetes in the elderly. Further prospective study is required to help explain the differential results between dietary and plasma magnesium levels.

Indexing -- Section 18-1 (Animal Nutrition)

Section cross-reference(s): 13, 14

Diabetes mellitus

Human

Human groups

(diabetes was inversely assocd. with plasma magnesium concn. but not low dietary magnesium in Taiwanese elderly)

Nutrition, animal

(diabetes was inversely assocd. with plasma magnesium concn. but not low dietary magnesium in Taiwanese elderly and vegans had significantly lower magnesium intake than ovo-lacto vegetarians and non-vegetarians)

Aging, animal

(elderly; magnesium status and assocn. with diabetes in the Taiwanese elderly)

Diet

Sex

(magnesium status and assocn. with diabetes in the Taiwanese elderly)

Diet

(vegetarian, lacto-ovo-; magnesium status and assocn. with diabetes in the Taiwanese elderly)

Diet

(vegetarian; magnesium status and assocn. with diabetes in the Taiwanese elderly)

50-99-7, D-Glucose, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; magnesium status and assocn. with diabetes in the Taiwanese elderly)

7439-95-4, Magnesium, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(diabetes was inversely assocd. with plasma magnesium concn. but not low dietary magnesium in Taiwanese elderly)

Supplementary Terms

magnesium diabetes elderly diet

Citations

1) Wacker, W; N Eng J Med 1968, 45, 658

2) Wester, P; Am J Clin Nutr 1987, 45, 1305

3) Saris, N; Clin Chem Acta 2000, 294, 1

4) Kelsay, J; Am J Clin Nutr 1979, 32, 1876

5) Wisker, E; Am J Clin Nutr 1991, 54, 553

6) Siener, R; Br J Nutr 1995, 73, 783

7) Hardwick, L; J Nutr 1991, 121, 13

8) Bohn, T; Am J Clin Nutr 2004, 79, 418

9) Institute Of Medicine; Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride 1997

10) Vormann, J; Mol Aspects Med 2003, 24, 27

11) Maier, J; Mol Aspects Med 2003, 24, 137

12) Barbagallo, M; Mol Aspects Med 2003, 24, 39

13) Delva, P; Mol Aspects Med 2003, 24, 63

14) Touyz, R; Mol Aspects Med 2003, 24, 107

15) Ma, J; J Clin Epidemiol 1995, 48, 927

16) Joffres, M; Am J Clin Nutr 1987, 45, 469

17) Sacks, F; Ann Epidemiol 1995, 5, 108

18) Peacock, J; Ann Epidemiol 1999, 9, 159

19) Rasmussen, H; Arch Int Med 1989, 149, 1050

20) Rubenowitz, E; Am J Epidemiol 1996, 143, 456

21) Ford, E; Int J Epidemiol 1999, 28, 645

22) Sjogren, A; Acta Med Scand 1988, 224, 461

23) Nadler, J; Hypertension 1993, 21, 1024

24) Paolisso, G; Diabetologia 1990, 33, 511

25) Schmidt, L; J Am Diet Assoc 1994, 94, 773

26) Paolisso, G; Am J Clin Nutr 1992, 55, 1161

27) Paolisso, G; Acta Endocrinol Copenh 1989, 121, 16

28) American Diabetes Association; Diab Care 1992, 15, 1065

29) Lima, M; Diabetes Care 1998, 21, 682

30) Kao, W; Arch Intern Med 1999, 159, 2151

31) Song, Y; Diabetes Care 2004, 27, 59

32) Lopez-Ridaura, R; Diabetes Care 2004, 27, 134

33) Pan, W; Asia Pac J Clin Nutr 2005, 14(3), 203

34) Wu, S; Asia Pac J Clin Nutr 2005, 14(3), 211

35) Sas Institute Inc; SAS/STAT User's Guide, Version 6, 4th ed 1990, 2

36) Shah, B; SUDAAN User's Manual Release 7.5 1997

37) Ford, E; J Nutr 2003, 133, 2879

38) Geleijnse, J; J Hypertens 1996, 14, 737

39) Vormann, J; J Clin Basic Cardiol 2002, 5, 49

40) Galan, P; Magnes Res 1997, 10, 321

41) Hendrix, P; Z Lebensm Unters Forsch 1995, 201, 213

42) Anon; Fourth Swiss Nutrition Report 1998, 18

43) Walti, M; Eur J Clin Nutr 2002, 56, 409

44) Department Of Health; Dietary Reference Intakes 6 th ed 2003

45) Liu, J; Nutr Sci J 2002, 27, 221

46) Singh, R; Magnes Res 1996, 9, 299

47) Kohlmeier, M; Versorgung Erwachsener mit Mineral-stoffen und Spurenelementen in der Bundesrepublik Deutschland 1995

48) Schimatschek, H; Magnes Res 2001, 14, 283

49) Rosolova, H; Metabol Clin Exp 2000, 49, 418

50) Fung, T; J Am Coll Nutr 2003, 22, 533

51) Barbagallo, M; J Am Geriatrics Soc 2000, 48, 1111

52) Paolisso, G; Diabetes Care 1989, 12, 265

53) Paolisso, G; J Clin Endocrinol Metab 1994, 78, 1510

20. McCarty, Mark F. Low-insulin-response diets may decrease plasma C-reactive protein by influencing adipocyte function. Medical Hypotheses (2005), 64(2), 385-387.

Abstract

A review. Hepatic prodn. of many acute phase reactants, including C-reactive protein (CRP), is induced primarily by interleukin-6 (IL-6). A significant fraction of the plasma pool of IL-6 derives from adipocytes. Physiol. concns. of insulin as well as of catecholamines have been shown to boost adipocyte prodn. of IL-6 dose-dependently. High fasting and postprandial insulin levels can increase adipocyte exposure to catcholamines by activating the sympathetic nervous system, as well as by provoking postabsorptive hypoglycemia that triggers adrenal secretion of epinephrine. It follows that diets which promote low diurnal insulin levels - by minimizing the stimulus to postprandial insulin release, and by aiding muscle insulin sensitivity - should be assocd. with lower CRP levels. In fact, recent epidemiol. demonstrates a correlation between dietary glycemic load and serum CRP in women, and a recent clin. study reports a 28% redn. in serum CRP following adoption of a whole-food vegan diet rich in sol. fiber. Whether very-low-fat diets which promote insulin sensitivity - and thus down-regulate insulin secretion - can influence CRP, remains to be seen. These considerations suggest that it may be possible to achieve worthwhile redns. in CRP by avoiding high-insulin-response starchy foods and by ingesting more sol. fiber, in foods or as a meal-time supplement.

Indexing -- Section 18-0 (Animal Nutrition)

Adipose tissue

(adipocyte; low-insulin-response diets may decrease plasma C-reactive protein by influencing adipocyte function)

Diet

(low-insulin-response diets may decrease plasma C-reactive protein by influencing adipocyte function)

C-reactive protein

Interleukin 6

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-insulin-response diets may decrease plasma C-reactive protein by influencing adipocyte function)

9004-10-8, Insulin, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-insulin-response diets may decrease plasma C-reactive protein by influencing adipocyte function)

Supplementary Terms

review diet insulin C reactive protein adipocyte

Citations

1) Clifton, P; Curr Atheroscler Rep 2003, 5, 431

2) Liu, S; Am J Clin Nutr 2002, 75, 492

3) Castell, J; FEBS Lett 1989, 242, 237

4) Heinrich, P; Z Ernahrungswiss 1998, 37(Suppl 1), 43

5) Mohamed-Ali, V; J Clin Endocrinol Metab 1997, 82, 4196

6) Fried, S; J Clin Endocrinol Metab 1998, 83, 847

7) Bastard, J; Circulation 1999, 99, 2221

8) McCarty, M; Med Hypotheses 1999, 52, 465

9) Bastard, J; J Clin Endocrinol Metab 2000, 85, 3338

10) Hotamisligil, G; J Clin Invest 1995, 95, 2409

11) Kern, P; J Clin Invest 1995, 95, 2111

12) Eckel, R; Lancet 1992, 340, 1452

13) Path, G; J Clin Endocrinol Metab 2001, 86, 2281

14) Mohamed-Ali, V; J Clin Endocrinol Metab 2001, 86, 5864

15) Vicennati, V; Int J Obes Relat Metab Disord 2002, 26, 905

16) Fasshauer, M; Horm Metab Res 2003, 35, 147

17) Krogh-Madsen, R; Am J Physiol Endocrinol Metab 2003

18) Tokunou, T; Arterioscler Thromb Vasc Biol 2001, 21, 1759

19) Hershko, D; Am J Physiol Regul Integr Comp Physiol 2002, 283, R1140

20) Takaki, A; Neuroimmunomodulation 1994, 1, 335

21) Yu, X; Life Sci 2001, 69, 167

22) Papanicolaou, D; Am J Physiol 1996, 271, E601

23) Landsberg, L; Blood Press Suppl 1996, 1, 25

24) Wolever, T; Diabetes Care 1995, 18, 962

25) Ludwig, D; Pediatrics 1999, 103, E26

26) Landsberg, L; Hypertension 1992, 19, 161

27) Reaven, G; N Engl J Med 1996, 334, 374

28) Fukagawa, N; Am J Clin Nutr 1990, 52, 524

29) Barnard, R; Am J Cardiol 1992, 69, 440

30) McDougall, J; J Altern Complem Med 2002, 8, 71

31) Heilbronn, L; Arterioscler Thromb Vasc Biol 2001, 21, 968

21. Rosell, Magdalena S.; Lloyd-Wright, Zoue; Appleby, Paul N.; Sanders, Thomas A. B.; Allen, Naomi E.; Key, Timothy J. Long-chain n-3 polyunsaturated fatty acids in plasma in british meat-eating, vegetarian, and vegan men. American Journal of Clinical Nutrition (2005), 82(2), 327-334.

Abstract

Plasma concns. of long-chain n-3 polyunsatd. fatty acids are lower in vegetarians and in vegans than in omnivores. No data are available on whether these concns. differ between long- and short-term vegetarians and vegans. Objectives of this study was to compare plasma fatty acid compn. in meat-eaters, vegetarians, and vegans and examd. whether the proportions of Eicosapentaenoic acid (20:5n-3; EPA), Docosapentaenoic acid (22:5n-3; DPA), and docosahexaenoic acid (22:6n-3; DHA) were related to the subjects' duration of adherence to their diets or to the proportions of plasma linoleic acid (18:2n-6; LA) and -linolenic acid (18:3n-3; ALA). The present cross-sectional study included 196 meat-eating, 231 vegetarian, and 232 vegan men in the United Kingdom. Information on anthropometry, diet, and smoking habits was obtained through a questionnaire. Total fatty acid compn. in plasma was measured. Results showed that proportions of plasma EPA and DHA were lower in the vegetarians and in the vegans than in the meat-eaters, whereas only small differences were seen for DPA. Plasma EPA, DPA, and DHA proportions were not significantly assocd. with the duration of time since the subjects became vegetarian or vegan, which ranged from < 1 y to > 20 y. In the vegetarians and the vegans, plasma DHA was inversely correlated with plasma LA. Thus, proportions of plasma long-chain n-3 fatty acids were not significantly affected by the duration of adherence to a vegetarian or vegan diet. This finding suggests that when animal foods are wholly excluded from the diet, the endogenous prodn. of EPA and DHA results in low but stable plasma concns. of these fatty acids.

Indexing -- Section 18-5 (Animal Nutrition)

Dietary energy

Egg

Human

Nutrition, animal

(long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(long-chain; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fish

(meal; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(monounsatd.; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Animals

(omnivore; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-3; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd.; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(satd.; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(total; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Animals

(vegetarian and vegan; long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

57-10-3, Hexadecanoic acid, biological studies

57-11-4, Octadecanoic acid, biological studies

60-33-3, 9,12-Octadecadienoic acid (9Z,12Z)-, biological studies

112-80-1, 9-Octadecenoic acid (9Z)-, biological studies

373-49-9

463-40-1

506-30-9, Eicosanoic acid

506-32-1

544-63-8, Tetradecanoic acid, biological studies

1783-84-2

2420-56-6

2540-56-9

6217-54-5

10417-94-4

24880-45-3

28929-01-3

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(long-chain n-3 polyunsatd. fatty acids in plasma in british meat-eating, vegetarian, and vegan men)

Supplementary Terms

long chain polyunsatd fatty acid meat eater vegetarian vegan

Citations

1) Marckmann, P; Eur J Clin Nutr 1999, 53, 585

2) Hu, F; JAMA 2002, 287, 1815

3) Hu, F; Circulation 2003, 107, 1852

4) He, K; JAMA 2002, 288, 3130

5) Sinclair, A; Lipids 1994, 29, 337

6) Meyer, B; Lipids 2003, 38, 391

7) Sanders, T; Am J Clin Nutr 1999, 70(suppl), S555

8) Davis, B; Am J Clin Nutr 2003, 78(suppl), S640

9) Muskiet, F; J Nutr 2004, 134, 183

10) Burdge, G; Br J Nutr 2002, 411

11) Burdge, G; Br J Nutr 2002, 88, 355

12) Brenna, J; Curr Opin Clin Nutr Metab Care 2002, 5, 127

13) Li, D; Am J Clin Nutr 1999, 69, 872

14) Sanders, T; Br J Nutr 1981, 45, 613

15) Fokkema, M; Prostaglandins Leukot Essent Fatty Acids 2004, 63, 287

16) Sanders, T; Am J Clin Nutr 1978, 31, 805

17) Li, D; Clin Sci 1999, 97, 175

18) Lee, H; Eur J Clin Nutr 2000, 54, 768

19) Fokkema, M; Prostaglandins Leukot Essent Fatty Acids 2000, 63, 279

20) Davey, G; Publ Health Nutr 2003, 6, 259

21) Allen, N; Br J Cancer 2000, 83, 95

22) Sanders, T; Arterioscler Thromb Vasc Biol 1997, 17, 3449

23) Lloyd-Wright, Z; PhD dissertation, University of London 2005

24) Arab, L; J Nutr 2003, 133(suppl), S925

25) Wolk, A; J Nutr 2001, 131, 828

26) Roshanai, F; Ann Nutr Metab 1985, 29, 189

27) Ritzenthaler, K; J Nutr 2001, 131, 1548

28) Terpstra, A; Am J Clin Nutr 2004, 79, 352

29) Riserus, U; Diabetologia 2004, 47, 1016

30) Tricon, S; Am J Clin Nutr 2004, 80, 614

31) Amiano, P; Eur J Clin Nutr 2001, 55, 827

32) Ma, J; Am J Clin Nutr 1995, 62, 564

33) Andersen, L; Am J Epidemiol 1999, 150, 75

34) Fusconi, E; Tumori 2003, 89, 624

35) Hjartaker, A; Eur J Clin Nutr 1997, 51, 736

36) Key, T; Am J Clin Nutr 2003, 78(suppl), S533

37) Key, T; Am J Clin Nutr 1999, 70(suppl), S516

38) Beilin, L; Clin Exp Pharmacol Physiol 1995, 22, 195

39) Thorogood, M; Br Med J 1987, 295, 351

40) Sanders, T; Eur J Clin Nutr 1992, 46, 823

22. Fields, Cheryl; Dourson, Michael; Borak, Jonathan. Iodine-deficient vegetarians: A hypothetical perchlorate-susceptible population? Regulatory Toxicology and Pharmacology (2005), 42(1), 37-46.

Abstract

A review. Recent risk assessments of environmental perchlorate have been subject to much debate. A particular concern is whether appropriate susceptible sub-populations have been identified. Iodine-deficient pregnant women, esp. vegetarians, have been proposed as such a potential susceptible sub-population, but there is no evidence of iodine deficiency in the US population and the adequacy of iodine nutrition has not been studied in US vegetarians. To understand the possibility that US vegetarians might be iodine deficient, we reviewed the prevalence, demog., and lifestyle characteristics of US vegetarians as well as the world literature on iodine nutrition in vegetarians. Our findings indicate that strict vegetarians and vegans, who comprise probably less than 0.1% of the US population, have higher education, higher incomes, and healthier lifestyles than the general population. Field studies indicate that vegetarian diets need not lead to iodine deficiency and vegans may suffer excess iodine intake. It is remains uncertain whether there are iodine-deficient vegans or pregnant women in the US. Of more general concern is whether the 10-fold default uncertainty factor is needed for intraspecies (i.e., within human) variability to protect such hypothetical susceptible sub-populations.

Indexing -- Section 18-0 (Animal Nutrition)

Section cross-reference(s): 4

Environmental pollution

Human

Nutrition, animal

Risk assessment

(I-deficient vegetarians and risk assessments of environmental perchlorate)

Diet

(vegetarian; I-deficient vegetarians and risk assessments of environmental perchlorate)

14797-73-0, Perchlorate

Role: ADV (Adverse effect, including toxicity); POL (Pollutant); BIOL (Biological study); OCCU (Occurrence)

(I-deficient vegetarians and risk assessments of environmental perchlorate)

7553-56-2, Iodine, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(deficiency; I-deficient vegetarians and risk assessments of environmental perchlorate)

Supplementary Terms

review vegetarian diet iodine deficiency perchlorate risk assessment

Citations

Abdulla, M; Am J Clin Nutr 1981, 34, 2464

Abdulla, M; Scand J Gastroenterol 1979, 14(Suppl 52), 185

American Dietetic Association and Dietitians of Canada; J Am Diet Assoc 2003, 103, 748

Applepy, P; Am J Clin Nutr 1999, 70, 525S

Barr, S; J Am Diet Assoc 2002, 102, 354

Borak, J; Conn Med 2005, 69, 73

Caron, P; Thyroid 1997, 7, 749

CDC (Centers for Disease Control and Prevention); http://www.cdc.gov/nchs/products/pubs/pubd/hestats/iodine.htm 2003

Delange, F; Postgrad Med J 2001, 77, 217

Dohan, O; Endocr Rev 2003, 24, 48

Dourson, M; Regul Toxicol Pharmacol 1996, 24, 108

Draper, A; Br J Nutr 1993, 69, 3

Dunn, J; Perchlorate State of the Art Symposium, http://www.perchloratesymposium.com/DunnPPT.ppt 2003

Dwyer, J; J Can Diet Assoc 1983, 44, 26

Dwyer, J; J Am Diet Assoc 1974, 64, 376

Ellis, F; Am J Clin Nutr 1970, 23, 249

Environmental Protection Agency; Perchlorate Environmental Contamination: Toxicological Review and Risk Characterization 2002

Frank, E; JAMA 1992, 268, 1566

Freeland-Graves, J; J Am Diet Assoc 1986, 86, 913

FF (Fruitarian Foundation); http://www.fruitarian.com/ao/WhatisFruitarianism.htm 2000

Glinoer, D; Thyroid 2001, 11, 471

Greer, M; Environ Health Perspect 2002, 110, 927

Ginsberg, C; http://www.vrg.org/nutshell/market.htm 2003

American Academy of Pediatrics and American College of Obstetricians and Gynecologists; Guidelines for Perinatal Care 1997

Haddad, E; Am J Clin Nutr 2003, 78(Suppl 3), 626S

Hollowell, J; Teratology 1997, 55, 389

Hollowell, J; J Clin Endocrinol Metab 1998, 83, 3401

Johnston, P; Am J Clin Nutr 2000, 71, 1212

Key, T; J Hum Nutr Diet 1992, 5, 323

Krajcovicova-Kudlackova, M; Ann Nutr Metab 2003, 47, 183

Lawrence, J; Thyroid 2000, 10, 659

Lightowler, H; Br J Nutr 1998, 80, 529

Living Foods; http://www.living-foods.com 2003

Messina, V; J Am Diet Assoc 2001, 101, 661

Moss, A; Use of Vitamin and Mineral Supplements in the United States: Current users, Types of Products, and Nutrients 1989, 174

National Academy of Sciences; Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2001

NAS (National Academy of Sciences); Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc 2001

NAS (National Academy of Sciences); http://www4.nas.edu/webcr.nsf/ProjectScopeDisplay/BEST-K-03-05-A?OpenDocument 2003

NCHS (National Center for Health Statistics); Vital and Health Statistics: Use of Dietary supplements in the United States, 1988-1994 1999

NRC (National Research Council); Science and Judgment in Risk Assessment 1994

NRA (National Restaurant Association); http://www.restaurant.org/rusa/magarticle.cfm?articleID = 324 1999

OEHHA (Office of Environmental Health Hazard Assessment); Public Health Goal for Perchlorate in Drinking Water 2004

Pearce, E; Thyroid 2004, 14, 327

Pearce, E; J Clin Endocrinol Metab 2004, 89, 3421

Pennington, J; J Food Comp Anal 1995, 8, 171

Perry, C; Arch Pediatr Adolesc Med 2002, 156, 431

Phillips, R; Am J Epidemiol 1980, 112, 296

Presidential/Congressional Commission (Presidential/Congressional Commission on Risk Assessment and Risk Management); Risk Assessment and Risk Management in Regulatory Decision-Making (Final Report) 1997, 2

Rauma, A; Nutr Res 1994, 14, 1789

Remer, T; Br J Nutr 1999, 81, 45

Strawson, J; Regul Toxicol Pharmacol 2004, 39, 44

Teas, J; Thyroid 2004, 14, 836

USDA (US Department of Agriculture); Continuing Survey of Food Intake by Individuals, 1994-1996, 1998 2000

US EPA (US Environmental Protection Agency); Risk Assessment Forum 2002, EPA/630/P-02/002A

VRG (Vegetarian Resource Group); Harris Interactive Survey 2003, http://www.vrg.org/journal/vj2003issue3/vj2003issue3poll.htm 2003

VRG (Vegetarian Resource Group); Roper Poll 1997, http://www.vrg.org/journal/vj97sep/979poll.htm 2003

VRG (Vegetarian Resource Group); Zogby Poll 2000, http://www.vrg.org/nutshell/poll2000.htm 2003

Weinsier, R; Am J Clin Nutr 2000, 71, 1211

White, R; West J Med 1994, 160, 465

White, R; J Am Diet Assoc 1999, 99, 595

WHO/UNICEF/ICCIDD; Assessment of Iodine Deficiency Disorders and Monitoring their Elimination 2001, WHO/NHD/01.1

Wiersinga, W; Contemporary Endocrinology: Diseases of the Thyroid 2003, 347

Wolff, J; Pharmacol Rev 1998, 50, 89

23. Waldmann, A.; Koschizke, J. W.; Leitzmann, C.; Hahn, A. German Vegan Study: Diet, Life-Style Factors, and Cardiovascular Risk Profile. Annals of Nutrition & Metabolism (2005), 49(6), 366-372.

Abstract

Background/Aim: Evaluation of cardiovascular risk profile in 154 German vegans. Methods: Cross-sectional study, Germany. Study instruments: 2 FFQ, 2 questionnaires, analyses of fasting venous blood samples. Results: The total study population had a low BMI (mean: 22.3 kg/m2), a moderate blood pressure (mean: 120/75 mm Hg), an extremely low consumption of alc. (mean: 0.77 g/day) and 96.8% were nonsmokers. Moderate phys. activity (PAL) was reported by nearly 50%, whereas 22.7% declared to have a high PAL (>3 h/wk). Median triacylglycerol (TG) was 0.81 mmol/l, total cholesterol (TC) was 4.33 mmol/l, HDL was 1.34 mmol/l. The mean TC/HDL-ratio was 3.3. Lipoprotein(a) (Lp(a)) was 8.13 mg/dL, concns. of >30 mg/dL were prevalent in 25% of the participants. In general, status of folate and pyridoxine were sufficient, while 49.7% showed cobalamin concns. <150 pmol/l. Plasma homocysteine levels were slightly elevated (median: 12.5 mol/l). Cobalamin concn. and duration of vegan nutrition were the main determinants of homocysteine in the total study population. Conclusion: Although TC and LDL concns. were favorable, low HDL and elevated homocysteine and Lp(a) concns. were unfavorable. Overall, these results confirm the notion that a vegan diet is deficient in vitamin B12, which may have an unfavorable effect on CHD risk.

Citations

1) Statistisches, B; http://www.destatis.de/basis/d/gesu/gesutab19.htm 2003

2) Hennekens, C; Cardiol Clin 1998, 16, 1

3) Hackman, D; JAMA 2003, 290, 947

4) Spiller, G; J Am Coll Nutr 1998, 17, 407

5) Refsum, H; Ann Rev Med 1998, 49, 31

6) Boushey, C; JAMA 1995, 274, 1049

7) Herrmann, W; Clin Chem 2001, 47, 1094

8) Selhub, J; JAMA 1993, 270, 2693

9) Gerhard, G; Curr Opin Lipidol 1999, 10, 417

10) Seman, L; Clin Chem 1999, 45, 1039

11) Rodriguez, C; Chem Phys Lipids 1994, 67/68, 389

12) Seman, L; Clin Chem 1994, 40, 400

13) Schaefer, E; JAMA 1994, 271, 999

14) Steinmetz, A; Internist 1992, 33, 24

15) Genest, J; Am J Cardiol 1991, 67, 1039

16) Pan, J; Metabolism 2002, 51, 1120

17) Hu, F; Am J Clin Nutr 2003, 78(suppl), S544

18) Key, T; Am J Clin Nutr 1999, 70, 516S

19) Waldmann, A; Eur J Clin Nutr 2003, 57, 947

20) Hoffmann, I; Am J Clin Nutr 1994, 59(suppl), 284

21) Brewster, M; Clinical Chemistry:Theory, Analysis, and Correlation 1989, 543

22) Chen, I; Clinical Chemistry:Theory, Analysis, and Correlation 1989, 569

23) McNeely, M; Clinical Chemistry:Theory, Analysis, and Correlation 1989, 539

24) Ubbink, J; J Chromatogr 1991, 565, 441

25) Canham, J; Am J Clin Nutr 1972, 25, 629

26) The International Task Force For Prevention Of Coronary Heart Disease In Cooperation With The Atherosclerosis Society; Nutr Metab Cardiovasc Dis 1998, 8, 205

27) Broenstrup, A; Ernahrungs-Umschau 1996, 43, 80

28) Hajar, K; Annu Rev Med 1996, 47, 423

29) Fraser, G; Prev Med 1999, 29(suppl), S18

30) Cooper, R; West J Med 1984, 140, 471

31) Davey, G; IARC Sci Publ 2002, 156, 113

32) Thorogood, M; Br Med J 1994, 308, 1667

33) Frentzel-Beyme, R; Am J Clin Nutr 1994, 59(suppl), 1143S

34) Rottka, H; Bibl Nutr Dieta 1990, 45, 176

35) Dge; Referenzwerte fur die Nahrstoffzufuhr 2000

36) Who; Diet, nutrition and the prevention of chronic diseases 1991

37) Davis, B; Am J Clin Nutr 2003, 78(suppl), 640S

38) Richter, V; Z Gerontol Geriat 2004, 37, 207

39) Bissoli, L; Ann Nutr Metabol 2002, 46, 73

40) Appleby, P; Am J Clin Nutr 1999, 70(suppl), 525S

41) Schwahn, B; Am J Pharmacogenomics 2001, 1, 189

42) Quinlinvan, E; Lancet 2002, 359, 227

43) Krajcovicova-Kudlackova, M; Ann Nutr Metabol 2000, 44, 135

44) Lewerin, C; Eur J Clin Nutr 2003, 57, 1426

45) Scanu, A; J Am Med Assoc 1992, 267, 3326

46) Li, D; Clin Sci 1999, 97, 175

24. Leblanc, J.-C.; Tard, A.; Volatier, J.-L.; Verger, P. Estimated dietary exposure to principal food mycotoxins from The First French Total Diet Study. Food Additives & Contaminants (2005), 22(7), 652-672.

Abstract

This study reports ests. on dietary exposure from the first French Total Diet Study (FTDS) and compares these ests. with both existing tolerable daily intakes for these toxins and the intakes calcd. during previous French studies. To est. the dietary exposure of the French population to the principal mycotoxins in the French diet (as consumed), 456 composite samples were prepd. from 2280 individual samples and analyzed for aflatoxins, ochratoxin A, trichothecenes, zearalenone, fumonisins and patulin. Av. and high percentile intakes were calcd. taking account of different eating patterns for adults, children and vegetarians. The results showed that contaminant levels obsd. in the foods examd. as consumed' complied fully with current European legislation. However, particular attention needs to be paid to the exposure of specific population groups, such as children and vegans/macrobiotics, who could be exposed to certain mycotoxins in quantities that exceed the tolerable or weekly daily intake levels. This observation is particularly relevant with respect to ochratoxin A, deoxynivalenol and zearalenone. For these mycotoxins, cereals and cereal products were the main contributors to high exposure.

Indexing -- Section 17-5 (Food and Feed Chemistry)

Bakery products

(biscuits; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Meat

(byproducts; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Bakery products

(cakes; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Development, mammalian postnatal

(child; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Alcoholic beverages

Beverages

Bread

Breakfast cereal

Butter

Cereal (grain)

Cheese

Chocolate

Coffea

Confectionery

Dairy products

Desserts

Diet

Egg, poultry

Food

Food contamination

Fruit

Human

Meat

Milk

Nut (seed)

Oryza sativa

Pasta

Soups

Vegetable

(estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Aflatoxins

Fumonisins

Mycotoxins

Role: POL (Pollutant); OCCU (Occurrence)

(estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Seed

(oilseed; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Bakery products

(pizza; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Meat

(poultry; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Food

(salads; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Sesquiterpenes

Role: POL (Pollutant); OCCU (Occurrence)

(trichothecane; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Diet

(vegetarian, lacto-ovo-; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Diet

(vegetarian; estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

149-29-1, Patulin

303-47-9, Ochratoxin A

1162-65-8, Aflatoxin B1

6795-23-9, Aflatoxin M1

17924-92-4, Zearalenone

23282-20-4, Nivalenol

51481-10-8, Deoxynivalenol

Role: POL (Pollutant); OCCU (Occurrence)

(estd. dietary exposure to principal food mycotoxins from The First French Total Diet Study)

Supplementary Terms

diet mycotoxin food contamination

Citations

Bhat, R; Third Joint FAO/WHO/UNEP International Conference on Mycotoxins 1999

Codex Committee On Food Additives And Contaminants; Thirty-fourth Session 2002

Codex Committee On Foods Additives And Contaminants; Thirty-sixth Session (CDR3, annex II) 2004

Combris, P; Rapport du laboratoire de recherches sur la consommation 2000

Credoc; Technical Note of the Credoc et de l'AFSSA pour l'INRA 2000

Credoc; Enquete INCA individuelle et nationale sur les consommations alimentaires, coordinated by Volatier JL 2000

Credoc; Rapport du Credoc No CP004 1996

Ec Commission; Regulation No 466/2001, setting maximum levels for certain contaminants in foodstuffs 2001

Ec Commission; Regulation No 1425/2003, amending Regulation (EC) No 466/2001 setting maximum levels for certain contaminants in foodstuffs 2003

Fao; Report of a FAO/WHO Consultation 1997

Jecfa; Forty-fourth Meeting of the Joint FAO/WHO Expert Committee on Food Additives Food Additives Series No 35 1995, 377

Jecfa; Forty-ninth Report Technical Report Series No 884 1999, 69

Jecfa; Safety evaluation of certain mycotoxins in food 2001

Leblanc, J; Etude de l'alimentation totale francaise-mycotoxines, mineraux et elements traces 2004

Leblanc, J; European Journal of Clinical Nutrition 2000, 54, 443

Mirocha, C; Journal of the Association of Official Analytical Chemistry 1974, 57, 1104

Scientific Committee For Food; Thirty-fifth Report Opinion on aflatoxins B1, B2, G1, G2, M1 and patulin 1994

Scientific Committee For Food; Opinion on ochratoxin A 1998

Scientific Committee For Food; Part 2: Evaluation of zearalenone 2000

Scientific Committee For Food; Part 3: Evaluation of Fumonisins 2000

Scientific Committee For Food; Part 6: Group evaluation of T-2 toxin, HT-2 toxin, nivalenol and deoxynivalenol 2002

Scoop; Task 3.2.7 Assessment of dietary intake of ochratoxin A by the population of EU Members States 1999

Scoop; Reports on Tasks 3.2.8 Assessment of dietary intake of patulin by the population of EU members states 2002

Scoop; Reports on Tasks 3.2.10 Assessment of dietary intake of fusariums by the population of EU members states 2003

Scudamore, K; Food Additives and Contaminants 1998, 15, 401

Tressou, J; Food Chemical and Toxicology 2004, 42, 1349

Trucksess, M; Journal of the AOAC International 1999, 82, 85

Trucksess, M; Journal of the Association of Official Analytical Chemistry 1991, 74, 81

Vannoort, R; Part 2: Elements 1997-1998

Verger, P; CSHPF, Les mycotoxines dans l'alimentation:Evaluation theorique de l'exposition aux aflatoxines 1999

Who; IWTDS, International Total Diet Workshop, 1st IWTDS 1999

Who; IWTDS, International Total Diet Workshop, 2nd IWTDS 2002

Who; IWTDS, International Total Diet Workshop, 3rd IWTDS 2004

25. Waldmann, Annika; Koschizke, Jochen W.; Leitzmann, Claus; Hahn, Andreas. Dietary intakes and blood concentrations of antioxidant vitamins in German vegans. International Journal for Vitamin and Nutrition Research (2005), 75(1), 28-36.

Abstract

The authors report on an evaluation of intake and blood concns. of antioxidant vitamins in a cross-sectional study of 104 German vegans, and examine the assocn. between blood concn. of antioxidant vitamins and their intake as well as fruit and vegetable intake. Comparisons are made with dietary ref. intakes and established threshold values (ETV) for blood concns. Mean intakes of vitamin C, E, and beta-carotene were higher than actual recommendations, but comparable to reported intakes in other vegan cohorts. Mean blood concns. were 0.76 mol/L for beta-carotene and 117 mol/L for vitamin C, so that nearly all participants showed concns. that were above the ETV for the prevention of chronic diseases. Although mean vitamin E intake was 24.8 mg/day, only 32% of female and 18% of male participants showed plasma concns. above the ETV. However, the mean vitamin E/cholesterol ratio was high (5.97), indicating a good protection of low-d. lipoprotein (LDL) against peroxidn. Of the reported antioxidant vitamins, only plasma vitamin C concn. was a good biomarker of fruit and vegetable intake. The high concn. of antioxidative compds. in plasma may be one of the reasons for the lower incidence of chronic diseases in people consuming a plant-only diet.

Indexing -- Section 18-2 (Animal Nutrition)

Vitamins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(antioxidant; dietary intakes and blood concns. of antioxidant vitamins in German vegans)

Blood

Fruit

Human

Sex

Vegetable

(dietary intakes and blood concns. of antioxidant vitamins in German vegans)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-3; dietary intakes and blood concns. of antioxidant vitamins in German vegans)

Diet

(vegetarian; dietary intakes and blood concns. of antioxidant vitamins in German vegans)

50-81-7, Vitamin C, biological studies

57-88-5, Cholesterol, biological studies

1406-18-4, Vitamin E

7235-40-7, -Carotene

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(dietary intakes and blood concns. of antioxidant vitamins in German vegans)

Supplementary Terms

vegan diet antioxidant vitamin intake

Citations

1) Appleby, P; Am J Clin Nutr 1999, 70(Suppl), 525S

2) Key, T; Proc Nutr Soc 1999, 58, 271

3) Key, T; Am J Clin Nutr 1999, 70(Suppl), 516S

4) Thorogood, M; Br Med J 1994, 308, 1667

5) Chang-Claude, J; Epidemiology 1992, 3, 395

6) Kris-Etherton, P; Am J Med 2002, 113(Suppl 9B), 71S

7) Gey, K; Bibl Nutr Dieta 1995, 52, 75

8) Heseker, H; VERA-Schriftenreihe, 2. uberarb Auflage 1994, III

9) Heseker, H; VERA-Schriftenreihe 1994, IV

10) Lowry, O; J Biol Chem 1943, 147, 609

11) Vuilleumier, J; Int J Vitam Nutr Res 1983, 53, 265

12) Eichholzer, M; Int J Vitam Nutr Res 2001, 71, 5

13) Virtamo, J; JAMA 2003, 290, 476

14) Baron, J; J Natl Cancer Inst 2003, 95, 717

15) Marchioli, R; Lipids 2001, 36(Suppl), S53

16) Hu, F; Am J Clin Nutr 2003, 78(Suppl), 544S

17) Ness, A; Int J Epidemiol 1997, 26, 1

18) Task-Force (The International Task Force for Prevention of Coronary Heart Disease); Nutr Metab Cardiovasc Dis 1998, 8, 205

19) WCRF (World Cancer Research Fund); Food, Nutrition and the Prevention of Cancer 1997, 670

20) WHO World Health Organization; Diet, nutrition and the prevention of chronic diseases 1991

21) Kobayashi, M; J Epidemiol 2003, 13(1 Suppl), S82

22) Rauma, A; Am J Clin Nutr 1995, 62, 1221

23) Ford, E; Am J Epidemiol 1999, 150, 290

24) Forman, M; Am J Clin Nutr 1993, 58, 519

25) Sinha, R; Cancer Epidemiol Biomarkers Prev 1993, 2, 473

26) Block, G; Am J Epidemiol 2001, 154, 1113

27) Drewnowski, A; Am J Clin Nutr 1997, 65, 1796

28) Krajcovicova-Kudlackova, M; Bratisl Lek Listy 2003, 104, 64

29) Krajcovicova-Kudlackova, M; Ann Nutr Metab 1995, 39, 334

30) Jacques, P; Am J Clin Nutr 1993, 57, 182

31) Khaw, K; Lancet 2001, 257, 657

32) Weber, P; Int J Vitam Nutr Res 1996, 66, 19

33) Davey, G; Public Health Nutr 2003, 6, 259

34) Donovan, U; J Adolesc Health 1996, 18(4), 292

35) Freeland-Graves, J; Am J Diet Assoc 1980, 77, 655

36) DGE (Deutsche Gesellschaft fur Ernahrung); Referenzwerte fur die Nahrstoffzufuhr 2000, 240

37) Draper, A; Br J Nutr 1993, 69, 3

38) Stryker, W; Am J Epidemiol 1988, 127, 283

39) Herbeth, B; Am J Epidemiol 1990, 132, 394

40) Krajcovicova-Kudlackova, M; Nahrung 1996, 40, 17

41) Johnson, L; J Agromedicine 2003, 9, 65

42) Gritschneder, K; Z Gerontol Geriat 1998, 31, 448

43) Scott, K; Br J Nutr 1996, 75, 409

44) Gassmann, B; Ernahrungs-Umschau 1995, 42, 80

45) Weber, P; Nutrition 1997, 13, 450

46) Meydani, M; Proc Nutr Soc 2002, 61, 165

47) Albertinti, R; Curr Mol Med 2002, 2, 579

48) Heinecke, J; Curr Atheroscler Rep 2003, 5, 83

49) Hodis, H; Circulation 2002, 106, 1453

50) Willett, W; Am J Clin Nutr 1983, 38, 559

51) Krajcovicova-Kudlackova, M; Oncol Rep 1995, 2, 77

52) Esterbauer, H; Free Radic Biol Med 1992, 13(4), 341

53) Holvoet, P; Arterioscler Thromb Vasc Biol 2001, 21, 844

54) Nordin Fredrikson, G; J Intern Med 2003, 253, 425

26. Stamp, Lisa K.; James, Michael J.; Cleland, Leslie G. Diet and Rheumatoid Arthritis: A Review of the Literature. Seminars in Arthritis and Rheumatism (2005), 35(2), 77-94.

Abstract

A review. Introduction: Rheumatoid arthritis is a common inflammatory condition. A large no. of patients seek alternative or complementary therapies of which diet is an important component. This article reviews the evidence for diet in rheumatoid arthritis along with the assocd. concept of oral tolerization. Methods: Refs. were taken from Medline from 1966 to Sept. 2004. The keywords, rheumatoid arthritis, diet, n-3 fatty acids, vitamins, and oral tolerization, were used. Results: Randomized controlled trials (RCTs) indicate that dietary supplementation with n-3 fatty acids provides modest symptomatic benefit in groups of patients with rheumatoid arthritis. Epidemiol. studies and RCTs show cardiovascular benefits in the broader population and patients with ischemic heart disease. A no. of mechanisms through which n-3 fats may reduce inflammation have been identified. In a small no. of patients with rheumatoid arthritis, other dietary manipulation such as fasting, vegan, and elimination diets may have some benefit. However, many of these diets are impractical or difficult to sustain long term. Conclusions: Dietary manipulation provides a means by which patients can a regain a sense of control over their disease. Dietary n-3 supplementation is practical and can be easily achieved with encapsulated or, less expensively, bottled fish oil.

Indexing -- Section 18-0 (Animal Nutrition)

Section cross-reference(s): 1

Antirheumatic agents

Cardiovascular system, disease

(cardiovascular disease, rheumatoid arthritis, and n-3 fatty acids)

Dietary supplements

Fasting

Human

Inflammation

Rheumatoid arthritis

(dietary supplementation with n-3 fatty acid reduces inflammation and provides modest symptomatic benefit in patient with rheumatoid arthritis)

Anti-inflammatory agents

(effect of fish oil on nsaid use in rheumatoid arthritis patients)

Fats and Glyceridic oils, biological studies

Role: BSU (Biological study, unclassified); PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(fish; dietary supplementation with n-3 fatty acid reduces inflammation and provides modest symptomatic benefit in patient with rheumatoid arthritis)

Food allergy

(food hypersensitivity and rheumatoid arthritis)

Anti-inflammatory agents

(nonsteroidal; effect of fish oil on nsaid use in rheumatoid arthritis patients)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(polyunsatd., omega-3; dietary supplementation with n-3 fatty acid reduces inflammation and provides modest symptomatic benefit in patient with rheumatoid arthritis)

Diet

(vegetarian; dietary supplementation with n-3 fatty acid reduces inflammation and provides modest symptomatic benefit in patient with rheumatoid arthritis)

Vitamins

Role: BSU (Biological study, unclassified); PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(vitamin supplements for patients with rheumatoid arthritis)

Supplementary Terms

review supplement fatty acid fish oil inflammation rheumatoid arthritis; vegan diet fasting antiinflammatory cardiovascular disease vitamin food review

Citations

1) Martin, R; Proc Nutr Soc 1998, 57, 231

2) Salminen, E; Prev Med 2002, 34, 529

3) Simopoulos, A; Am J Clin Nutr 1991, 54, 438

4) Salmon, J; Br Med Bull 1987, 43, 285

5) Caughey, G; J Immunol 1997, 158, 351

6) Hawkes, J; Prostaglandins 1991, 42, 355

7) Hawkes, J; Agents Actions 1992, 35, 85

8) Prescott, S; J Biol Chem 1984, 259, 7615

9) Goldman, D; Biochem Biophys Res Commun 1983, 117, 282

10) Lee, T; N Engl J Med 1985, 312, 1217

11) Arend, W; Arthritis Rheum 1995, 38, 151

12) Badolato, R; Semin Arthritis Rheum 1996, 26, 526

13) Brennan, F; Br J Rheumatol 1992, 31, 293

14) Moreland, L; Ann Intern Med 1999, 130, 478

15) Weinblatt, M; N Engl J Med 1999, 340, 253

16) Maini, R; Arthritis Rheum 1998, 41, 1552

17) Bresnihan, B; Arthritis Rheum 1998, 41, 2196

18) Grimble, R; Am J Clin Nutr 2002, 76, 454

19) Jump, D; Ann Rev Nutr 1999, 19, 63

20) de Urquiza, A; Science 2000, 275, 721

21) Curtis, C; J Biol Chem 2000, 275, 721

22) Penglis, P; J Immunol 2000, 165, 1605

23) Serhan, C; J Exp Med 2000, 192, 1197

24) Serhan, C; J Exp Med 2002, 196, 1025

25) Zerva, L; J Exp Med 1996, 183, 829

26) Abbas, A; Cellular and Molecular Immunology (ed 4) 2000

27) Firestein, G; Arthritis Rheum 1987, 30, 857

28) Fujikawa, M; Immunology 1992, 75, 330

29) Hughes, D; J Nutr 1996, 126, 603

30) Hughes, D; Am J Clin Nutr 2000, 71, 357S

31) Hughes, D; Am J Clin Nutr 1996, 63, 267

32) Liao, H; Rheum Dis Clin North Am 1995, 21, 715

33) Kavanagh, A; Arthritis Rheum 1994, 37, 992

34) Curtis, C; Arthritis Rheum 2002, 46, 1544

35) James, M; Semin Arthritis Rheum 1997, 27, 85

36) Fortin, P; J Clin Epidemiol 1995, 48, 1379

37) Ariza-Ariza, R; Semin Arthritis Rheum 1998, 27, 366

38) Kremer, J; Lancet 1985, 185

39) Adam, O; Rheumatol Int 2003, 23, 27

40) Volker, D; J Rheumatol 2000, 27, 2343

41) Cleland, L; Am J Clin Nutr 1992, 55, 395

42) Kremer, J; Arthritis Rheum 1990, 33, 810

43) Cleland, L; Lipids 2003, 38, 419

44) Kremer, J; Arthritis Rheum 1995, 38, 1107

45) Kjeldsen-Kragh, J; J Rheumatol 1992, 19, 1531

46) Lau, C; Br J Rheumatol 1993, 32, 982

47) Skoldstam, L; Scand J Rheumatol 1992, 21, 178

48) Caughey, G; Am J Clin Nutr 1996, 63, 116

49) Demasi, M; Inflamm Res 2000, 49, 737

50) Mantzioris, E; Am J Clin Nutr 2000, 72, 42

51) Myllykangas-Luosujarvi, R; Semin Arthritis Rheum 1995, 25, 193

52) Symmons, D; J Rheumatol 1998, 25, 1072

53) Bacon, P; Arthritis Rheum 2001, 44, 2707

54) Roubenoff, R; Arthritis Rheum 1997, 40, 718

55) Landewe, R; Lancet 2000, 355, 1616

56) Haagsma, C; Ann Rheum Dis 1999, 58, 79

57) Rogers, T; Transplantation 1988, 45, 153

58) Elzinga, L; Transplantation 1987, 43, 271

59) Busnach, G; J Nephrol 1998, 11, 87

60) van der Heide, H; Transplantation 1990, 49, 523

61) Catella-Lawson, F; N Engl J Med 2001, 345, 1809

62) Bombardier, C; N Engl J Med 2000, 343, 1520

63) Clark, D; Drug Saf 2004, 27, 427

64) Solomon, S; N Engl J Med 2005, 352, 1071

65) Merck; www.vioxx.com/rofecoxib/vioxx/consumer/index 2004

66) Bresalier, R; N Engl J Med 2005, 325, 1092

67) Lorenz, R; Circulation 1983, 67, 504

68) Von Schaky, C; J Clin Invest 1985, 76, 1626

69) Albert, C; J Am Med Assoc 1998, 279, 23

70) Albert, C; N Engl J Med 2002, 346, 1113

71) James, M; www.goldncanola.com.au 2000

72) Burr, M; Lancet 1989, 334, 757

73) Anon; Lancet 1999, 354, 447

74) Marcholi, R; Circulation 2002, 105, 1897

75) Kang, J; Am J Clin Nutr 2000, 71, 202S

76) Schrepf, R; Lancet 2004, 363, 1441

77) Metcalf, R; Heart Lung Circ 2004, 13S, 132

78) Horowitz, M; Gastroenterology 1993, 105, 382

79) Metcalf, R; Eur J Clin Nutr 2003, 57, 1605

80) Cleland, L; J Rheumatol 1988, 15, 1471

81) Shapiro, J; Epidemiology 1996, 7, 256

82) Shichikawa, K; Ryumachi 1981, 21, 35

83) Nishimoto, T; Tissue Antigens 1993, 42, 497

84) Tokunaga, N; Nephron 1999, 81, 165

85) Gibson, R; Am J Clin Nutr 1981, 34, 252

86) Barrett, J; Arthritis Rheum 2000, 43, 1010

87) James, D; J Rheumatol 1983, 10, 184

88) Farrell, A; Ann Rheum Dis 1992, 51, 1219

89) Halliwell, B; Ann Rheum Dis 1995, 54, 505

90) McNeil, J; Ann Rheum Dis 1985, 44, 780

91) Sato, M; J Rheumatol 1996, 23, 432

92) Remans, P; Eur J Clin Nutr 2004, 58, 839

93) Kulmacz, R; Biochem Biophys Res Commun 1985, 130, 918

94) Wu, D; J Nutr 2001, 131, 382S

95) Devaraj, S; J Clin Invest 1996, 98, 756

96) Devaraj, S; Arterscler Thromb Vasc Biol 1998, 19, 1125

97) de Bandt, M; Arthritis Rheum 2002, 46, 522

98) Venkatraman, J; J Am Coll Nutr 1999, 18, 602

99) Abate, A; Free Radic Biol Med 2000, 29, 1135

100) Paredes, S; J Rheumatol 2002, 29, 2271

101) Edmonds, S; Ann Rheum Dis 1997, 56, 649

102) Wittenborg, A; J Rheumatol 1998, 57, 215

103) Sakai, A; Arch Orthop Trauma Surg 1999, 119, 121

104) Davis, R; J Am Podiatr Med Assoc 1990, 80, 414

105) Mangge, H; Scand J Rheumatol 1999, 28, 201

106) Peretz, A; Semin Arthritis Rheum 1991, 20, 305

107) O'Dell, J; Ann Rheum Dis 1991, 50, 376

108) Kose, K; Biol Trace Element Res 1996, 53, 51

109) Heinle, K; Med Klin 1997, 92, 29

110) Stone, J; Semin Arthritis Rheum 1997, 27, 180

111) Tarp, U; Scand J Rheumatol 1985, 14, 364

112) Petersson, I; Scand J Rheumatol 1991, 20, 218

113) Jantti, J; Scand J Rheumatol 1991, 20, 225

114) Peretz, A; Scand J Rheumatol 2001, 30, 208

115) Tarp, U; Ann Rheum Dis 1992, 51, 1044

116) Roubenoff, R; Arthritis Rheum 1995, 38, 105

117) Bekpinar, S; Clin Chim Acta 2002, 329, 143

118) Chiang, E; Am J Med 2003, 114, 283

119) Schumacher, H; Am J Clin Nutr 1975, 28, 1200

120) Bae, S; J Am Coll Nutr 2003, 22, 311

121) Heliovaara, M; Ann Rheum Dis 1994, 53, 51

122) Comstock, G; Ann Rheum Dis 1997, 56, 323

123) Cerhan, J; Am J Epidemiol 2003, 157, 345

124) Lunardi, C; Clin Exp Rheumatol 1988, 6, 423

125) Williams, R; Br Med J 1981, 283, 563

126) Parke, A; BMJ 1981, 282, 2027

127) Holst-Jensen, S; Scand J Rheumatol 1998, 27, 329

128) Kavanagh, R; Br J Rheumatol 1995, 34, 270

129) Haugen, M; Clin Exp Rheumatol 1994, 12, 275

130) Kjeldsen-Kragh, J; Lancet 1991, 338, 899

131) Kjeldsen-Kragh, J; Scand J Rheumatol 1995, 24, 85

132) Kjeldsen-Kragh, J; Clin Exp Rheumatol 1995, 13, 167

133) Skoldstam, L; Scand J Rheumatol 1979, 8, 249

134) Nenonen, M; Br J Rheumatol 1998, 37, 274

135) Hafstrom, I; Rheumatology 2001, 40, 1175

136) Muller, H; Scand J Rheumatol 2001, 30, 1

137) Skoldstam, L; Ann Rheum Dis 2003, 62, 207

138) McDougall, J; J Altern Complement Med 2002, 8, 71

139) Sarzi-Puttini, P; Scand J Rheumatol 2000, 29, 302

140) Hafstrom, I; Arthritis Rheum 1988, 31, 585

141) Uden, A; Ann Rheum Dis 1983, 42, 45

142) Panush, R; Arthritis Rheum 1986, 29, 220

143) Panush, R; J Rheumatol 1990, 17, 291

144) van der Laar, M; Ann Rheum Dis 1992, 51, 303

145) van der Laar, M; Semin Arthritis Rheum 1991, 21, 12

146) Darlington, L; Lancet 1986, 236

147) Beri, D; Ann Rheum Dis 1988, 47, 69

148) Panush, R; Arthritis Rheum 1983, 26, 462

149) van der Laar, M; Ann Rheum Dis 1992, 51, 298

150) Kjeldsen-Kragh, J; Br J Rheumatol 1994, 33, 569

151) Chandra, R; Am J Clin Nutr 1991, 53, 1087

152) Roubenoff, R; J Clin Invest 1994, 93, 2379

153) Haugen, M; Br J Nutr 1994, 72, 555

154) Fraser, D; Clin Exp Rheumatol 2000, 18, 357

155) Shinebaum, R; Br J Rheumatol 1987, 26, 329

156) Wilson, C; Ann Rheum Dis 1995, 54, 216

157) Deighton, C; Br J Rheumatol 1992, 31, 241

158) Kjeldsen-Kragh, J; Ann Rheum Dis 1995, 54, 221

159) Peltonen, R; Br J Rheumatol 1997, 86, 64

160) Cordain, L; Br J Nutr 2000, 83, 207

161) Weiner, H; Ann Rev Immunol 1994, 12, 809

162) Trentham, D; Science 1993, 261, 1727

163) Seiper, J; Arthritis Rheum 1996, 39, 41

164) Barnett, M; Arthritis Rheum 1998, 41, 290

165) McKown, K; Arthritis Rheum 1999, 42, 1204

166) Hauselmann, H; Br J Rheumatol 1998, 17, 1110

167) Kalden, J; Arthritis Rheum 1998, 41, 191

168) Bardos, T; Clin Exp Immunol 2002, 129, 224

169) Garcia, G; J Autoimmun 1999, 13, 315

170) Endres, S; N Engl J Med 1989, 320, 265

171) Molvig, J; Scand J Immunol 1991, 34, 399

172) Meydani, S; J Nutr 1991, 121, 547

173) Meydani, S; J Biol Chem 1993, 92, 105

174) Gallai, V; J Neuroimmunol 1995, 56, 143

175) Schmidt, E; Scand J Clin Lab Invest 1996, 56, 87

176) Blok, W; Eur J Clin Invest 1997, 27, 1003

177) Kelley, D; Lipids 1999, 34, 317

178) Yaqoob, P; Eur J Clin Invest 2000, 30, 260

179) Geusens, P; Arthritis Rheum 1994, 37, 824

180) Nielsen, G; Eur J Clin Invest 1992, 22, 687

181) van der Tempel, H; Ann Rheum Dis 1990, 49, 76

182) Tulleken, J; Arthritis Rheum 1990, 33, 1416

183) Kremer, J; Ann Intern Med 1987, 106, 497

27. Smith, G. Richard; Collinson, Paul O.; Kiely, Patrick D. W. Diagnosing hypovitaminosis D: serum measurements of calcium, phosphate, and alkaline phosphatase are unreliable, even in the presence of secondary hyperparathyroidism. Journal of Rheumatology (2005), 32(4), 684-689.

Abstract

To ascertain the ability of routine biochem. markers of bone turnover to predict vitamin D insufficiency. Receiver operating characteristic (ROC) anal. was used to assess the value of serum, alk. phosphatase, calcium, and phosphate concns. in the detection of hypovitaminosis D (< 20 nmol/l) in 467 patients between 1998 and 2000 (Cohort 1). The same anal. was repeated in a subsequent group of 719 patients between 2001 and 2003 (Cohort 2), in whom values of parathyroid hormone (PTH) were also available. Samples with elevated parathyroid levels from Cohort 2 were also analyzed to det. whether, in this subset, serum levels of calcium, phosphate, and alk. phosphatase could reliably predict hypovitaminosis D. A subset of 50 patients from Cohort I, with serum Vitamin D < 12 nmol/l, were reviewed by case note and telephone interview to det. demog. characteristics and the prevalence of risk factors for severe hypovitaminosis D. The areas under the ROC curves for alk. phosphatase, calcium, and phosphate were all less than 0.7 (the criterion for a useful test) in both Cohorts 1 and 2. In the subset of Cohort 2 with elevated serum PTH levels (n = 337), the area under the ROC curve for calcium was 0.701 (95% confidence interval 0.643-0.758), and less than 0.7 for alk. phosphatase and phosphate. In the 50 patients from Cohort I with severe hypovitaminosis D, risk factors were prevalent: 66% were vegetarian or vegan, clothing was partially or completely occlusive of sunlight (veiling) in 72%, and 60% of this cohort went outdoors less than 5 times per wk. Symptoms were non-specific in the majority. Routine measurements of calcium, phosphate, and alk. phosphatase are not reliable predictors of hypovitaminosis D, even when vitamin D insufficiency has been sufficient to produce a PTH response. Clin. suspicion based upon history and an awareness of risk factors should remain the gold std. for requesting serum vitamin D measurements.

Inadequate sunlight exposure (through veiling and poor outdoor exposure) and poor dietary intake are highly prevalent features of hypovitaminosis D in severely affected patients.

Indexing -- Section 14-14 (Mammalian Pathological Biochemistry)

Section cross-reference(s): 18

Diet

(restricted; serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in presence of secondary hyperparathyroidism to diagnose hypovitaminosis D in relation to risk factors, sunlight exposure and poor dietary intake)

Hyperparathyroidism

(secondary; serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in presence of secondary hyperparathyroidism to diagnose hypovitaminosis D in relation to risk factors, sunlight exposure and poor dietary intake)

Biomarkers

Blood analysis

Blood serum

Bone resorption

Diagnosis

Human

Risk assessment

Solar radiation

(serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in presence of secondary hyperparathyroidism to diagnose hypovitaminosis D in relation to risk factors, sunlight exposure and poor dietary intake)

1406-16-2, Vitamin D

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); DGN (Diagnostic use); BIOL (Biological study); USES (Uses)

(hypovitaminosis; diagnosing hypovitaminosis D in relation to serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in the presence of secondary hyperparathyroidism)

9002-64-6, Parathyroid hormone

Role: ADV (Adverse effect, including toxicity); ANT (Analyte); BSU (Biological study, unclassified); DGN (Diagnostic use); ANST (Analytical study); BIOL (Biological study); USES (Uses)

(serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in presence of secondary hyperparathyroidism to diagnose hypovitaminosis D in relation to risk factors, sunlight exposure and poor dietary intake)

7440-70-2, Calcium, biological studies

9001-78-9, Alkaline phosphatase

14265-44-2, Phosphate, biological studies

Role: ANT (Analyte); BSU (Biological study, unclassified); DGN (Diagnostic use); ANST (Analytical study); BIOL (Biological study); USES (Uses)

(serum measurements of calcium, phosphate, and alk. phosphatase are unreliable, even in presence of secondary hyperparathyroidism to diagnose hypovitaminosis D in relation to risk factors, sunlight exposure and poor dietary intake)

Supplementary Terms

hypovitaminosis D diagnosis calcium phosphate alk phosphatase nutrition

Citations

1) Pfeifer, M; Osteoporosis Int 2002, 13, 187

2) Pfeifer, M; Exp Clin Endocrinol Diabetes 2001, 109, 87

3) Eastell, R; Vitamin D 1997, 695

4) Chapuy, M; Vitamin D 1997, 679

5) Chiu, K; J Trauma 1992, 32, 584

6) Merlino, L; Arthritis Rheum 2004, 50, 72

7) Wilkinson, R; Lancet 2000, 355, 618

8) Chapuy, M; Osteoporos Int 1997, 7, 439

9) Pfeifer, M; J Bone Miner Res 2000, 15, 1113

10) Bischoff, H; Arch Phys Med Rehab 1999, 80, 54

11) Glerup, H; Calcif Tissue Int 2000, 66, 419

12) National Center For Health Statistics; Vital and health statistics; series 1 1994, 32

13) Looker, A; N Engl J Med 1998, 339, 344

14) Bettica, P; Osteoporos Int 1999, 9, 226

15) Aguado, P; Osteoporos Int 2000, 11, 739

16) Thomas, M; N Engl J Med 1998, 338, 777

17) Gloth, F; JAMA 1995, 274, 1683

18) Peach, H; J Clin Pathol 1982, 35, 625

19) Campbell, G; Age Ageing 1986, 15, 156

20) Serhan, E; Bone 1999, 25, 609

21) Dhesi, J; Age Ageing 2002, 31, 267

22) Collinson, P; Heart 1998, 80, 215

23) Malabanan, A; Lancet 1998, 351, 805

24) Lips, P; J Clin Endocrinol Metab 2001, 86, 1212

25) Sahota, O; Age Ageing 2001, 30, 467

26) McKenna, M; Am J Med 1992, 93, 69

27) Fuleihan, G; New Engl J Med 1999, 340, 1840

28. Dyett, Patricia Adelle. Developing a valid screening tool for assessing nutritional adequacy and osteoporosis risk among vegans in the United States. (2005), 209 pp.

Indexing -- Section 18-1 (Animal Nutrition)

Section cross-reference(s): 14

Nutrition, animal

Osteoporosis

Risk assessment

(Developing a valid screening tool for assessing nutritional adequacy and osteoporosis risk among vegans in the United States)

Diet

(vegetarian; Developing a valid screening tool for assessing nutritional adequacy and osteoporosis risk among vegans in the United States)

Supplementary Terms

vegan nutrition osteoporosis risk

29. Winiarska-Mieczan, Anna; Mazurek, Katarzyna. Comparison of the nutritional value of traditional, semivegetarian and vegan diets. Zywienie Czlowieka i Metabolizm (2005), 32(3), 203-213.

Abstract

The nutritional value of traditional, semivegetarian, and vegan diets was compared using model 7-day menu and a computer simulation program. The crude protein and carbohydrates contents in the analyzed model diets were similar, but the vegan diet had higher content of dietary fiber. A pos. correlation between crude fat and cholesterol in the diets and the consumption of animal products was noted. The contents of minerals and vitamins B1 and B2 in the vegan diets were lower than in semivegetarian and non-vegetarian diets. Higher level of vitamin C was noted in the vegan vs. the other diets.

Indexing -- Section 18-7 (Animal Nutrition)

Dietary energy

Dietary fiber

Human

Nutrition, animal

(comparison of nutritional value of traditional, semivegetarian and vegan diets using 7-day model menu and computer simulation program)

Carbohydrates, biological studies

Fats and Glyceridic oils, biological studies

Mineral elements, biological studies

Role: FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(comparison of nutritional value of traditional, semivegetarian and vegan diets using 7-day model menu and computer simulation program)

Proteins

Role: FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(dietary; comparison of nutritional value of traditional, semivegetarian and vegan diets using 7-day model menu and computer simulation program)

Diet

(vegetarian; comparison of nutritional value of traditional, semivegetarian and vegan diets using 7-day model menu and computer simulation program)

50-81-7, Vitamin c, biological studies

57-88-5, Cholesterol, biological studies

59-43-8, Vitamin b1, biological studies

83-88-5, Vitamin b2, biological studies

7439-89-6, Iron, biological studies

7439-95-4, Magnesium, biological studies

7440-23-5, Sodium, biological studies

7440-70-2, Calcium, biological studies

7723-14-0, Phosphorus, biological studies

Role: FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(comparison of nutritional value of traditional, semivegetarian and vegan diets using 7-day model menu and computer simulation program)

Supplementary Terms

nutrition semivegetarian vegan diet nutrient content

30. Codazzi Daniela; Sala Francesca; Parini Rossella; Langer Martin Coma and respiratory failure in a child with severe vitamin B(12) deficiency. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies (2005), 6(4), 483-5.

Abstract

OBJECTIVE: Psychofunctional follow-up of severe vitamin B(12) deficit. DESIGN: Case report. SETTING: Pediatric intensive care unit. Patient: Ten-month-old boy. INTERVENTION: Follow-up at 3 yrs. MEASUREMENTS AND MAIN RESULTS: A 10-month-old boy was admitted to the pediatric intensive care unit with respiratory failure, muscular hypotonia, and involuntary movements. Although a central nervous system infection was excluded, computed tomography scan showed a diffuse cortical-subcortical atrophy. Vitamin B(12) deficiency was suspected because of a red-cell count of 1,350,000/mm(3) and a hemoglobin value 5.9 g/dL (MCV 116). The baby had been exclusively breast-fed, but his mother had been a strict vegan for 10 yrs. Chronic dietary vitamin B(12) deprivation was confirmed by blood and urinary samples. Treatment with vitamin B(12) led in 2 wks to rapid and complete hematological improvement and to partial regression of neurologic symptoms. During the following 3 yrs the boy had normal vitamin intake and underwent intensive rehabilitative treatment. The brain atrophy regressed, but linguistic and psychomotor delay persisted. CONCLUSIONS: Rapid clinical improvement after vitamin supply does not correlate with a complete recovery.

Controlled Terms

Check Tags: Female; Male

*Breast Feeding: AE, adverse effects

*Coma: ET, etiology

Developmental Disabilities: ET, etiology

*Diet, Vegetarian: AE, adverse effects

Humans

Infant

*Respiratory Insufficiency: ET, etiology

Vitamin B 12 Deficiency: CO, complications

*Vitamin B 12 Deficiency: ET, etiology

31. Petzke, Klaus J.; Boeing, Heiner; Metges, Cornelia C. Choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance. Rapid Communications in Mass Spectrometry (2005), 19(11), 1392-1400.

Abstract

Stable isotopic (15N, 13C) compn. of tissues depends on isotopic pattern of food sources. We investigated whether the isotopic compns. of human hair protein and amino acids reflect the habitual dietary protein intake. Hair samples were analyzed from 100 omnivores (selected randomly out of the 1987-1988 German nutrition survey VERA), and from 15 ovo-lacto-vegetarians (OLV), and from 6 vegans recruited sep. Hair bulk and amino acid specific isotopic compns. were analyzed by isotope-ratio mass spectrometry (EA/IRMS and GC/C/IRMS, resp.) and the results were correlated with data of the 7 day dietary records. Hair bulk 15N and 13C abundances clearly reflect the particular eating habits. Vegans can be distinguished from OLV and both are significantly distinct from omnivores in both 15N and 13C abundances. 15N and 13C abundances rose with a higher proportion of animal to total protein intake (PAPI). Individual proportions of animal protein consumption (IPAP) were calcd. using isotopic abundances and a linear regression model using animal protein consumption data of vegans (PAPI = 0) and omnivores (mean PAPI = 0.639). IPAP values pos. correlated with the intake of protein, meat, meat products, and animal protein. Distinct patterns for hair amino acid specific 15N and 13C abundances were measured but with lower resoln. between food preference groups compared with bulk values. In conclusion, hair 13C and 15N values both reflected the extent of animal protein consumption. Bulk isotopic abundance of hair can be tested for future use in the validation of dietary assessment methods.

Indexing -- Section 18-3 (Animal Nutrition)

Section cross-reference(s): 8

Body weight

Cheese

Egg, poultry

Hair

Human

Meat

(choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Amino acids, biological studies

Gliadins

Zeins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(dietary; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Animals

(omnivore; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(pea and potato; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Globulins, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(pig; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Gelatins, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(porcine skin; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Albumins, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(serum, bovine and porcine; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Glycinins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(soybean; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Diet

(vegetarian, lacto-ovo-; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Diet

(vegetarian; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Glutens

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(wheat; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(whey; choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

14390-96-6, Nitrogen 15, analysis

14762-74-4, Carbon 13, analysis

Role: ANT (Analyte); ANST (Analytical study)

(choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

56-40-6, Glycine, biological studies

56-41-7, L-Alanine, biological studies

56-45-1, L-Serine, biological studies

56-84-8, L-Aspartic acid, biological studies

56-86-0, L-Glutamic acid, biological studies

56-87-1, L-Lysine, biological studies

60-18-4, L-Tyrosine, biological studies

61-90-5, L-Leucine, biological studies

63-91-2, L-Phenylalanine, biological studies

71-00-1, L-Histidine, biological studies

72-18-4, L-Valine, biological studies

72-19-5, L-Threonine, biological studies

73-32-5, L-Isoleucine, biological studies

147-85-3, L-Proline, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(choice of dietary protein of vegetarians and omnivores is reflected in their hair protein 13C and 15N abundance)

Supplementary Terms

dietary protein vegetarian omnivore hair carbon 15 nitrogen 13

Citations

1) World Cancer Research Fund and American Institute for Cancer Research; Food, Nutrition and the Prevention of Cancer: A Global Perspective 1997

2) Fung, T; Am J Clin Nutr 2003, 78, 357

3) Flood, A; Am J Epidemiol 2003, 158, 59

4) Metges, C; J Nutr 2000, 130, 886

5) Rolland-Cachera, M; Eur J Clin Nutr 2000, 54(Suppl 1), S41

6) Kroke, A; Am J Clin Nutr 1999, 70, 439

7) McKoewn, N; Am J Clin Nutr 2002, 74, 188

8) Macko, S; Phil Trans R Soc Lond B 1999, 354, 65

9) Macko, S; FASEB J 1999, 13, 559

10) O'Connell, T; Am J Phys Anthropol 1999, 108, 409

11) Nakamura, K; Biomed Mass Spectrom 1982, 9, 390

12) Yoshinaga, J; Am J Phys Anthropol 1996, 100, 23

13) Tokui, N; J UOEH 2000, 22, 219

14) Minagawa, M; Appl Geochem 1992, 7, 145

15) Schoeller, D; Ecol Food Nutr 1986, 18, 159

16) Bol, R; Rapid Commun Mass Spectrom 2002, 16, 2195

17) Minagawa, M; Geochim Cosmochim Acta 1984, 48, 1135

18) Schoeller, D; J Archaeol Sci 1999, 26, 667

19) Focken, U; Isotopes Environ Health Stud 2001, 37, 199

20) Metges, C; Anal Biochem 1997, 247, 158

21) Petzke, K; Isotopes Environ Health Stud 1997, 33, 267

22) Heseker, H; VERA-Schriftenreihe 1994, III

23) Anon; VERA-Schriftenreihe 1992-1995, I-XIV

24) Federal Institute for Risk Assessment (BfR); BgVV-Heft 1999, 10

25) Metges, C; J Mass Spectrom 1996, 31, 367

26) Metges, C; Anal Biochem 2000, 278, 156

27) Craig, H; Geochim Cosmochim Acta 1953, 3, 53

28) Petzke, K; J Nutr 2000, 130, 2889

29) Wada, E; Crit Rev Food Sci Nutr 1991, 30, 361

30) Schoeller, D; Am J Clin Nutr 1980, 33, 2375

31) Schulze, A; Z Ernahrungswiss 1995, 34, 190

32) O'Leary, M; BioScience 1988, 38, 328

33) DeNiro, M; Geochim Cosmochim Acta 1978, 42, 495

34) DeNiro, M; Geochim Cosmochim Acta 1981, 45, 342

35) Mensink, G; Beitrage zur Gesundheitsberichterstattung des Bundes. Was essen wir heute? Ernahrungsverhalten in Deutschland (Contributions to the health report refund of the federation. What do we eat today? Diet behavior in Germany) 2002

36) Macko, S; Geochim Cosmochim Acta 1986, 50, 2143

37) Sick, H; Z Ernahrungswiss 1997, 36, 340

38) Petzke, K; Z Ernahrungswiss 1998, 37, 368

39) O'Connell, T; J Archaeol Sci 2001, 28, 1247

40) Hare, P; J Archaeol Sci 1991, 18, 277

32. Bergesio F; Monzani G; Guasparini A; Ciuti R; Gallucci M; Cristofano C; Castrignano E; Cupisti A; Barsotti G; Marcucci R; Abbate R; Bandini S; Gallo M; Tosi P L; Salvadori M Cardiovascular risk factors in severe chronic renal failure: the role of dietary treatment. Clinical nephrology (2005), 64(2), 103-12. Journal code: 0364441.

Abstract

BACKGROUND: Lipoprotein abnormalities and increased oxidized LDL (OxLDL) are often observed in uremia and are reported to play a central role in the development of cardiovascular disease (CVD). Vegan diet, known for its better lipoprotein profile and antioxidant vitamins content, could protect against CVD. Aim of this study was to investigate the influence of vegan diet supplemented with essential amino acids (EAA) and ketoanalogues (VSD) on both traditional and non-traditional cardiovascular risk factors (CVRF). METHODS: Twenty-nine patients (18 M, 11 F) aged 55 years (range 29-79 years) with advanced chronic renal failure (median sCr: 5.6 mg/dl) on very low protein vegetarian diet (0.3 g/kg/day) supplemented with a mixture of EAA and ketoacids (VSD) and 31 patients (20 M, 11 F) aged 65 years (range 29 - 82 years) on conventional low-protein diet (CD: 0.6 g/kg/day) with a similar renal function (median sCr: 5.2 mg/dl), were investigated for lipids and apolipoprotein parameters (traditional CVRF) as well as for oxidative stress (oxidized LDL, antibodies against OxLDL and thiobarbituric acid-reactive substances (TBARS)), total homocysteine (tHcy), lipoprotein(a) (Lp(a)), albumin and c-reactive protein (CRP) (non-traditional CVRF) including vitamins A, E, B12 and folic acid. RESULTS: Compared to patients on CD, those on VSD showed increased HDL cholesterol levels (p < 0.005) with a reduction of LDL cholesterol (p < 0.01) and an increase of apoA1/apoB ratio (p < 0.02). Among non-traditional CVRF, a mild but significant reduction of OxLDL (p < 0.05) with lower TBARS concentrations (p < 0.01) and a significant reduction of total homocysteine (p < 0.002), Lp(a) (p < 0.002) and CRP levels (p < 0.05) were also observed in these patients. Concentrations of vitamin E and A were not different between the two groups while vitamin B12 and folic acid resulted markedly increased in patients on VSD. OxLDL significantly correlated with total and LDL cholesterol, triglycerides and Apo B in CD but not in VSD patients.

Patients on CD also showed a significant correlation between urea and CRP. After a multivariate analysis, only urea (p < 0.001) and OxLDL (p < 0.006) were associated to a risk of CRP > 0.3 mg/dl. CONCLUSIONS: These results indicate a better lipoprotein profile in patients on vegan diet including non-traditional CVRF. In particular, these patients show a reduced oxidative stress with a reduced acute-phase response (CRP) as compared to patients on conventional diet. We hypothesize that urea, significantly lower in patients on VSD, may account, possibly together with the reduction of other protein breakdown products, for the decreased acute-phase response observed in these patients. Our findings suggest that low-protein diets, and vegan in particular, may exert a beneficial effect on the development of cardiovascular disease in patients with end-stage renal disease (ESRD).

Controlled Terms

Check Tags: Female; Male

Adult

Aged

Aged, 80 and over

C-Reactive Protein: ME, metabolism

Cardiovascular Diseases: BL, blood

*Cardiovascular Diseases: PC, prevention & control

Creatinine: BL, blood

Cross-Sectional Studies

*Diet, Vegetarian

Homocysteine: BL, blood

Humans

Kidney Failure, Chronic: BL, blood

*Kidney Failure, Chronic: DH, diet therapy

Lipids: BL, blood

Middle Aged

Regression Analysis

Risk Factors

Serum Albumin: ME, metabolism

Thiobarbituric Acid Reactive Substances: ME, metabolism

Treatment Outcome

Vitamins: BL, blood

Registry Numbers

454-28-4 (Homocysteine)

60-27-5 (Creatinine)

9007-41-4 (C-Reactive Protein)

Chemical Names

0 (Lipids)

0 (Serum Albumin)

0 (Thiobarbituric Acid Reactive Substances)

0 (Vitamins)

33. Wagnon J; Cagnard B; Bridoux-Henno L; Tourtelier Y; Grall J-Y; Dabadie A Breastfeeding and vegan diet. Journal de gynecologie, obstetrique et biologie de la reproduction (2005), 34(6), 610-2.

Abstract

Vegan diet in lactating women can induce vitamin B12 deficiency for their children with risk of an impaired neurological development. A 9.5-month-old girl presented with impaired growth and severe hypotonia. She had a macrocytic anemia secondary to vitamin B12 deficiency. MRI showed cerebral atrophy. She was exclusively breastfed. Her mother was also vitamin B12 deficient, secondary to a vegan diet. She had a macrocytic anemia when discharged from the maternity. Vegan diet is a totally inadequate regimen for pregnant and lactating women, especially for their children. Prevention is based on screening, information and vitamin supplementation.

Controlled Terms

Check Tags: Female

Brain: PA, pathology

*Breast Feeding

*Diet, Vegetarian: AE, adverse effects

Growth Disorders

Humans

Infant

Lactation

Magnetic Resonance Imaging

Muscle Hypotonia

*Vitamin B 12 Deficiency: DI, diagnosis

Vitamin B 12 Deficiency: ET, etiology

34. Hobbs Suzanne Havala Attitudes, practices, and beliefs of individuals consuming a raw foods diet. Explore (New York, N.Y.) (2005), 1(4), 272-7.

Abstract

OBJECTIVE: Describe dietary practices of U.S. raw foods leaders, examine diet rationale, attitudes and health practices of raw foodists. DESIGN: Nonexperimental, descriptive, using semistructured qualitative interview data. PARTICIPANTS: Purposeful (nonrandom) sample of 17 U.S. raw foods leaders, including 11 males and 6 females. Leaders were targeted to provide insights into practices modeled for larger community. PHENOMENA OF INTEREST: Attitudes, practices, and beliefs of individuals consuming a raw foods diet. ANALYSIS: Text analysis and simple descriptive statistics. RESULTS: Subjects averaged 13 years on the diet (range: 3-32 years). Twelve subjects reported a diet at least 85% raw. All diets were primarily vegan. Primary constituents included fruits and juices, vegetables, nuts and seeds, and vegetable fats. Subjects consumed no dairy, eggs, meat, fish, poultry, commercial sweets or alcohol in a typical week. Only one subject used a commercial, nonfood-based supplement weekly (vitamin B12). Six subjects consumed food-based supplements, and remainder used no supplements at all. On average, subjects met or exceeded recommended intakes of vegetables, fruits, and fats and did not meet recommendations for calcium-rich foods, protein-rich foods, and grains. CONCLUSIONS AND IMPLICATIONS: Those counseling raw foodists must understand the rationale and practices that characterize this eating style. Further research is needed on larger populations to validate findings and determine the extent to which reported health benefits may compare to those from other vegetarian diets. Further studies should examine food-handling and preparation practices in relation to food safety and raw produce.

Controlled Terms

Check Tags: Female; Male

Adult

Aged

*Diet, Vegetarian

*Food Habits

*Food Preferences

Health Behavior

*Health Food

*Health Knowledge, Attitudes, Practice

Health Promotion

Health Status

Humans

Middle Aged

Questionnaires

35. McCarty, Mark F. An ezetimibe-policosanol combination has the potential to be an OTC agent that could dramatically lower LDL cholesterol without side effects. Medical Hypotheses (2005), 64(3), 636-645.

Abstract

A review. Although many risk factors influence atherogenesis, LDL appears to play a primary role in this process. In prospective epidemiol., coronary risk increases as LDL cholesterol increases, throughout the entire range of concns. encountered in healthy humans. Coronary risk is minimal in individuals and populations whose serum cholesterol remains quite low throughout life. Thus, practical strategies for achieving large redns. of LDL cholesterol in the general population could have a dramatic impact on coronary mortality rates. Dietary measures have limited potential in this regard; modest restriction of satd. fat has a rather trivial effect on LDL cholesterol, and the very-low-fat quasi-vegan diets that do have a notable effect in this regard currently have little appeal to the majority of the population. With respect to pharmacotherapy, most available hypolipidemic agents with reasonably potent activity entail side effects or compliance difficulties that would render their use too expensive or impractical for population-wide application. However, two agents may have great potential in this regard: policosanol and ezetimibe. The former, a mixt. of long-chain alcs. derived from sugar cane wax, has effects on serum lipids comparable to those of statins, and may work by down-regulating expression of HMG-CoA reductase. However, unlike statins, policosanol appears to be devoid of side effects or risks. Ezetimibe is a newly approved drug that is a potent and highly specific inhibitor of an intestinal sterol permease; in daily doses as low as 10 mg, it suppresses intestinal absorption of cholesterol and decreases serum LDL cholesterol by approx. 18%. No side effects have been seen in clin. doses, and the fact that its hypolipidemic activity is additive to that of statins has generated considerable interest. Both policosanol and ezetimibe can be administered once daily. Future studies should det. whether policosanol, like statins, interacts additively with ezetimibe.

If so, it may be feasible someday to produce a tablet combining policosanol and ezetimibe that could reduce LDL cholesterol by about 40%, without side effects, and that could be recommended to virtually anyone whose LDL cholesterol levels were not already ideal.

Indexing -- Section 1-0 (Pharmacology)

Combination chemotherapy

(ezetimibe-policosanol combination has potential as OTC agent that could dramatically lower LDL cholesterol without side effects in patient)

Atherosclerosis

Human

Hypolipemic agents

(policosanol and intestinal sterol permease inhibitor ezetimibe dramatically lower LDL cholesterol without side effects in patient)

Low-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(policosanol and intestinal sterol permease inhibitor ezetimibe dramatically lower LDL cholesterol without side effects in patient)

163222-33-1, Ezetimibe

Role: PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(intestinal sterol permease inhibitor ezetimibe suppressed intestinal absorption of cholesterol and decreased serum LDL cholesterol with no side effects in patient)

57-88-5, Cholesterol, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(policosanol and intestinal sterol permease inhibitor ezetimibe dramatically lower LDL cholesterol without side effects in patient)

9028-35-7, Hydroxymethyl glutaryl-CoA reductase

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(policosanol effects on serum lipids is comparable to that of statins and down-regulate HMG-CoA reductase expression with no side effects or risks in patient)

142583-61-7, Policosanol

Role: PAC (Pharmacological activity); THU (Therapeutic use); BIOL (Biological study); USES (Uses)

(policosanol effects on serum lipids is comparable to that of statins and down-regulate HMG-CoA reductase expression with no side effects or risks in patient)

Supplementary Terms

review ezetimibe policosanol LDL cholesterol hypolipemic

Citations

1) Roberts, W; Am J Cardiol 1989, 64, 552

2) Evans, M; Curr Opin Lipidol 2002, 13, 663

3) Szatrowski, T; J Chronic Dis 1984, 37, 569

4) Chen, Z; BMJ 1991, 303, 276

5) Verschuren, W; JAMA 1995, 274, 131

6) Howard, B; Arterioscler Thromb Vasc Biol 2000, 20, 830

7) Mediene-Benchekor, S; Lancet 2001, 358, 1064

8) Anon; Lancet 2002, 360, 7

9) Braun, L; J Cardiovasc Nurs 2003, 18, 44

10) Taubes, G; Science 2001, 291, 2536

11) Jacobs, D; Circulation 1992, 86, 1046

12) Law, M; BMJ 1994, 308, 373

13) Iribarren, C; Circulation 1995, 92, 2396

14) Hebert, P; JAMA 1997, 278, 313

15) Peto, R; BMJ 1989, 298, 1249

16) Campbell, T; Am J Clin Nutr 1994, 59, 1153S

17) Tang, J; BMJ 1998, 316, 1213

18) Barnard, R; Arch Intern Med 1991, 151, 1389

19) Ornish, D; JAMA 1998, 279, 1345

20) Sacks, F; New Engl J Med 1975, 292, 1148

21) Ornish, D; JAMA 1998, 280, 2001

22) Esselstyn, C; J Fam Pract 1995, 41, 560

23) Esselstyn, C; Am J Cardiol 1999, 84, 339

24) Robbins, J; Diet for a New America 1998

25) Barnard, N; Food for life:how the new four food groups can save your life 1994

26) McCarty, M; Eating to live - How a low-fat, low-salt, whole-food vegan diet can help you stay lean and healthy into ripe old age 2002

27) Hamilton-Craig, I; Med J Aust 2002, 177, 407

28) Simons, L; BMJ 2000, 321, 1084

29) Jackevicius, C; JAMA 2002, 288, 462

30) Garg, R; Am Heart J 1999, 138, 1082

31) Brown, L; Am J Clin Nutr 1999, 69, 30

32) Vuksan, V; Diabetes Care 1999, 22, 913

33) Vuksan, V; Diabetes Care 2000, 23, 9

34) Katan, M; Mayo Clin Proc 2003, 78, 965

35) Judd, J; Lipids 2002, 37, 33

36) Jones, P; J Lipid Res 2003, 44, 1713

37) Szapary, P; JAMA 2003, 290, 765

38) Gouni-Berthold, I; Am Heart J 2002, 143, 356

39) Pons, P; Curr Ther Res 1992, 52, 507

40) Pons, P; Curr Ther 1993, 53, 265

41) Aneiros, E; Curr Ther Res 1993, 54, 304

42) Pons, P; Int J Clin Pharmacol Res 1994, 14, 27

43) Canetti, M; Int J Clin Pharmacol Res 1995, 15, 159

44) Torres, O; Diabetes Care 1995, 18, 393

45) Batista, J; Int J Clin Pharmacol Ther 1996, 34, 134

46) Castano, G; Curr Ther Res 1996, 57, 691

47) Mas, R; Clin Pharmacol Ther 1999, 65, 439

48) Castano, G; Gynecol Endocrinol 2000, 14, 187

49) Castano, G; J Gerontol A: Biol Sci Med Sci 2001, 56, M186

50) Stusser, R; Int J Clin Pharmacol Ther 1998, 36, 469

51) Castano, G; Angiology 1999, 50, 123

52) Castano, G; Angiology 2001, 52, 115

53) Valdes, S; Int J Clin Pharmacol Res 1996, 16, 67

54) Arruzazabala, M; Pharmacol Res 1996, 34, 181

55) Arruzazabala, M; Pharmacol Res 1997, 36, 293

56) Carbajal, D; Prostag Leukotr Ess Fatty Acids 1998, 58, 61

57) Arruzazabala, M; Int J Tissue React 1998, 20, 119

58) Prat, H; Rev Med Chil 1999, 127, 286

59) Castano, G; Int J Clin Pharmacol Res 1999, 19, 105

60) Crespo, N; Int J Clin Pharmacol Res 1999, 19, 117

61) Castano, G; Curr Ther Res 2000, 61, 137

62) Hernandez, F; Curr Ther Res 1992, 51, 568

63) Aleman, C; Teratog Carcinog Mutagen 1994, 14, 239

64) Rodriguez, M; Teratog Carcinog Mutagen 1994, 14, 107

65) Aleman, C; Toxicol Lett 1994, 70, 77

66) Rodriguez-Echenique, C; Food Chem Toxicol 1994, 32, 565

67) Mesa, A; Toxicol Lett 1994, 73, 81

68) Aleman, C; Food Chem Toxicol 1995, 33, 573

69) Rodriguez, M; Toxicol Lett 1997, 90, 97

70) Rodriguez, M; Teratog Carcinog Mutagen 1998, 18, 1

71) Menendez, R; Brit J Nutr 1997, 77, 923

72) Menendez, R; Biol Res 1996, 29, 253

73) Menendez, R; Arch Med Res 2001, 32, 8

74) Mirkin, A; Int J Clin Pharmacol Res 2001, 21, 31

75) Castano, G; Int J Clin Pharmacol Res 2002, 22, 55

76) Rosenblum, S; J Med Chem 1998, 41, 973

77) Sudhop, T; Circulation 2002, 106, 1943

78) Repa, J; J Lipid Res 2002, 43, 1864

79) van Heek, M; Brit J Pharmacol 2003, 138, 1459

80) Brown, W; Clin Cardiol 2003, 26, 259

81) Turley, S; Curr Opin Lipidol 2003, 14, 233

82) Knopp, R; Int J Clin Pract 2003, 57, 363

83) Davis, H; Metabolism 2001, 50, 1234

84) Kosoglou, T; Brit J Clin Pharmacol 2002, 54, 309

85) Gagne, C; Am J Cardiol 2002, 90, 1084

86) Davidson, M; J Am Coll Cardiol 2002, 40, 2125

87) Kerzner, B; Am J Cardiol 2003, 91, 418

88) Melani, L; Eur Heart J 2003, 24, 717

89) Aide, M; Pharma Note 2003, 18, 1

90) Zhu, Y; Clin Pharmacol Ther 2000, 67, 152

91) Harris, M; Drugs Today (Barc) 2003, 39, 229

92) Arsenio, L; Acta Biomed Ateneo Parmense 1984, 55, 25

93) Gaddi, A; Atherosclerosis 1984, 50, 73

94) Murai, A; Artery 1985, 12, 234

95) Arsenio, L; Clin Ther 1986, 8, 537

96) Donati, C; Clin Nephrol 1986, 25, 70

97) Bertolini, S; Int J Clin Pharmacol Ther Toxicol 1986, 24, 630

98) Eto, M; Artery 1987, 15, 1

99) Coronel, F; Am J Nephrol 1991, 11, 32

100) Ranganathan, S; Atherosclerosis 1982, 44, 261

101) Cighetti, G; Biochim Biophys Acta 1988, 963, 389

102) Cighetti, G; Atherosclerosis 1986, 60, 67

103) Cighetti, G; J Lipid Res 1987, 28, 152

104) McCarty, M; Med Hypotheses 2001, 56, 314

105) Wittwer, C; Atherosclerosis 1987, 68, 41

106) Vuksan, V; Diabetes Care 1999, 22, 913

36. Rosell M; Appleby P; Spencer E; Key T Weight gain over 5 years in 21,966 meat-eating, fish-eating, vegetarian, and vegan men and women in EPIC-Oxford. International journal of obesity (2005) (2006), 30(9), 1389-96.

Abstract

BACKGROUND: Cross-sectional studies have shown that vegetarians and vegans are leaner than omnivores. Longitudinal data on weight gain in these groups are sparse. OBJECTIVE: We investigated changes in weight and body mass index (BMI) over a 5-year period in meat-eating, fish-eating, vegetarian, and vegan men and women in the UK. DESIGN: Self-reported anthropometric, dietary and lifestyle data were collected at baseline in 1994-1999 and at follow-up in 2000-2003; the median duration of follow-up was 5.3 years. SUBJECTS: A total of 21,966 men and women participating in Oxford arm of the European Prospective Investigation into Cancer and Nutrition aged 20-69 years at baseline. RESULTS: The mean annual weight gain was 389 (SD 884) g in men and 398 (SD 892) g in women. The differences between meat-eaters, fish-eaters, vegetarians and vegans in age-adjusted mean BMI at follow-up were similar to those seen at baseline. Multivariable-adjusted mean weight gain was somewhat smaller in vegans (284 g in men and 303 g in women, P<0.05 for both sexes) and fish-eaters (338 g, women only, P<0.001) compared with meat-eaters. Men and women who changed their diet in one or several steps in the direction meat-eater --> fish-eater --> vegetarian --> vegan showed the smallest mean annual weight gain of 242 (95% CI 133-351) and 301 (95% CI 238-365) g, respectively. CONCLUSION: During 5 years follow-up, the mean annual weight gain in a health-conscious cohort in the UK was approximately 400 g. Small differences in weight gain were observed between meat-eaters, fish-eaters, vegetarians and vegans. Lowest weight gain was seen among those who, during follow-up, had changed to a diet containing fewer animal food.

Controlled Terms

Check Tags: Female; Male

Adult

Aged

Body Mass Index

*Diet: SN, statistics & numerical data

*Diet, Vegetarian: SN, statistics & numerical data

Exercise: PH, physiology

Great Britain

Humans

Life Style

Longitudinal Studies

*Meat: SN, statistics & numerical data

Middle Aged

*Weight Gain: PH, physiology

37. Smith Annabelle M Veganism and osteoporosis: a review of the current literature. International journal of nursing practice (2006), 12(5), 302-6.

Abstract

The purpose of this review is to examine the current literature regarding calcium and Vitamin D deficiencies in vegan diets and the possible relationship to low bone mineral density and incidence for fracture. Prominent databases were searched for original research publications providing data capable of answering these questions: (i) Do vegans have lower-than-recommended levels of calcium/Vitamin D? (ii) Do vegans have lower bone mineral density than their non-vegan counterparts? (iii) Are vegans at a greater risk for fractures than non-vegans? The findings gathered consistently support the hypothesis that vegans do have lower bone mineral density than their non-vegan counterparts. However, the evidence regarding calcium, Vitamin D and fracture incidence is inconclusive. More research is needed to definitively answer these questions and to address the effects of such deficiencies on the medical and socioeconomic aspects of life.

Controlled Terms

Bone Density

Calcium: DF, deficiency

*Diet, Vegetarian

Humans

*Osteoporosis: ET, etiology

Osteoporosis: NU, nursing

Risk Factors

Vitamin D Deficiency: CO, complications

Registry Numbers

7440-70-2 (Calcium)

38. Jagannathan Narasimhan Vegan ? Sorry, we have porcine heparin on the menu!. Anesthesia and analgesia (2006), 102(3), 976.

Controlled Terms

Animals

*Diet, Vegetarian

*Heparin

Humans

Swine

Registry Numbers

9005-49-6 (Heparin)

39. McCarty Mark F; Block Keith I Toward a core nutraceutical program for cancer management. Integrative cancer therapies (2006), 5(2), 150-71.

Abstract

As previously suggested, it may be feasible to impede tumorevoked angiogenesis with a nutraceutical program composed of glycine, fish oil, epigallocatechin-3-gallate, selenium, and silymarin, complemented by a low-fat vegan diet, exercise training, and, if feasible, a salicylate and the drug tetrathiomolybdate. It is now proposed that the scope of this program be expanded to address additional common needs of cancer patients: blocking the process of metastasis; boosting the cytotoxic capacity of innate immune defenses (natural killer [NK] cells); preventing cachexia, thromboembolism, and tumor-induced osteolysis; and maintaining optimal micronutrient status. Modified citrus pectin, a galectin-3 antagonist, has impressive antimetastatic potential. Mushroombeta-glucans and probiotic lactobacilli can amplify NK activity via stimulatory effects on macrophages. Selenium, beta-carotene, and glutamine can also increase the number and/or cytotoxic activity of NK cells. Cachectic loss of muscle mass can be opposed by fish oil, glutamine, and beta-hydroxy-beta-methylbutyrate. Fish oil, policosanol, and vitamin D may have potential for control of osteolysis. High-dose aspirin or salicylates, by preventing NF-B activation, can be expected to aid prevention of metastasis and cachexia while down-regulating osteolysis, but their impacts on innate immune defenses will not be entirely favorable. A nutritional insurance formula crafted for the special needs of cancer patients can be included in this regimen. To minimize patient inconvenience, this complex core nutraceutical program could be configured as an oil product, a powder, and a capsule product, with the nutritional insurance formula provided in tablets. It would be of interest to test this program in nude mouse xenograft models.

Controlled Terms

Animals

Cachexia: PC, prevention & control

*Chemistry, Pharmaceutical: TD, trends

Health Services Needs and Demand: TD, trends

Health Status

Humans

Immune System: GD, growth & development

Killer Cells, Natural: PH, physiology

Micronutrients: AD, administration & dosage

Neoplasm Metastasis: PC, prevention & control

*Neoplasms: DH, diet therapy

*Neoplasms: DT, drug therapy

*Nutrition Physiology: PH, physiology

Osteolysis, Essential: PC, prevention & control

Patient Satisfaction

Thromboembolism: PC, prevention & control

Chemical Names

0 (Micronutrients)

40. Ingenbleek, Yves. The nutritional relationship linking sulfur to nitrogen in living organisms. Journal of Nutrition (2006), 136(6S), 1641S-1651S.

Abstract

A review. Nitrogen (N) and sulfur (S) coexist in the biosphere as free elements or in the form of simple inorg. NO3- and SO42- oxyanions, which must be reduced before undergoing anabolic processes leading to the prodn. of methionine (Met) and other S-contg. mols. Both N and S pathways are tightly regulated in plant tissues so as to maintain S:N ratios ranging from 1:20 to 1:35. As a result, plant products do not adequately fulfill human tissue requirements, whose mean S:N ratios amt. to 1:14.5. The evolutionary patterns of total body N (TBN) and of total body S (TBS) offer from birth to death sex- and age-related specificities well identified by the serial measurement of plasma transthyretin (TTR). Met is regarded as the most limiting of all indispensable amino acids (IAAs) because of its participation in a myriad of mol., structural, and metabolic activities of survival importance. Met homeostasis is regulated by subtle competitive interactions between transsulfuration and remethylation pathways of homocysteine (Hcy) and by the actual level of TBN reserves working as a direct sensor of cystathionine--synthase activity. Under steady-state conditions, the dietary intake of SO42- is essentially equal to total sulfaturia. The recommended dietary allowances for both S-contg. AAs allotted to replace the minimal obligatory losses resulting from endogenous catabolism is largely covered by Western customary diets. By contrast, strict vegans and low-income populations living in plant-eating countries incur the risk of chronic N and Met dietary deficiencies causing undesirable hyperhomocysteinemia best explained by the down-sizing of their TBN resources and documented by declining TTR plasma values.

Indexing -- Section 18-0 (Animal Nutrition)

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(dietary; nutritional relationship linking sulfur to nitrogen in living organisms)

Diet

Human

Nutrition, animal

(nutritional relationship linking sulfur to nitrogen in living organisms)

Transthyretin

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(nutritional relationship linking sulfur to nitrogen in living organisms)

14808-79-8, Sulfate, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(balance; nutritional relationship linking sulfur to nitrogen in living organisms)

6027-13-0, L-Homocysteine

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); BIOL (Biological study)

(nutritional relationship linking sulfur to nitrogen in living organisms)

7704-34-9, Sulfur, biological studies

7727-37-9, Nitrogen, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(nutritional relationship linking sulfur to nitrogen in living organisms)

Supplementary Terms

review nutrition sulfur nitrogen diet protein hyperhomocysteinemia transthyretin

Citations

1) Rose, W; Nutr Abstr Rev 1957, 27, 631

2) Holt, L; Nutr Abstr Rev 1965, 35, 1

3) Hegsted, D; Fed Proc 1963, 22, 1424

4) Cynober, L; Amino acid metabolism and therapy in health and nutritional disease 1995

5) Reeds, P; Present knowledge in nutrition 7th ed 1996, 67

6) Young, V; J Nutr 2000, 130(Suppl), S1841

7) Nickless, G; Inorganic sulfur chemistry 1968

8) Schmidt, M; Comprehensive inorganic chemistry 1973, 2, 795

9) Bowmann, B; Russell RM Present knowledge in nutrition, 8th ed 2001

10) Caballero, B; British encyclopedia of nutrition, 2nd ed 2005

11) Martin, A; Apports nutritionnels conseilles pour la population francaise, 3rd ed 2001

12) McCance, R; The composition of foods 5th ed 1991

13) Beutler, E; Annu Rev Nutr 1989, 9, 287

14) McCully, K; Nat Med 1996, 2, 386

15) Holland, H; Orig Life 1974, 5, 87

16) Jones, K; Comprehensive inorganic chemistry 1973, 2, 147

17) Mohr, H; Plant physiology 1994

18) Winnewisser, G; Top Curr Chem 1987, 139, 119

19) Huxtable, R; Biochemistry of sulfur 1986

20) Mitchell, S; Biological interactions of sulfur compounds 1996

21) Ault, W; Geochim Cosmochim Acta 1959, 16, 201

22) Kelly, D; Sulphur in biology, CIBA Foundation Symposium 72 1980, 3

23) Bothe, H; Biology of inorganic nitrogen and sulfur 1981

24) Miflin, B; Annu Rev Plant Physiol 1977, 28, 299

25) Fowden, L; Nitrogen metabolism in man 1981, 87

26) Losada, M; Biology of inorganic nitrogen and sulfur 1981, 30

27) Schwenn, J; Biology of inorganic nitrogen and sulfur 1981, 334

28) Stetten de, W; J Biol Chem 1942, 144, 501

29) Laidlaw, S; Am J Clin Nutr 1988, 47, 660

30) Smith, I; Plant Physiol 1975, 55, 303

31) Hart, J; Plant Physiol 1969, 44, 1253

32) Reuveny, Z; J Biol Chem 1977, 252, 1858

33) Friedrich, J; Plant Physiol 1978, 61, 900

34) Bergmann, L; Biology of inorganic nitrogen and sulfur 1981, 341

35) Datko, A; Plant Physiol 1978, 62, 629

36) Food And Agriculture Organization; Amino-acid content of foods and biological data on proteins 1970

37) Souci, S; Food composition and nutrition tables, 5th ed 1994

38) Young, V; Am J Clin Nutr 1984, 39, 16

39) Forbes, G; Present knowledge in nutrition, 7th ed 1996, 7

40) Cohn, S; Am J Physiol 1983, 244, E305

41) Dabek, J; J Radioanal Chem 1977, 37, 325

42) Cohn, S; Metabolism 1981, 30, 222

43) Stamatelatos, I; Phys Med Biol 1993, 38, 615

44) Olesen, K; Biochim Biophys Acta 1954, 15, 95

45) Ingenbleek, Y; Clin Chem Lab Med 2002, 40, 1281

46) Lohman, T; Advances in body composition assessment Monograph 3 1992

47) Picou, D; Clin Sci 1969, 36, 283

48) Ellis, K; Biol Trace Elem Res 1990, 26-27, 385

49) Winterer, J; Exp Gerontol 1976, 11, 79

50) Fomon, S; Am J Clin Nutr 1982, 35, 1169

51) Baur, L; Human body composition:methods, models and assessment 1993

52) Forbes, G; Human body composition Growth, aging, nutrition and activity 1987

53) Ingenbleek, Y; Lancet 1972, 2, 106

54) Bienvenu, J; Serum proteins in clinical medicine 1996, 9.011

55) Lewis, H; J Biol Chem 1916, 26, 61

56) Wilson, H; Biochem J 1925, 19, 322

57) Kennedy, P; Aust J Agric Res 1974, 25, 1015

58) Florin, T; J Food Compos Anal 1993, 6, 140

59) Young, V; Am J Clin Nutr 1994, 59(Suppl), S1203

60) Friedman, M; Annu Rev Nutr 1992, 12, 119

61) Ingenbleek, Y; Nutr Res Rev 2004, 17, 135

62) Raguso, C; Am J Clin Nutr 1997, 66, 283

63) Womack, M; J Biol Chem 1937, 121, 403

64) Wellers, G; J Physiol (Paris) 1959, 51, 723

65) Gaull, G; Pediatr Res 1972, 6, 538

66) Rassin, D; Early Hum Dev 1978, 2, 1

67) Fugakawa, N; Am J Clin Nutr 1998, 68, 380

68) Fao; Energy and protein requirements:Report of an FAO/WHO/UNU Expert Consultation Geneva: WHO Tech Rep Series 724 1985

69) Millward, D; Proc Nutr Soc 1999, 58, 249

70) Institute Of Medicine; Energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids 2000

71) Horowitz, J; Gastroenterology 1981, 81, 668

72) Stipanuk, M; Annu Rev Nutr 2004, 24, 539

73) Bauer, J; J Appl Physiol 1976, 40, 648

74) Florin, T; Gut 1991, 32, 766

75) Anast, C; J Lab Clin Med 1965, 65, 903

76) Hoffman, D; Eur J Clin Pharmacol 1990, 39, 143

77) Ryan, R; J Clin Invest 1956, 35, 1119

78) Pierson, R; J Chronic Dis 1982, 35, 419

79) Walser, M; J Clin Invest 1953, 32, 299

80) Becker, E; J Clin Invest 1960, 39, 1909

81) Chakmakjian, Z; N Engl J Med 1966, 275, 862

82) Bostrom, H; Scand J Clin Lab Invest 1960, 12, 323

83) Ramakrishna, B; J Clin Pathol 1989, 42, 620

84) Sabry, Z; Nature 1965, 206, 931

85) Clark, H; Am J Clin Nutr 1970, 23, 731

86) Bressani, R; J Nutr 1966, 87, 77

87) Wright, J; J Nutr 1960, 72, 314

88) Lakshmanan, F; Am J Clin Nutr 1976, 29, 1367

89) Sherman, H; Am J Physiol 1900, 4, 25

90) Kennedy, P; Aust J Biol Sci 1975, 28, 31

91) Jackson, S; Clin Chim Acta 1968, 22, 443

92) Tateishi, N; J Nutr 1977, 107, 51

93) Hofmann, K; Adv Food Res 1978, 24, 1

94) Jacobsen, J; Physiol Rev 1968, 48, 424

95) Furst, P; Proc Nutr Soc 1983, 42, 451

96) Kilberg, M; Annu Rev Nutr 2005, 25, 59

97) Jousse, C; Curr Opin Clin Nutr Metab Care 1999, 2, 297

98) Stephen, J; Br J Nutr 1968, 22, 153

99) Lecker, S; J Nutr 1999, 129(Suppl), S227

100) Mortimore, G; Annu Rev Nutr 1987, 7, 539

101) Young, V; J Nutr 2000, 130, 761

102) Young, V; J Nutr 2000, 130(Suppl), S892

103) Garrow, J; J Clin Invest 1965, 44, 417

104) Addis, T; J Biol Chem 1936, 115, 111

105) Waterlow, J; Protein-energy malnutrition 1995

106) Morgan, W; Am J Clin Nutr 1992, 56(Suppl), S262

107) Russell, D; Am J Clin Nutr 1983, 38, 229

108) Baur, L; Am J Clin Nutr 1991, 53, 503

109) Jourdan, M; Am J Clin Nutr 1980, 33, 236

110) Hamadeh, M; Am J Physiol 2001, 281, E341

111) Anderson, M; J Biol Chem 1980, 255, 9530

112) Martensson, J; Metabolism 1986, 35, 118

113) Steiner, M; Am J Physiol 1968, 215, 75

114) Cho, E; J Nutr 1981, 111, 914

115) Douglas, G; J Biol Chem 1956, 222, 581

116) Hochberg, A; Biochim Biophys Acta 1964, 90, 464

117) Kutzbach, C; Biochim Biophys Acta 1967, 139, 217

118) Finkelstein, J; Biochem Biophys Res Commun 1975, 66, 81

119) Meier, M; EMBO J 2001, 20, 3910

120) Kang, S; Metabolism 1987, 36, 458

121) Stabler, S; Blood 1990, 76, 871

122) Ubbink, J; J Clin Invest 1996, 98, 177

123) Lussier-Cacan, S; Am J Clin Nutr 1996, 64, 587

124) Saw, S; Am J Clin Nutr 2001, 73, 232

125) Fuller, M; Br J Nutr 1989, 62, 255

126) Owens, F; J Anim Sci 1983, 57(Suppl 2), S498

127) Storch, K; Am J Physiol 1990, 258, E790

128) Ingenbleek, Y; Am J Clin Nutr 1986, 43, 310

129) Ingenbleek, Y; Nutrition 2002, 18, 40

130) Stolzenberg-Solomon, R; Am J Clin Nutr 1999, 69, 467

131) Antener, I; Int J Vitam Nutr Res 1981, 51, 64

132) Finkelstein, J; Arch Biochem Biophys 1971, 146, 84

133) Finkelstein, J; J Biol Chem 1984, 259, 9508

134) Straus, D; J Nutr 1994, 124, 1041

135) Kanda, Y; J Biol Chem 1974, 249, 6796

136) Ingenbleek, Y; Nutrition 1999, 15, 305

137) Ingenbleek, Y; J Clin Ligand Assay 1999, 22, 259

138) Arnold, J; Clin Sci 1993, 84, 655

139) Zoico, E; Nutr Rev 2002, 60, 39

140) Cuthertson, D; Biochem J 1931, 25, 236

141) O'Keefe, S; Lancet 1974, 2, 1035

142) Beisel, W; Annu Rev Med 1975, 26, 9

143) Kotler, D; Am J Clin Nutr 1985, 42, 1255

144) Ratnam, S; J Biol Chem 2002, 277, 42912

145) Zou, C; J Biol Chem 2003, 278, 16802

146) Malmezat, T; Am J Physiol 2000, 279, E1391

147) Malmezat, T; J Nutr 2000, 130, 1239

148) Yu, Y; J Trauma 1993, 35, 1

149) Carpenter, K; Am J Clin Nutr 1992, 55, 913

150) Murakami, T; Biochem Biophys Res Commun 1988, 155, 554

151) Wood, C; J Parenter Enterol Nutr 1984, 8, 665

152) Heymsfield, S; Am J Clin Nutr 1982, 35, 1192

153) Briend, A; Eur J Clin Nutr 1989, 43, 715

154) Krajcovicova-Kudlackova, M; Ann Nutr Metab 2000, 44, 135

155) Hung, C; J Nutr 2002, 132, 152

156) Stabler, S; Annu Rev Nutr 2004, 24, 299

41. Agostoni, Carlo; Axelsson, Irene; Goulet, Olivier; Koletzko, Berthold; Michaelsen, Kim Fleischerm; Puntis, John; Rieu, Daniel; Rigo, Jacques; Shamir, Raanan; Szajewska, Hania; Turck, Dominique. Soy protein infant formulae and follow-on formulae: A commentary by the ESPGHAN Committee on nutrition. Journal of Pediatric Gastroenterology and Nutrition (2006), 42(4), 352-361.

Abstract

A review. This comment by the European Society for Paediatric Gastroenterol. Hepatol. and Nutrition (ESPGHAN) Committee on Nutrition summarizes available information on the compn. and use of soy protein formulas as substitutes for breastfeeding and cows' milk protein formulas as well as on their suitability and safety for supporting adequate growth and development in infants. Soy is a source of protein that is inferior to cows' milk, with a lower digestibility and bioavailability as well as a lower methionine content. For soy protein infant formulas, only protein isolates can be used, and min. protein content required in the current European Union legislation is higher than that of cows' milk protein infant formulas (2.25 g/100 kcal vs. 1.8 g/100kcal). Soy protein formulas can be used for feeding term infants, but they have no nutritional advantage over cows' milk protein formulas and contain high concns. of phytate, aluminum, and phytoestrogens (isoflavones), which might have untoward effects. There are no data to support the use of soy protein formulas in preterm infants. Indications for soy protein formulas include severe persistent lactose intolerance, galactosemia, and ethical considerations (e.g., vegan concepts). Soy protein formulas have no role in the prevention of allergic diseases and should not be used in infants with food allergy during the first 6 mo of life. If soy protein formulas are considered for therapeutic use in food allergy after the age of 6 mo because of their lower cost and better acceptance, tolerance to soy protein should first be established byclin. challenge. There is no evidence supporting the use of soy protein formulas for the prevention or management of infantile colic, regurgitation, or prolonged crying.

Indexing -- Section 17-0 (Food and Feed Chemistry)

Milk substitutes

(human; nutrition of soy protein infant formula and follow-on formula)

Food allergy

Glycine max

Human

Nutrition, animal

(nutrition of soy protein infant formula and follow-on formula)

Proteins

Role: FFD (Food or feed use); BIOL (Biological study); USES (Uses)

(soybean; nutrition of soy protein infant formula and follow-on formula)

Supplementary Terms

review soy protein infant formula nutrition

Citations

1) Ruhrah, J; Arch Pediatr 1909, 26, 494

2) Hill, L; JAMA 1929, 93, 985

3) American Academy of Pediatrics Committee on Nutrition; Pediatrics 1998, 101, 148

4) Zoppi, G; J Pediatr Gastroenterol Nutr 1999, 5, 541

5) Bocquet, A; Arch Pediatr 2001, 8, 1226

6) Miniello, V; Acta Paediatr Suppl 2003, 441, 93

7) Scientific Committee on Food; Report on the revision of essential requirements of infant formulae and follow-up formulae (adopted on 4 April 2003) 2003, SCF/CS/NUT/IF/65

8) Committee on Toxicity; Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment. Phyloestrogens and health 2003

9) Agence Francaise de Securite Sanitaire des Aliments (French Food Safety Agency); Report of the working group on phytoestrogens [French], www.afssa.fr 2005

10) Walker-Smith, J; J Pediatr Gastroenterol Nutr 1997, 24, 619

11) Host, A; Arch Dis Child 1999, 81, 80

12) American Academy of Pediatrics Committee on Nutrition; Pediatrics 2000, 106, 346

13) Osborn, D; Cochrane Database Syst Rev 2004, CD003741

14) Bos, C; J Nutr 2003, 133, 1308

15) Fomon, S; Am J Clin Nutr 1979, 32, 2460

16) ESPGAN Committee on Nutrition; Acta Paediatr Scand 1990, 79, 1001

17) Olson, A; Am J Clin Nutr 1989, 49, 624

18) Life Sciences Research Office American Society for Nutritional Sciences; J Nutr 1998, 128(Suppl 11), 2059S

19) Anon; Official J European Communities 1991, L 175, 35

20) Anon; Official J European Communities 1996, L 49

21) Fomon, S; Acta Paediatr Scand 1973, 62, 33

22) Fomon, S; J Nutr 1986, 116, 1405

23) Fomon, S; Nutrition of Normal Infants 1993, 424

24) Mendez, M; J Nutr 2002, 132, 2127

25) Venkataraman, P; Am J Dis Child 1992, 146, 1302

26) Mimouni, F; J Pediatr 1993, 122, 348

27) Hall, R; J Pediatr Gastroenterol Nutr 1984, 3, 571

28) Hurrell, R; Am J Clin Nutr 1992, 56, 573

29) Davidsson, L; Pediatr Res 1994, 36, 816

30) Lonnerdal, B; Am J Clin Nutr 1999, 69, 490

31) Davidsson, L; Br J Nutr 2004, 91, 287

32) Hydrovitz, J; N Engl J Med 1960, 262, 351

33) Shepard, T; N Engl J Med 1960, 262, 1099

34) Chorazy, P; Pediatrics 1995, 96, 148

35) Jabbar, M; J Am Coll Nutr 1997, 16, 280

36) Conrad, S; Arch Dis Child 2004, 89, 37

37) Kuchan, M; J Am Coll Nutr 2000, 19, 16

38) American Academy of Pediatrics Committee on Nutrition; Pediatrics 1996, 97, 413

39) World Health Organization; WHO Tech Rep Ser 1989, 776, 1

40) Zung, A; J Pediatr Gastroenterol Nutr 2001, 33, 112

41) Setchell, K; Am J Clin Nutr 1998, 68(Suppl), 1453s

42) Setchell, K; J Am Coll Nutr 2001, 20, 354s

43) Hawrylewicz, E; J Nutr 1991, 121, 1693

44) Naik, H; Anticancer Res 1994, 14, 2617

45) Barnes, S; Adv Exp Med Biol 1994, 354, 135

46) Birt, D; Modern Nutrition in Health and Disease 1998, 1263

47) Anderson, J; Am J Clin Nutr 1999, 70(Suppl), 464s

48) Velasquez, M; Am J Kidney Dis 2001, 37, 1056

49) Setchell, K; J Chromatograph 1987, 368, 315

50) Setchell, K; Lancet 1997, 350, 23

51) Franke, A; Am J Clin Nutr 1998, 68(Suppl), 1466s

52) Irvine, C; Am J Clin Nutr 1998, 68(Suppl), 1462s

53) Benneteau-Pelissero, C; Cah Nutr Dietet 2004, 39, 24

54) Antignac, J; Food Chem 2004, 87, 275

55) Markiewicz, L; J Steroid Biochem Mol Biol 1993, 45, 399

56) Yellayi, S; Proc Natl Acad Sci U S A 2002, 99, 7616

57) Bennetts, H; Aust J Agric Res 1946, 22, 131

58) Levy, J; Proc Soc Exp Biol Med 1995, 208, 60

59) Fort, P; J Am Coll Nutr 1990, 9, 164

60) Divi, R; Biochem Pharmacol 1997, 54, 1087

61) Freni-Titulaer, L; Am J Dis Child 1986, 140, 1263

62) Strom, B; JAMA 2001, 286, 807

63) Ostrom, K; J Pediatr Gastroenterol Nutr 2002, 34, 137

64) Cordle, C; J Pediatr Gastroenterol Nutr 2002, 34, 145

65) Walter, J; Arch Dis Child 1999, 80, 93

66) Wiesmann, U; Eur J Pediatr 1995, 154(Suppl 2), 93

67) Brown, K; Pediatrics 1994, 93, 17

68) Sandhu, B; J Pediatr Gastroenterol Nutr 1997, 24, 522

69) Darmon, N; Pediatr Res 1998, 44, 931

70) Li, X; J Allergy Clin Immunol 1999, 103, 206

71) Zeiger, R; J Pediatr Gastroenterol Nutr 2000, 30(Suppl 1), 77

72) Perkkio, M; Eur J Pediatr 1981, 137, 63

73) Sicherer, S; J Pediatr Gastroenterol Nutr 2000, 30(Suppl 1), 45

74) Powell, G; J Pediatr 1976, 88, 840

75) Halpin, T; J Pediatr 1977, 91, 404

76) Kerner, J; J Pediatr Gastroenterol Nutr 1997, 24, 442

77) American Academy of Pediatrics Committee on Nutrition; Pediatrics 1983, 72, 359

78) Zeiger, R; J Pediatr 1999, 134, 614

79) Klemola, T; J Pediatr 2002, 140, 219

80) Lack, G; N Engl J Med 2003, 348, 977

81) Sicherer, S; Allergy 2000, 55, 515

82) Businco, L; Am J Clin Nutr 1998, 68(Suppl), 1447s

83) Kjellman, N; Clin Allergy 1979, 9, 347

84) Gruskay, F; Clin Pediatr 1982, 21, 486

85) Moore, W; Arch Dis Child 1985, 60, 722

86) Merrett, T; Ann Allergy 1988, 61, 13

87) Chandra, R; J Pediatr Gastroenterol Nutr 1997, 24, 380

88) Iacono, G; J Pediatr Gastroenterol Nutr 1991, 12, 332

89) Garrisson, M; Pediatrics 2000, 106, 184

90) Campbell, J; J R Coll Gen Pract 1989, 39, 11

91) Lothe, L; Pediatrics 1982, 70, 7

92) Lucassen, P; BMJ 1998, 316, 1563

43. Ambroszkiewicz, J.; Klemarczyk, W.; Chelchowska, M.; Gajewska, J.; Laskowska-Klita, T. Serum homocysteine, folate, vitamin B12 and total antioxidant status in vegetarian children. Advances in Medical Sciences (2006), 51 265-268.

Abstract

Purpose: The results of several studies point to the pos. role of vegetarian diets in reducing the risk of diabetes, some cancers and cardiovascular diseases. However, exclusion of animal products in vegetarian diets may affect the cobalamin status and cause an elevation of the plasma homocysteine level. The aim of this study was to assess the effect of vegetarian diets on serum concns. of homocysteine, folate, vitamin B12 and total antioxidant status (TAS) in children. Material and methods: The study included 32 vegetarians (including 5 vegans), age 2-10 years. Dietary constituents were analyzed using a local nutritional program. Serum homocysteine, folate and vitamin B12 were detd. with fluorescence and chemiluminescence immunoassays. The concn. of TAS was measured by a colorimetric method. Results: Av. daily energy intake and the percentage of energy from protein, fat and carbohydrates in the diets of the studied children were just above or similar to the recommended amts. It could be shown that vegetarian diets contain high concns. of folate. In vegan diets it even exceeds the recommended dietary allowance. Mean daily intake of vitamin B12 in the studied diets was adequate but in vegans was below the recommended range. The serum concns. of homocysteine, folate, vitamin B12 and TAS in vegetarian children remained within the physiol. range. Conclusions: The presented data indicate that vegetarian children, contrary to adults, have enough vitamin B12 in their diet (excluding vegans) and normal serum concns. of homocysteine, folate and vitamin B12. Therefore, in order to prevent deficiencies in the future, close monitoring of vegetarian children (esp. on a vegan diet) is important to make sure that they receive adequate quantities of nutrients needed for healthy growth.

Indexing -- Section 18-2 (Animal Nutrition)

Section cross-reference(s): 13

Glycerides, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; vegetarian diet maintained moderate physiol. range of serum triglyceride in children)

Development, mammalian postnatal

(child; vegetarian diets excluding vegan diet provided adequate quantities of nutrients from diet and achieved normal physiol. range of serum homocysteine, folate, vitamin B12 and total antioxidant status in children)

Low-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(cholesterol of; vegetarian diet maintained low or physiol. range of serum low-d. lipoprotein-cholesterol in children)

High-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(cholesterol of; vegetarian diet maintained lower ref. range of serum high-d. lipoprotein-cholesterol in children)

Growth, animal

(serum homocysteine, folate, vitamin B12 and total antioxidant status in vegetarian children)

Carbohydrates, biological studies

Fats and Glyceridic oils, biological studies

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(serum homocysteine, folate, vitamin B12 and total antioxidant status in vegetarian children)

Dietary energy

(vegetarian children achieved above or similar to recommended amts. of av. daily energy intake and percentage of energy from protein, fat and carbohydrates)

Antioxidants

(vegetarian diets excluding vegan diet achieved normal physiol. range of serum total antioxidant status in children)

Human

Nutrition, animal

(vegetarian diets excluding vegan diet provided adequate quantities of nutrients from diet and achieved normal physiol. range of serum homocysteine, folate, vitamin B12 and total antioxidant status in children)

Diet

(vegetarian, lacto-ovo-; lacto-ovovegetarian diet provided adequate quantities of nutrients from diet and achieved normal physiol. range of serum homocysteine, folate, vitamin B12 and total antioxidant status in children)

Diet

(vegetarian; vegetarian diets excluding vegan diet provided adequate quantities of nutrients from diet and achieved normal physiol. range of serum homocysteine, folate, vitamin B12 and total antioxidant status in children)

57-88-5, Cholesterol, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(vegetarian diet maintained low or physiol. range of serum total cholesterol in children)

59-30-3, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(vegetarian diets excluding vegan diet achieved normal physiol. range of serum folate in children)

6027-13-0, Homocysteine

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(vegetarian diets excluding vegan diet achieved normal physiol. range of serum homocysteine in children)

68-19-9, Vitamin B12

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(vegetarian diets excluding vegan diet achieved normal physiol. range of serum vitamin B12 in children)

Supplementary Terms

vegetarian diet homocysteine folate vitamin B12 antioxidant child

Citations

1) Rajaram, S; Nutrition 2000, 16, 531

2) Mangels, A; J Am Diet Assoc 2003, 103, 748

3) Leitzmann, C; Forum Nutr 2005, 57, 147

4) Sebekowa, K; Clin Chem 2003, 49, 983

5) Key, T; Proc Nutr Soc 2006, 65, 35

6) Refsum, H; Br J Nutr 2001, 85(Suppl 2), 109

7) Herrmann, W; Clin Chem 2001, 47, 1094

8) Sauders, T; Pediatr Clin North Am 1995, 42(4), 955

9) Thane, C; J Hum Nutr Diet 2000, 13, 149

10) Huang, Y; Eur J Nutr 2003, 42, 84

11) Krajcovicova-Kudlackova, M; Ann Nutr Metab 1994, 38, 331

12) Laskowska-Klita, T; Pol Merk Lek 2004, 94, 340

13) Ambroszkiewicz, J; Ann Acad Med Bial 2004, 49, 103

14) Geisel, J; Clin Chem Lab Med 2005, 43, 1164

15) Su, T; Atherosclerosis 2006, 184, 356

16) Hung, C; J Nutr 2002, 132, 152

17) Gamble, M; A M J Clin Nutr 2005, 81, 1372

18) Krajcovicova-Kudlackova, M; Biologia 2002, 57, 395

19) Szymczak, E; Med Wieku Rozwoj 2001, 2, 157

20) Laskowska-Klita, T; Clin Pediatr 2001, 40, 149

21) Krajcovicova-Kudlackova, M; Physiol Res 2004, 53, 219

22) Ullegaddi, R; J Parenter Enteral Nutr 2006, 30, 108

23) Chelchowska, M; Med Wieku Rozwoj 2003, 4(2), 577

24) Rauma, A; Nutrition 2000, 16, 111

25) Hozyasz, K; Ped Pol 2005, 80, 72

26) Drabko, K; Med Wieku Rozwoj 2004, 8, 215

27) Krajcovicova-Kudlackova, M; Scand J Clin Lab Invest 2000, 60, 657

28) Waldmann, A; Public Health Nutr 2004, 7, 467

44. Higuchi, Hisa; Okuda, Toyoko; Sasaki, Kimiko; Kogirima, Miho; Ioku, Kana; Kajiwara, Naemi; Okada, Yuki; Okada, Mariko. Relationship between the dietary pattern and the blood rheology in the middle-aged women. Nippon Kasei Gakkaishi (2006), 57(3), 159-167.

Abstract

We analyzed the relationship between the dietary pattern and blood rheol. in 34 vegetarian and 65 omnivorous middle-aged female volunteers. The vegetarian diet consisted mainly of unpolished rice, green vegetables, and tofu (bean curd), under a physician's guidance, and there were individual variations. The blood rheol. was evaluated by measuring the passage time of whole blood with a microchannel array flow analyzer (MC-FAN). A cluster anal. was performed on the nutrient intake of each subject. Four clusters representing different dietary patterns could be readily identified. These were (a) a vegan diet, (b) vegetarian diet, contg. only two omnivores, (c) eating moderately, all omnivores, (d) tendency to overeat, all omnivores. The intakes of Ca, Mg, Fe, Cu, vitamins K and B1, and folic acid by the vegetarian group were significantly more than those by the other three groups. BMI, body fat percentage, waist circumference, and diastolic pressure of the vegan and vegetarian groups were significantly lower than those of the omnivorous groups. The serum folic acid level for the vegan group was significantly higher than that for the two omnivorous groups, and the plasma quercetin level for the vegan and vegetarian groups was significantly higher than that in the two other groups. The blood rheol. parameters for the vegan and vegetarian groups tended to be higher than those for the two omnivorous groups. These data suggest that the vegetarian diet stimulated the blood rheol., and subsequently decreased the risk of impairing the microcirculation.

Indexing -- Section 18-7 (Animal Nutrition)

Blood

(blood rheol. during a vegetarian diet)

Diet

(vegetarian; blood rheol. during a vegetarian diet)

Supplementary Terms

blood diet vegetarian diet

45. Miyamoto, Emi; Tanioka, Yuri; Nakao, Tomoyuki; Barla, Florin; Inui, Hiroshi; Fujita, Tomoyuki; Watanabe, Fumio; Nakano, Yoshihisa. Purification and characterization of a corrinoid compound in an edible Cyanobacterium Aphanizomenon flos-aquae as a nutritional supplementary food. Journal of Agricultural and Food Chemistry (2006), 54(25), 9604-9607.

Abstract

The vitamin B12 concn. of the dried cells of Aphanizomenon flos-aquae was detd. by both microbiol. method with Lactobacillus delbrueckii ATCC7830 and chemiluminescence method with intrinsic factor. The Aphanizomenon cells contained 616.3  30.3 g (n = 4) of vitamin B12 per 100 g of the dried cells by the microbiol. method. The values detd. with the chemiluminescence method, however, were only about 5.3% of the values detd. by the microbiol. method. A corrinoid compd. was purified from the dried cells and characterized. The purified corrinoid compd. was identified as pseudovitamin B12 (an inactive corrinoid compd. for humans) by silica gel 60 TLC, C18 reversed-phase HPLC, UV-visible spectroscopy, and 1H NMR spectroscopy. The results suggest that the Aphanizomenon cells are not suitable for use as a vitamin B12 source, esp. in vegans.

Indexing -- Section 10-1 (Microbial, Algal, and Fungal Biochemistry)

Section cross-reference(s): 17

Aphanizomenon flos-aquae

Dietary supplements

(corrinoid compds. in edible cyanobacterium Aphanizomenon flos-aquae as nutritional supplement and purifn. and characterization)

Corrinoids

Role: BSU (Biological study, unclassified); PUR (Purification or recovery); BIOL (Biological study); PREP (Preparation)

(corrinoid compds. in edible cyanobacterium Aphanizomenon flos-aquae as nutritional supplement and purifn. and characterization)

Lactobacillus delbrueckii

(microbiol. detn. using; corrinoid compds. in edible cyanobacterium Aphanizomenon flos-aquae as nutritional supplement and purifn. and characterization)

13408-75-8P, Pseudovitamin B12

Role: BSU (Biological study, unclassified); PUR (Purification or recovery); BIOL (Biological study); PREP (Preparation)

(corrinoid compds. in edible cyanobacterium Aphanizomenon flos-aquae as nutritional supplement and purifn. and characterization)

Supplementary Terms

pseudovitamin vitamin B12 corrinoid cyanobacterium Aphanizomenon food supplement

Citations

1) Millet, P; Am J Clin Nutr 1989, 50, 718

2) Herbert, V; J Am Nutr Assoc 1982, 248, 3096

3) Dagnelie, P; Am J Clin Nutr 1991, 53, 695

4) Watanabe, F; Appl Biol Sci 1995, 5, 99

5) Watanabe, F; Biosci Biotechnol Biochem 2000, 64, 2712

6) Miyamoto, E; J Agric Food Chem 2001, 49, 3486

7) Kittaka-Katsura, H; J Agric Food Chem 2002, 50, 4994

8) Watanabe, F; J Agric Food Chem 1999, 47, 4736

9) Pulz, O; Appl Microbiol Biotechnol 2004, 65, 635

10) Jensen, G; J Am Nutr Assoc 2000, 2, 50

11) Kushak, R; J Am Nutr Assoc 2000, 2, 59

12) Drapeau, C; Abstracts from the 25th Annual Scientific Congerence of the American Holistic Medical Association, Complementary Health Practice Review 2003, 8, 161

13) Kay, R; Crit Rev Food Sci Nutr 1991, 30, 555

14) Watanabe, F; J Agric Food Chem 1998, 46, 1433

15) Stupperich, E; Eur J Biochem 1991, 199, 299

16) Pugh, N; Phytomedicine 2001, 8, 445

17) Benedetti, S; Life Sci 2004, 75, 2353

18) Pugh, N; Planta Med 2001, 67, 737

46. Myles, Paul S.; Chan, Matthew T. V.; Forbes, Andrew; Leslie, Kate; Paech, Michael; Peyton, Philip. Preoperative folate and homocysteine status in patients undergoing major surgery. Clinical Nutrition (2006), 25(5), 736-745.

Abstract

Background & aims: Patients with folate deficiency and elevated homocysteine (Hcy) levels have increased risk of cerebrovascular and cardiovascular disease. They may also be at increased risk of complications after surgery because nitrous oxide interferes with folate metab. The aim of this study was to assess the incidence of folate deficiency and hyperhomocysteinemia in patients presenting for major surgery. We also tested the utility of a brief preoperative medical and dietary questionnaire to identify those with low folate or elevated Hcy levels. Methods: We enrolled 390 patients and obtained a preoperative fasting blood sample from each of the study participants (folate [ n = 386 ], homocysteine [ n = 387 ]). Results: Although only one patient had folate deficiency preoperatively (incidence 0.3%), there were 29 patients with elevated Hcy concns. (incidence 7.5%). The meanSD folate and Hcy concns. were 23.75.2 nmol/l and 9.44.2 mol/l, resp. There was a neg. correlation between folate and Hcy, r = - 0.27 , P < 0.001 . Multivariate analyses indicated that vegan status and folate supplementation prevented low folate status (P < 0.05), while age of the patient, and history of heart failure and anemia predicted elevated Hcy concn. Conclusions: Some factors identified by a brief medical and dietary questionnaire are assocd. with folate and homocysteine status. Hyperhomocysteinemia occurs in about 7.5% of surgical patients; however, both low folate status and elevated Hcy concn. are less likely in those taking folate or vitamin B supplements. This has implications for patients undergoing nitrous oxide anesthesia because of its inhibition of folate metab., and should prompt clinicians to consider folate and other nutritional supplementation before elective surgery.

Indexing -- Section 14-2 (Mammalian Pathological Biochemistry)

Section cross-reference(s): 18

Anemia (disease)

(pernicious anemia; predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

Aging, animal

Body weight

Coronary artery disease

Diet

Dietary supplements

Human

Hypertension

Infection

Prognosis

Sex

Surgery

Tobacco smoke

(predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

Embolism

(thromboembolism; predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

59-30-3, biological studies

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); DGN (Diagnostic use); BIOL (Biological study); USES (Uses)

(deficiency; predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

6027-13-0, Homocysteine

Role: ADV (Adverse effect, including toxicity); BSU (Biological study, unclassified); DGN (Diagnostic use); BIOL (Biological study); USES (Uses)

(predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

68-19-9, Vitamin B12

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(predictors of folate deficiency and hyperhomocysteinemia in patients undergoing major surgery and effect of diet and nutritional supplements)

Supplementary Terms

folate deficiency hyperhomocysteinemia prognosis surgery

Citations

1) Clarke, R; Am J Clin Nutr 2003, 77, 1241

2) Tucker, K; J Nutr 1996, 126, 3025

3) Drogan, D; Br J Nutr 2004, 92, 489

4) Allen, L; Nutr Rev 2004, 62, S29

5) Rosener, M; J Neurol Neurosurg Psychiatry 1996, 60, 354

6) Ogundipe, O; Clin Lab Haematol 1999, 21, 409

7) Schilling, R; J Am Med Assoc 1986, 255, 1605

8) Myles, P; Anaesth Intens Care 2004, 32, 165

9) Marie, R; Arch Neurol 2000, 57, 380

10) Badner, N; Anesth Analg 2000, 91, 1073

11) Ravaglia, G; Am J Clin Nutr 2005, 82, 636

12) Chambers, J; Circulation 1999, 99, 1156

13) Ganji, V; Am J Clin Nutr 2004, 80, 1500

14) He, K; Stroke 2004, 35, 169

15) Maze, M; Anaesthesia 2000, 55, 311

16) Ermens, A; Clin Pharmacol Ther 1991, 49, 385

17) Amos, R; Lancet 1982, 2, 835

18) Murphy, M; Eur J Clin Nutr 2000, 54, 555

19) Flood, V; Public Health Nutr 2004, 7, 751

20) Pufulete, M; Br J Nutr 2002, 87, 383

21) Lumbers, M; Br J Nutr 2001, 85, 733

22) Sungurtekin, H; J Am Coll Nutr 2004, 23, 227

23) Fettes, S; Clin Nutr 2002, 21, 249

24) Quere, I; Lancet 2002, 359, 747

25) Badner, N; Anesth Analg 2001, 93, 1507

26) Tepaske, R; Lancet 2001, 358, 696

27) Marik, P; Crit Care Med 2001, 29, 2264

47. Schecter, Arnold; Harris, T. Robert; Paepke, Olaf; Tung, K. C.; Musumba, Alice. Polybrominated diphenyl ether (PBDE) levels in the blood of pure vegetarians ( vegans ). Toxicological and Environmental Chemistry (2006), 88(1), 107-112.

Abstract

Intake of many persistent org. pollutants (POPs) including dioxins, dibenzofurans and PCBs is almost exclusively from gastrointestinal ingestion of animal fats in the diet. With polybrominated di-Ph ether (PBDE) brominated flame retardants (BFRs), no consensus exists at present as to the extent of intake from food, from indoor dust or other routes of intake. Vegans, or pure vegetarians, were previously found to have low body burden of dioxins and dibenzofurans in blood. Data reported here for the first time show a trend towards lower PBDE levels with longer time periods without ingestion of food of animal origin in 8 adult residents of the United States. A stronger relationship between lower PBDE levels and time without meat, specifically, is consistent with substantial PBDE intake from meat relative to fish or dairy products in Americans. These vegans had somewhat lower PBDE levels with a range 12.4-127 and a median 23.9 ppb than published reports of US general population samples which had a range of 4-366 and median of 26 ppb. Our findings suggest that food of animal origin may be a major but not the sole contributor to human body burden of PBDEs.

Indexing -- Section 4-3 (Toxicology)

Section cross-reference(s): 17

Aging, animal

Blood

Fire-resistant materials

Food contamination

Human

(polybrominated di-Ph ether in blood of pure vegetarians (vegans)

Diet

(vegetarian; polybrominated di-Ph ether in blood of pure vegetarians (vegans)

101-84-8D, Diphenyl ether, bromine derivs.

1163-19-5, BDE 209

5436-43-1, BDE 47

41318-75-6, BDE 28

60348-60-9, BDE 99

68631-49-2, BDE 153

147217-75-2, BDE 17

182346-21-0, BDE 85

182677-30-1, BDE 138

189084-61-5, BDE 66

189084-64-8, BDE 100

207122-15-4, BDE 154

207122-16-5, BDE 183

Role: POL (Pollutant); OCCU (Occurrence)

(polybrominated di-Ph ether in blood of pure vegetarians (vegans)

Supplementary Terms

polybrominated diphenyl ether blood vegetarian food contamination

Citations

1) Bayen, S; J Toxicol Environ Health-Part A 2005, 68, 151

2) EPA; Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds National Academy Sciences (NAS) Review Draft, http://www.epa.gov/ncea/pdfs/dioxin/nas-review/ 2004

3) Schecter, A; Organohalogen Compd 1998, 38, 179

4) Startin, J; Dioxins and Health, 2nd ed 2003, 89

5) Craan, A; Arch Environ Contam Toxicol 1998, 35, 702

6) Lind, Y; Environ Res 2003, 93, 186

7) Mazdai, A; Environ Health Perspect 2003, 111, 1249

8) Meironyte, D; J Toxicol Environ Health Part A 1999, 58, 329

9) Noren, K; Chemosphere 2000, 40, 1111

10) Papke, O; Organohalogen Compd 2001, 52, 197

11) Schecter, A; J Toxicol Environ Health A 2005, 68, 501

12) Sjodin, A; Environ Health Perspect 2004, 112, 654

13) Solomon, G; Environ Health Perspect 2002, 110, A339

14) Schecter, A; Environ Health Perspect 2003, 111, 1723

15) Schecter, A; Environ Sci Technol 2004, 38, 5306

16) Schecter, A; J Occup Environ Med 2005, 47, 199

17) Jones-Otazo, H; Environ Sci Technol 2005, 39, 5121

18) Stapleton, H; Environ Sci Technol 2005, 39, 925

19) Webster, T; Organohalogen Compd 2005, 67, 505

20) Wu, N; Organohalogen Compd 2005, 67, 657

21) Betts, K; Environ Sci Technol 2004, 38, 50A

22) Birnbaum, L; Environ Health Perspect 2004, 112, 9

23) NTP National Toxicology Program; Toxicology and Carcinogenesis Studies of Decabromodiphenyl Oxide (CAS No 1163-19-5) in F344/N Rats and B6C3F1 Mice (Feed Studies), http://www.epa.gov/iris/subst/0035.htm 1986, TR-309

24) Branchi, I; Neurotoxicology 2002, 23, 375

25) Branchi, I; Neurotoxicology 2003, 24, 449

26) Eriksson, P; Toxicol Sci 2002, 67, 98

27) Viberg, H; Toxicol Sci 2003, 76, 112

28) Hallgren, S; Toxicology 2002, 177, 227

29) Meerts, I; Environ Health Perspect 2001, 109, 399

30) Meerts, I; Toxicol Sci 2002, 68, 361

31) Papke, O; Talanta 2004, 63, 1203

32) Lehmann, E; Nonparametrics: Statistical methods based on ranks 1975

48. Blanchard Dawn S Omega-3 fatty acid supplementation in perinatal settings. MCN. The American journal of maternal child nursing (2006), 31(4), 250-6.

Abstract

The purpose of this article is (a) to explain the role of omega-3 fatty acids in human health, specifically in fetal/neonatal development, (b) to summarize the recent research behind the innovations in infant formula manufacturing and advertisement of omega-3 fatty acid supplementation for pregnant and lactating mothers, and (c) to relate the research findings to clinical practice. Omega-3 fatty acid supplementation in perinatal settings is discussed here from three vantage points: (a) supplementation of the third-trimester pregnant woman to enhance fetal development, (b) supplementation of the lactating mother to enhance development of the breastfeeding infant, and (c) supplementation of infant formulas to enhance development of the bottle-feeding infant. Supplementation can occur by increasing one's intake of foods high in omega-3 fatty acids or by ingesting fatty acid nutritional supplements. The challenge of supplementation for vegan and vegetarian women is also addressed.

Controlled Terms

Check Tags: Female

Animals

Diet, Vegetarian: AE, adverse effects

*Dietary Supplements

Evidence-Based Medicine

Fatty Acids, Omega-3: PD, pharmacology

*Fatty Acids, Omega-3: TU, therapeutic use

Fetal Development

Fishes

Food Habits

Humans

Infant Formula: CH, chemistry

Infant Nutrition Physiology

Infant, Newborn

Lactation: PH, physiology

Maternal Nutrition Physiology

*Maternal-Child Nursing

Maternal-Child Nursing: MT, methods

Nurse's Role

Nutrition Policy

Nutritional Requirements

Nutritional Sciences: ED, education

*Patient Education

Patient Education: MT, methods

*Perinatal Care

Perinatal Care: MT, methods

Pregnancy

Pregnancy Trimester, Third

Chemical Names

0 (Fatty Acids, Omega-3)

49. Steinman Gary Mechanisms of twinning: VII. Effect of diet and heredity on the human twinning rate. The Journal of reproductive medicine (2006), 51(5), 405-10.

Abstract

OBJECTIVE: To evaluate the possible biochemical effect of diet and heredity on the rates of monozygotic and dizygotic twinning. STUDY DESIGN: In that insulin-like growth factor (IGF) has been found to be elevated in cows selected for their demonstrated increased twinning rate, the effect of agents that influence the level of IGF in women was examined. This was correlated with their prior history of singleton versus twin birthing. In particular, the effect of diets consisting of or excluding animal products that have elevated IGF content (e.g., milk) was considered. RESULTS: Vegan women, who exclude dairy products from their diets, have a twinning rate which is one-fifth that of vegetarians and omnivores. CONCLUSION: The results reported here support the proposed IGF model of dizygotic twinning. Genotypes favoring elevated IGF and diets including dairy products, especially in areas where growth hormone is given to cattle, appear to enhance the chances of multiple pregnancies due to ovarian stimulation.

Controlled Terms

Check Tags: Female

Dairy Products

*Diet

Diet, Vegetarian

Genetic Predisposition to Disease

Humans

Pregnancy

Somatomedins: GE, genetics

*Somatomedins: PH, physiology

Triplets: PH, physiology

*Twins: PH, physiology

Chemical Names

0 (Somatomedins)

50. Daubenmier Jennifer J; Weidner Gerdi; Marlin Ruth; Crutchfield Lila; Dunn-Emke Stacey; Chi Christine; Gao Billy; Carroll Peter; Ornish Dean Lifestyle and health-related quality of life of men with prostate cancer managed with active surveillance. Urology (2006), 67(1), 125-30.

Abstract

OBJECTIVES: To assess the impact of lifestyle on health-related quality of life (HR-QOL), perceived stress, and self-reported sexual function in men with early-stage prostate cancer electing active surveillance. METHODS: A total of 44 intervention and 49 usual-care control participants were enrolled in a randomized clinical trial examining the effects of lifestyle changes on prostate cancer progression. The intervention consisted of a low-fat, vegan diet, exercise, and stress management. Participants completed the Medical Outcomes Study Short Form-36 Health Status Survey (a measure of mental and physical HR-QOL), the Perceived Stress Scale, the Sexual Function subscale of the University of California, Los Angeles, Prostate Cancer Index, and measures of lifestyle behaviors (to yield an overall lifestyle index) at baseline and 12 months. The data were analyzed using analysis of variance for repeated measures. The relationship between lifestyle and QOL was also analyzed using multiple linear regression analyses. RESULTS: Intervention participants had significantly improved their lifestyle compared with controls at 12 months. The quality-of-life scores were high across groups and time points. However, a healthier lifestyle was related to better QOL at baseline. Participants in both groups who reported a healthier lifestyle also reported better mental and physical HR-QOL and sexual function. Furthermore, participants whose lifestyle improved over time showed enhanced physical HR-QOL and decreased perceived stress. CONCLUSIONS: Men who choose active surveillance for early-stage prostate cancer are able to make comprehensive lifestyle changes. Although the average QOL was already high in this sample, individuals who improved their lifestyle enhanced their QOL further.

Controlled Terms

Check Tags: Male

Aged

Humans

*Life Style

Middle Aged

Population Surveillance

*Prostatic Neoplasms: TH, therapy

*Quality of Life

51. Herbal cosmetic products containing vegetable oils and waxes. Ger. Gebrauchsmusterschrift (2006), 3pp.

Abstract

The invention concerns cosmetic or tech. products that contain vegetable oils, vegetable waxes in combination with essential oils and/or Vitamin E. Thus a viscous vegan bio mammary fat for milking contained (g): rape oil 555; palm kernel oil 90; olive oil 80; castor oil 60; jojoba oil 30; palm stearin 120; shea butter 20; coco fat 30; Vitamin E 2; perfumes 10.

Indexing -- Section 62-4 (Essential Oils and Cosmetics)

Castor oil

Essential oils

Jojoba oil

Olive oil

Palm kernel oil

Rape oil

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(herbal cosmetic products contg. vegetable oils and waxes)

Coconut oil

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(hydrogenated; herbal cosmetic products contg. vegetable oils and waxes)

Fats and Glyceridic oils, biological studies

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(shea butter; herbal cosmetic products contg. vegetable oils and waxes)

Palm oil

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(stearins; herbal cosmetic products contg. vegetable oils and waxes)

Fats and Glyceridic oils, biological studies

Waxes

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(vegetable; herbal cosmetic products contg. vegetable oils and waxes)

1406-18-4, Vitamin E

Role: COS (Cosmetic use); BIOL (Biological study); USES (Uses)

(herbal cosmetic products contg. vegetable oils and waxes)

Supplementary Terms

herbal cosmetic product vegetable oil wax

52. Giannini Alberto; Mirra Nadia; Patria Maria Francesca Health risks for children raised on vegan or vegetarian diets. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies (2006), 7(2), 188.

Controlled Terms

Check Tags: Male

*Anemia, Iron-Deficiency: ET, etiology

Cardiomegaly: ET, etiology

Diarrhea: ET, etiology

*Diet, Vegetarian: AE, adverse effects

Heart Murmurs: ET, etiology

Humans

Infant

53. Key, Timothy J.; Appleby, Paul N.; Rosell, Magdalena S. Health effects of vegetarian and vegan diets. Proceedings of the Nutrition Society (2006), 65(1), 35-41.

Abstract

A review. Vegetarian diets do not contain meat, poultry or fish; vegan diets further exclude dairy products and eggs. Vegetarian and vegan diets can vary widely, but the empirical evidence largely relates to the nutritional content and health effects of the av. diet of well-educated vegetarians living in Western countries, together with some information on vegetarians in non-Western countries. In general, vegetarian diets provide relatively large amts. of cereals, pulses, nuts, fruits and vegetables. In terms of nutrients, vegetarian diets are usually rich in carbohydrates, n-6 fatty acids, dietary fiber, carotenoids, folic acid, vitamin C, vitamin E and Mg, and relatively low in protein, satd. fat, long-chain n-3 fatty acids, retinol, vitamin B12 and Zn; vegans may have particularly low intakes of vitamin B12 and low intakes of Ca. Cross-sectional studies of vegetarians and vegans have shown that on av. they have a relatively low BMI and a low plasma cholesterol concn.; recent studies have also shown higher plasma homocysteine concns. than in non-vegetarians. Cohort studies of vegetarians have shown a moderate redn. in mortality from IHD but little difference in other major causes of death or all-cause mortality in comparison with health-conscious non-vegetarians from the same population. Studies of cancer have not shown clear differences in cancer rates between vegetarians and non-vegetarians. More data are needed, particularly on the health of vegans and on the possible impacts on health of low intakes of long-chain n-3 fatty acids and vitamin B12. Overall, the data suggest that the health of Western vegetarians is good and similar to that of comparable non-vegetarians.

Indexing -- Section 18-0 (Animal Nutrition)

Body weight

Human

(relatively low BMI, plasma cholesterol concn., higher plasma homocysteine concn. and moderate redn. in mortality from IHD were seen in Western vegetarians and vegans than in non-vegetarians)

Diet

(vegetarian, lacto-ovo-; relatively low BMI, plasma cholesterol concn., higher plasma homocysteine concn. and moderate redn. in mortality from IHD were seen in Western vegetarians and vegans than in non-vegetarians)

Diet

(vegetarian; relatively low BMI, plasma cholesterol concn., higher plasma homocysteine concn. and moderate redn. in mortality from IHD were seen in Western vegetarians and vegans than in non-vegetarians)

57-88-5, Cholest-5-en-3-ol (3)-, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; relatively low BMI, plasma cholesterol concn., higher plasma homocysteine concn. and moderate redn. in mortality from IHD were seen in Western vegetarians and vegans than in non-vegetarians)

6027-13-0, Homocysteine

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(relatively low BMI, plasma cholesterol concn., higher plasma homocysteine concn. and moderate redn. in mortality from IHD were seen in Western vegetarians and vegans than in non-vegetarians)

Supplementary Terms

review vegetarian vegan diet health mortality

Citations

Allen, N; Cancer Epidemiology, Biomarkers & Prevention 2002, 11, 1441

Allen, N; British Journal of Cancer 2000, 83, 95

American Dietetic Association And Dietitians Of Canada; Journal of the American Dietetic Association 2003, 103, 748

Antony, A; American Journal of Clinical Nutrition 2003, 78, 3

Appleby, P; Public Health Nutrition 2002, 5, 645

Armstrong, B; American Journal of Clinical Nutrition 1974, 27, 712

Barr, S; Nutrition 2004, 20, 696

Beilin, L; American Journal of Clinical Nutrition 1988, 48, 806

Chang-Claude, J; Cancer Epidemiology, Biomarkers & Prevention 2005, 14, 963

Dagnelie, P; Journal of Nutrition 1997, 127, 379

Dagnelie, P; American Journal of Clinical Nutrition 1991, 53, 695

Davey, G; Public Health Nutrition 2003, 6, 259

Davis, B; American Journal of Clinical Nutrition 2003, 78(Suppl), 640S

Department Of Health; Dietary Reference Values for Food Energy and Nutrients for the United Kingdom Report on Health and Social Subjects no 41 1991

Dos Santos Silva, I; International Journal of Cancer 2002, 99, 238

Eaton, N; British Journal of Cancer 1999, 80, 930

Fraser, G; American Journal of Clinical Nutrition 1999, 70(Suppl), 532S

Henderson, L; National Diet and Nutrition Survey:Adults Aged 19 to 64 Years vol 1: Types and Quantities of Foods Consumed 2002

Herbert, V; American Journal of Clinical Nutrition 1988, 48(Suppl), 852

Herrmann, W; Clinica Chimica Acta 2002, 326, 47

Herrmann, W; American Journal of Clinical Nutrition 2003, 78, 131

Hung, C; Journal of Nutrition 2002, 132, 152

International Vegetarian Union; 37th IVU World Vegetarian Congress, http://www.ivu.org/congress/2006/whyindia.html 2006

Jebb, S; Public Health Nutrition 2004, 7, 461

Jenkins, D; Journal of the American Medical Association 2003, 290, 502

Key, T; Journal of the National Cancer Institute 2002, 94, 606

Key, T; British Medical Journal 1996, 313, 816

Key, T; American Journal of Clinical Nutrition 2003, 78(Suppl), 533S

Key, T; Proceedings of the Nutrition Society 1999, 58, 271

Key, T; American Journal of Clinical Nutrition 1999, 70(Suppl), 516S

Key, T; Public Health Nutrition 2004, 7, 187

Koebnick, C; Journal of Nutrition 2004, 134, 3319

Kwok, T; American Journal of Hematology 2002, 70, 186

Law, M; British Medical Journal 1994, 308, 363

Mann, N; European Journal of Clinical Nutrition 1999, 53, 895

Mezzano, D; Thrombosis Research 2000, 100, 153

Mills, P; Cancer 1989, 64, 582

Mills, P; Cancer 1989, 64, 598

New, S; Osteoporosis International 2004, 15, 679

Nieman, D; American Journal of Clinical Nutrition 1999, 70(Suppl), 570S

Norat, T; Journal of the National Cancer Institute 2005, 97, 906

Pais, P; Lancet 1996, 348, 358

Peeters, P; Breast Cancer Research and Treatment 2003, 77, 171

Rao, D; British Journal of Cancer 1994, 70, 129

Reddy, S; British Journal of Nutrition 1998, 79, 495

Refsum, H; American Journal of Clinical Nutrition 2001, 74, 233

Renehan, A; Lancet 2004, 363, 346

Rosell, M; Public Health Nutrition 2005, 8, 870

Rosell, M; International Journal of Obesity In the Press 2005

Rosell, M; American Journal of Clinical Nutrition 2005, 82, 327

Sanders, T; Proceedings of the Nutrition Society 1999, 58, 265

Sanders, T; American Journal of Clinical Nutrition 1999, 70(Suppl), 555S

Sanders, T; American Journal of Clinical Nutrition 1978, 31, 805

Sanders, T; British Journal of Nutrition 1978, 40, 9

Sanjoaquin, M; Public Health Nutrition 2004, 7, 77

Sanjoaquin, M; British Journal of Cancer 2004, 90, 118

Scientific Advisory Committee On Nutrition; Salt and Health 2003

Shetty, P; Public Health Nutrition 2002, 5, 175

Spencer, E; International Journal of Obesity and Related Metabolic Disorders 2003, 27, 728

Stabler, S; Annual Review of Nutrition 2004, 24, 299

Steinfeld, H; Veterinary Parasitology 2004, 125, 19

Thomas, H; British Journal of Cancer 1999, 80, 1470

Waldmann, A; Annals of Nutrition and Metabolism 2004, 48, 103

Willett, W; American Journal of Clinical Nutrition 1999, 78(Suppl), 539S

Williams, C; Proceedings of the Nutrition Society 2006, 65, 42

World Health Organization; Diet, Nutrition and the Prevention of Chronic Diseases WHO Technical Report Series no 916 2003

54. Mann, Neil; Pirotta, Yvonne; O'Connell, Stella; Li, Duo; Kelly, Fiona; Sinclair, Andy. Fatty acid composition of habitual omnivore and vegetarian diets. Lipids (2006), 41(7), 637-646.

Abstract

High-fat diets are implicated in the onset of cardiovascular disease (CVD), cancer, and obesity. Large intakes of satd. and trans FA, together with low levels of PUFA, particularly long-chain (LC) omega-3 (n-3) PUFA, appear to have the greatest impact on the development of CVD. A high n-6:n-3 PUFA ratio is also considered a marker of elevated risk of CVD, though little accurate data on dietary intake is available. A new Australian food compn. database that reports FA in foods to 2 decimal places was used to assess intakes of FA in 4 habitual dietary groups. Anal. using the database found correlations between the dietary intakes of LC n-3 PUFA and the plasma phospholipid LC n-3 PUFA concns. of omnivore and vegetarian subjects. High meat-eaters (HME), who consumed large amts. of food generally, had significantly higher LC n-3 PUFA intakes (0.29 g/d) than moderate meat-eaters (MME) (0.14 g/d), whose intakes in turn were significantly higher than those of ovolacto-vegetarians or vegans (both 0.01 g/d). The satd. FA intake of MME subjects (typical of adult male Australians) was not different from ovolacto-vegetarian intakes, whereas n-6:n-3 intake ratios in vegetarians were significantly higher than in omnivores. Thus, accurate dietary and plasma FA analyses suggest that regular moderate consumption of meat and fish maintains a plasma FA profile possibly more conducive to good health.

Indexing -- Section 18-5 (Animal Nutrition)

Blood plasma

Human

(fatty acid compn. of habitual omnivore and vegetarian diets)

Fatty acids, biological studies

Phospholipids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(fatty acid compn. of habitual omnivore and vegetarian diets)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(monounsatd.; fatty acid compn. of habitual omnivore and vegetarian diets)

Diet

(omnivore; fatty acid compn. of habitual omnivore and vegetarian diets)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-3; fatty acid compn. of habitual omnivore and vegetarian diets)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(polyunsatd., omega-6; fatty acid compn. of habitual omnivore and vegetarian diets)

Fatty acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(satd.; fatty acid compn. of habitual omnivore and vegetarian diets)

Diet

(vegetarian, lacto-ovo-; fatty acid compn. of habitual omnivore and vegetarian diets)

Diet

(vegetarian; fatty acid compn. of habitual omnivore and vegetarian diets)

57-10-3, Hexadecanoic acid, biological studies

57-11-4, Octadecanoic acid, biological studies

60-33-3, 9,12-Octadecadienoic acid (9Z,12Z)-, biological studies

112-80-1, 9-Octadecenoic acid (9Z)-, biological studies

463-40-1

506-17-2

506-30-9, Eicosanoic acid

506-32-1

544-63-8, Tetradecanoic acid, biological studies

6217-54-5

10417-94-4

24880-45-3

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(fatty acid compn. of habitual omnivore and vegetarian diets)

Supplementary Terms

vegetarian omnivore diet blood fatty acid

Citations

1) Institute of Medicine of the National Academies; Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (Macronutrients) 2002, 335

2) Kwiterovich, P; J Am Diet Assoc 1997, 97, S31

3) Ravnskov, U; J Clin Epidemiol 1998, 51, 443

4) Kris-Etherton, P; Am J Clin Nutr 1994, 60, 1029S

5) Kinsella, J; Am J Clin Nutr 1990, 52, 1

6) Fischer, S; Prostaglandins 1986, 32, 235

7) DeLorgeril, M; Circulation 1999, 99, 779

8) Mann, N; Lipids 1997, 32, 635

9) Arterburn, L; Omega-3 Fatty Acids: Recommendations for Therapeutics and Prevention Symposium 2005

10) Mori, T; Am J Clin Nutr 2000, 71, 1085

11) Mantzioris, E; Am J Clin Nutr 1994, 59, 1304

12) Mann, N; J Nutr 1995, 125, 2528

13) Bang, H; Acta Med Scand 1972, 192(1-2), 85

14) Harper, C; Arch Intern Med 2001, 161, 2185

15) Burr, M; Lancet 1989, 2, 757

16) Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico; Lancet 1999, 354, 447

17) Hibbeln, J; Lancet 1998, 351, 1213

18) Hibbeln, J; World Rev Nutr Diet 2001, 88, 41

19) Phillipson, B; N Engl J Med 1985, 312, 1210

20) Von Schacky, C; J Clin Invest 1985, 76, 1626

21) Delarue, J; Am J Physiol 1996, 270, E353

22) Li, D; Am J Clin Nutr 1999, 69, 872

23) Roche, H; Proc Nutr Soc 1999, 58, 397

24) Gerster, H; Int J Vitamin Nutr Res 1995, 65(1), 3

25) de Deckere, E; Eur J Clin Nutr 1998, 52, 749

26) ISSFAL (International Society for the Study of Fatty Acids and Lipids); Recommendations for PUFA Intakes [Online], http://www.issfal.org.uk/welcome/PolicyStatement3.asp 2004

27) Astorg, P; Lipids 2004, 39, 527

28) Kris-Etherton, P; Circulation 2002, 106, 2747

29) Kris-Etherton, P; Am J Clin Nutr 2000, 71, 179S

30) WHO (World Health Organisation); Technical report series, http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf 2003, 916

31) Meyer, B; Food Australia 1999, 51(3), 82

32) Sinclair, A; Lipids 1994, 29, 337

33) Australian Bureau of Statistics; Apparent Consumption of Food Stuffs (1996/7) 1998

34) Cordain, L; Am J Clin Nutr 2005, 81, 341

35) McLennan, W; National Nutrition Survey of Australia 1995: Foods Eaten, Australia 1995 1999

36) CSIRO Human Nutrition in conjunction with Foundation SA; Nutrition in South Australia from 1988 to 1993: Results from the CSIRO State Nutrition Surveys 1994

37) McLennan, W; National Nutrition Survey of Australia 1995: Nutrient Intakes and Physical Measurements, Australia 1995 1998

38) Anon; NUTTAB 95, Data Tables for Use in Australia 1995

39) ANZFA: Australia New Zealand Food Authority; Supplement to NUTTAB 95 Database 1999

40) Mann, N; Nutr Dietetics 2003, 60(1), 42

41) Li, D; Eur J Clin Nutr 1999, 53, 612

42) Thomas, S; Metric Tables of Composition of Australian Foods 1977

43) Mann, N; J Nutr Diet (Aust) 2006, 63(2), 69

44) Gurr, M; Role of Fats in Food and Nutrition 1986, 3

45) Tefft, M; Eur J Clin Nutr 2002, 56, 786

46) Kelly, F; Comp Biochem Physiol Part A: Physiol 1991, 98, 581

47) Meyer, B; Lipids 2003, 38, 391

48) Berner, L; J Nutr 1993, 123, 1175

49) Howe, P; Nutrition 2006, 22, 47

50) Health and Welfare Canada; Nutrition Recommendations: The Report of the Scientific Review Committee 1990

51) Sugano, M; Lipids 1996, 31, S283

52) Hibbeln, J; Recommendations for Therapeutics and Prevention Symposium 2005

53) Department of Health and Ageing Australian Government; Nutrient Reference Values for Australia and New Zealand, http://www.nhmrc.gov.au/publications/_files/n36.pdf 2005

54) Kuriki, K; J Nutr 2003, 133, 3643

55) Roshanai, F; Hum Nutr Appl Nutr 1984, 38, 345

56) Rosell, M; Am J Clin Nutr 2005, 82, 327

57) Li, D; Asia Pacific J Clin Nutr 2005, 14, 113

58) Mann, N; Lipid Technol 2005, 17(4), 79

59) De Lorgeril, M; Asia Pac J Clin Nutr 2004, 13, S2

60) Donaldson, M; Nutr J 2004, 3, 19

55. Moerkbak, Anne L.; Hvas, Anne-Mette; Lloyd-Wright, Zoue; Sanders, Tom A. B.; Bleie, Oeyvind; Refsum, Helga; Nygaard, Ottar K.; Nexoe, Ebba. Effect of vitamin B12 treatment on haptocorrin. Clinical Chemistry (Washington, DC, United States) (2006), 52(6), 1104-1111.

Abstract

Haptocorrin (HC) carries the major part of circulating cobalamin, but whether HC is altered on treatment with vitamin B12 remains unknown. Our study included 3 populations: a population of vegan men (n = 174; vegan population), of whom 63 were treated daily with 5 mg of oral vitamin B12 for 3 mo; a group of patients with a previous methylmalonic acid (MMA) concn. >0.4 mol/L (n = 140; population with suspected deficiency), of which 69 were treated with weekly vitamin B12 injections (1 mg) for 4 wk; and a subgroup of participants in a vitamin B intervention study (n = 88; nondeficient population), of whom 45 were treated daily with 0.4 mg of oral vitamin B12 for 3 mo. Total HC and holoHC were measured by ELISA. Cobalamin was measured by an intrinsic factor (IF)-based assay. Samples were collected at baseline and 3 mo after start of treatment. Compared with baseline results for the 3 study populations, total HC and holoHC increased 30 pmol/L for every 100 pmol/L increase in cobalamin. After treatment with vitamin B12, holoHC (P <0.0001) and total HC (P <0.0001) increased significantly in the vegan population. Only holoHC increased in the population with suspected deficiency (P <0.0001), whereas no alteration was obsd. in the nondeficient population. The HC concn. is decreased in severely cobalamin-deficient individuals and increases on treatment. The concn. of cobalamin also relates significantly to the HC concn. in nondeficient individuals.

Indexing -- Section 18-2 (Animal Nutrition)

Section cross-reference(s): 1

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(haptocorrins; vitamin B12 treatment effect on haptocorrin)

Diet

(vegetarian; vitamin B12 treatment effect on haptocorrin)

Dietary supplements

Human

(vitamin B12 treatment effect on haptocorrin)

516-05-2, Methylmalonic acid

6027-13-0, Homocysteine

13408-78-1, Cobalamin

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(vitamin B12 treatment effect on haptocorrin)

68-19-9, Vitamin B12

Role: BSU (Biological study, unclassified); PAC (Pharmacological activity); BIOL (Biological study)

(vitamin B12 treatment effect on haptocorrin)

Supplementary Terms

vitamin B12 deficiency vegan diet haptocorrin cobalamin

Citations

1) Hall, C; Clin Sci Mol Med 1977, 53, 453

2) Nexo, E; Vitamin B12 and B12-Binding Proteins 1997, 459

3) Markle, H; Crit Rev Clin Lab Sci 1996, 33, 247

4) Kolhouse, J; N Engl J Med 1978, 299, 785

5) Carmel, R; Am J Clin Pathol 2001, 116, 576

6) Morkbak, A; Clin Chim Acta 2005, 356, 184

7) Carmel, R; Clin Chem 2003, 49, 1367

8) Nexo, E; Scand J Clin Lab Invest 1977, 37, 723

9) Lindemans, J; Clin Chim Acta 1983, 132, 53

10) Morelli, T; Clin Chim Acta 1977, 77, 365

11) Carmel, R; JAMA 1983, 250, 1886

12) Nexo, E; Clin Chem 2002, 48, 561

13) Lloyd-Wright, Z; Clin Chem 2003, 49, 2076

14) Hvas, A; J Intern Med 2005, 257, 289

15) Nexo, E; Clin Chem 2002, 48, 1768

16) Bleie, O; Am J Clin Nutr 2004, 80, 641

17) Rasmussen, K; Clin Chem 1996, 42, 630

18) Rasmussen, K; Clin Chem 1989, 35, 260

19) Husek, P; J Chromatogr B Biomed Sci Appl 1998, 717, 57

20) Nexo, E; Clin Chem 2000, 46, 1150

21) Carmel, R; Am J Clin Pathol 1978, 69, 319

22) Eussen, S; Arch Intern Med 2005, 165, 1167

23) Rajan, S; J Am Geriatr Soc 2002, 50, 1789

24) Gullberg, R; Scand J Haematol 1972, 9, 639

56. Waldmann A; Dorr B; Koschizke J W; Leitzmann C; Hahn A Dietary intake of vitamin B6 and concentration of vitamin B6 in blood samples of German vegans. Public health nutrition (2006), 9(6), 779-84.

Abstract

OBJECTIVE: The study aimed to evaluate the dietary vitamin B6 intake and determine the vitamin B6 concentration in blood samples of German vegans. DESIGN AND SETTING: Cross-sectional study with 33 examination sites all over Germany.Subjects Ninety-three vegans (50 females) with a mean (+/- standard deviation (SD)) age of 43.7 +/- 15.7 years who took no vitamin supplements. METHODS: Dietary intake was assed using a semi-quantitative food-frequency questionnaire. Erythrocyte aspartate aminotransferase activity coefficient (EAST-AC) was calculated as the ratio of stimulated (pyridoxal 5'-phosphate added) to unstimulated activity in blood samples that were provided after an overnight fast. RESULTS: Mean +/- SD vitamin B6 intake was 2.83 +/- 0.98 mg day(-1) and mean +/- SD protein intake was 56.6 +/- 21.7 g day(-1). Of the participants 4% showed vitamin B6 intakes lower than daily recommended intakes for Germany, 16% showed EAST-AC > 1.85, and a further 58% showed EAST-AC of 1.5-1-85. Moderate vegans were affected to a lesser extent than strict vegans. None of the established confounders was a significant predictor of EAST-AC. In logistic regression analyses the contribution of nutriments and cereals to pyridoxine intake was the only predictor of EAST-AC classified as < or = 1.85 and > 1.85, respectively. CONCLUSIONS: In spite of the high total intake of vitamin B6, an adequate concentration in blood samples could not be realised for a majority of the participants. Due to the health implications of a marginal pyridoxine status, vegans should be encouraged to include foods with a high bioavailability of pyridoxine, such as beans, lentils and bananas, in the daily diet.

Controlled Terms

Check Tags: Female; Male

Adult

Aspartate Aminotransferases: ME, metabolism

Biological Availability

Cross-Sectional Studies

*Diet, Vegetarian

Erythrocytes: EN, enzymology

Germany

Humans

Logistic Models

*Nutrition Assessment

*Nutritional Status

Questionnaires

*Vitamin B 6: AD, administration & dosage

*Vitamin B 6: BL, blood

Vitamin B 6 Deficiency: BL, blood

Vitamin B 6 Deficiency: EP, epidemiology

Vitamin B 6 Deficiency: PC, prevention & control

*Vitamin B Complex: AD, administration & dosage

Vitamin B Complex: BL, blood

Registry Numbers

12001-76-2 (Vitamin B Complex)

8059-24-3 (Vitamin B 6)

Chemical Names

EC 2.6.1.1 (Aspartate Aminotransferases)

57. Harrad, Stuart; Ren, Jianzhang; Hazrati, Sadegh; Robson, Matthew. Chiral signatures of PCB#s 95 and 149 in indoor air, grass, duplicate diets and human faeces. Chemosphere (2006), 63(8), 1368-1376.

Abstract

Chiral signatures of PCB#s 95 and 149 are reported for indoor air, grass, omnivorous and vegan duplicate human diet homogenates, and human feces. Comparison of chiral signatures of both congeners in grass with those reported previously for outdoor air (measured at a height of 1.5 m) and soil at the same location suggest that volatilization of PCBs present in soil may exert a significant influence on concns. in grass. Duplicate diet homogenates display racemic signatures for both congeners. Alongside the racemic signatures in both outdoor and indoor air, this implies that human intake via diet and inhalation is racemic, and that the previously obsd. variation between individuals in the extent of enantioselective degrdn. in human liver samples indicates possible inter-individual variation in ability to metabolise PCBs. Chiral signatures of PCB# 95 in the 10 human fecal samples analyzed indicate 8 to be racemic, but 2 to display an excess of the 2nd eluting enantiomer. This is consistent with the excess of the 1st eluting enantiomer reported elsewhere for human liver samples, as it implies enantioselective excretion of the 2nd eluting enantiomer. However, the racemic residues for PCB# 95 in the majority of fecal samples are a possible indication that enantioselective interaction of chiral PCBs with cytochrome P 450 occurs slowly. The racemic or near-racemic signatures obsd. for PCB# 95 and 149 in indoor air match closely those in outdoor air, but differ from those in soil, adding to the wt. of evidence that ventilation of indoor air is a far more significant contributor to outdoor air concns. than volatilization of PCBs from soil.

Indexing -- Section 4-1 (Toxicology)

Section cross-reference(s): 59

Feces

Human

Indoor air pollution

Poaceae

Soil pollution

(chiral signatures of PCBs 95 and 149 in indoor air, grass, duplicate diets and human feces)

Diet

(omnivorous and vegan; chiral signatures of PCBs 95 and 149 in indoor air, grass, duplicate diets and human feces)

38379-99-6, PCB 95

38380-04-0, PCB 149

Role: ANT (Analyte); POL (Pollutant); ANST (Analytical study); OCCU (Occurrence)

(chiral signatures of PCBs 95 and 149 in indoor air, grass, duplicate diets and human feces)

Supplementary Terms

PCB 95 149 indoor air grass diet feces

Citations

Ayris, S; Chemosphere 1997, 35, 905

Bidleman, T; Environ Sci Technol 1999, 33, 206A

Blanch, G; Eur Food Res Technol 1999, 209, 294

Bordajandi, L; Organohalogen Compd 2004, 66, 440

Buser, H; Organohalogen Compd 1997, 31, 225

Chu, S; Environ Res 2003, 93, 167

Currado, G; Environ Sci Technol 1998, 32, 3043

Currado, G; Persistent Organic Pollutants:Environmental Behaviour and Pathways of Human Exposure 2001, 53

Finizio, A; Chemosphere 1998, 36, 345

Food Standards Agency; Food Survey Information Sheet Number 04/00 2000

Food Standards Agency; Food Survey Information Sheet 38/03 2003

Glausch, A; J High Resolut Chromatogr 1994, 17, 347

Harrad, S; Organohalogen Compd 2004, 66, 3786

Harrad, S; Environ Pollut 1994, 85, 131

Harrad, S; J Environ Monit 2003, 5, 224

Harrad, S; Environ Sci Technol 2004, 38, 2345

Huhnerfuss, H; Mar Pollut Bull 1995, 30, 332

Krauss, M; Organohalogen Compd 2004, 66, 2345

Mao, H; Organohalogen Compd 2002, 58, 65

M; Issues Enviro Sci Technol 1996, 6, 31

Moser, G; Chemosphere 2001, 45, 201

Pakdeesusuk, U; Environ Sci Technol 2003, 37, 1100

Puttmann, M; Biochem Pharmacol 1989, 38, 1345

Robson, M; Environ Sci Technol 2004, 38, 1662

Rodman, L; Biochem Pharmacol 1991, 41, 915

Trapp, S; Environ Sci Technol 1997, 31, 71

Vetter, W; J Chromatogr A 1997, 774, 143

Welsch-Pausch, K; Environ Sci Technol 1995, 29, 1090

Wilford, B; Environ Sci Technol 2004, 38, 5312

Wong, C; J Chromatogr A 2000, 866, 213

Wong, C; Environ Sci Technol 2001, 35, 2448

58. Cundiff David K; Harris William Case report of 5 siblings: malnutrition? Rickets? DiGeorge syndrome? Developmental delay?. Nutrition journal (2006), 5 1.

Abstract

BACKGROUND: Parents of six children are facing a trial on charges of aggravated manslaughter in the care a 5 1/2 month old infant who died suddenly and neglect of their four older children for causing them to be malnourished by feeding them all an exclusively raw foods vegan diet. Both parents declined plea bargains and plan to defend themselves in court. CASE PRESENTATION: The fifth child born to a married couple was breast-fed until 2 1/2 months. Subsequently, the parents fed the baby an exclusively raw foods diet prepared in a blender at home. The four older children, ages 18 months-6 1/2 years also ate an exclusively raw foods vegan diet. None of the four older children had significant previous injuries or serious illnesses. At autopsy, the infant weighed 3180 mg (6.99 pounds) and appeared emaciated. The thymus gland was absent and parathyroid glands were not located. The lungs were "congested." DiGeorge anomaly cannot be ruled out from these findings. Although, the coroner ruled that "malnutrition" was the sole cause of death, malnutrition, according to the World Health Organization definition, cannot be diagnosed in this infant. Compared with standard growth charts, the older children fell 2.1-4.1 standard deviations below the mean for North American children in height and weight. Labs were normal except for a low cholesterol level in all and a low prealbumin in one of three children tested. Therefore, malnutrition cannot be diagnosed in these children. The pediatrician diagnosed rickets in the four-year-old. However, chest x-rays were normal in all and long bone x-rays showed minimal changes in one child--no sign of rickets. The clinical diagnosis of rickets was not confirmed by the Center for Disease Control's criteria. A psychologist diagnosed the 18-month-old as developmentally delayed to the level of a 15-month-old, but this diagnosis is questionable.

CONCLUSION: The raw foods vegan diet and possibly inherited small stature from the father's side account for their relatively low heights and weights. Catch-up growth will probably occur on the standard American diet but would have also been expected if they had remained on a vegan diet.

Controlled Terms

Check Tags: Female

Body Height

Body Weight

Child

*Child Abuse: LJ, legislation & jurisprudence

Child Nutrition Physiology

Child, Preschool

*Developmental Disabilities: DI, diagnosis

*DiGeorge Syndrome: DI, diagnosis

*Diet, Vegetarian: AE, adverse effects

Energy Intake

Fatal Outcome

Humans

Infant

Infant Nutrition Physiology

*Malnutrition: DI, diagnosis

Nutrition Policy

*Rickets: DI, diagnosis

59. Krajcovicova-Kudlackova, Marica; Ursinyova, Monika; Masanova, Vlasta; Bederova, Alzbeta; Valachovicova, Martina. Cadmium blood concentrations in relation to nutrition. Central European Journal of Public Health (2006), 14(3), 126-129.

Abstract

Cadmium is a toxic element ubiquitous in the environment, which damages biol. systems in various ways. The major source of cadmium exposure is food. High cadmium content in the soil leads to high cadmium concns. in certain plants such as grains (above all surface layers and germs), oil or non-oil seeds, fruit and vegetables. These food commodities are the crucial components of a vegetarian nutrition. Blood cadmium concns. were measured in two non-smoking population groups: the vegetarian group (n = 80) and the non-vegetarian (control) group of general population on traditional mixed diet (n = 84). The significantly higher blood cadmium content (1.780.22 vs. 0.450.04 g/l) was measured in vegetarian group. Healthy risk values > 5g/l were found in 6 vegetarians vs. no non-vegetarian. The highest cadmium concn. (3.150.77 g/l) was measured in vegan subgroup (plant food only, n = 10) and that value decreased with increasing animal food consumption (1.750.36 g/l, lactovegetarian and lactoovovegetarian subgroup/added dairy products and eggs, n = 41/, 1.340.21 g/l, semivegetarian subgroup/as a previous subgroup and added white meat, n = 29/). Risk vegetarians vs. non-risk vegetarians consume significantly higher amts. of whole grain products, grain sprouts and oil seeds. Blood cadmium content is directly influenced by age (r = 0.32, p < 0.001), by whole grain product intake (r = 0.66, p < 0.001) and by duration of vegetarianism (r = 0.5, p < 0.001). Oxidative stress plays a major role in chronic cadmium induced hepatic and renal toxicity as well as in other consequences of cadmium injuries. Vegetarians have significantly higher plasma concns. of natural antioxidants. The sufficient antioxidative protection against cadmium induced free radical formation in vegetarians may inhibit the harmful effects of greater cadmium intake from plant food.

Indexing -- Section 4-3 (Toxicology)

Section cross-reference(s): 18

Blood

Fruit

Health

Human

Nutrition, animal

Vegetable

(cadmium blood concns. in relation to nutrition examd. in vegetarians)

Diet

(vegetarian; cadmium blood concns. in relation to nutrition examd. in vegetarians)

7440-43-9, Cadmium, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(cadmium blood concns. in relation to nutrition examd. in vegetarians)

Supplementary Terms

cadmium blood nutrition

Citations

1) Nordberg, G; Biometals 2004, 17(5), 485

2) Boguszewska, A; Ann Univ Mariae Curie Sklodowska 2004, 59(2), 519

3) Wing, A; Nutr Res 1992, 12, 1205

4) Reeves, P; Environ Health Perspect 1997, 105(10), 1098

5) Donma, O; Med Hypotheses 2005, 65(4), 699

6) Anon; Analyses of hazardous substances in biological materials 1985, 1, 81

7) Recknagel, R; Methods in enzymology 1984, 331

8) Krajcovicova-Kudlackova, M; Cesk Pediatr (In Slovak) 1999, 54(9), 482

9) Puklova, V; Cent Eur J Public Health 2005, 13(1), 11

10) Benes, B; Cent Eur J Public Health 2000, 8(2), 117

11) Benes, B; Cent Eur J Public Health 2001, 9(4), 190

12) Koreckova-Sysalova, J; Biol Trace Elem Res 1997, 56(3), 321

13) Krajcovicova-Kudlackova, M; Physiol Res 2004, 53(2), 219

14) Tietz, N; Clinical guide to laboratory tests 1995

15) Kaczmarek-Wdowiak, B; Med Pr (In Polish) 2004, 55(5), 403

16) Krajcovicova-Kudlackova, M; Vet Med 1995, 40(9), 293

17) Stohs, S; Free Radic Biol Med 1995, 18(2), 321

18) Klaassen, C; Annu Rev Pharmacol Toxicol 1999, 39, 267

19) Kamiyama, T; Res Commun Mol Pathol Pharmacol 1995, 88(2), 177

20) Barany, E; Environ Res 2005, 98(2), 215

21) Kazantzis, G; Biometals 2004, 17(5), 493

22) Kuriwaki, J; Toxicol Lett 2005, 156(3), 369

23) Grosicki, A; J Trace Elem Med Biol 2004, 18(2), 183

24) Krajcovicova-Kudlackova, M; Klin Biochem Metab (In Slovak) 2001, 9(4), 187

25) Krajcovicova-Kudlackova, M; Bratisl Lek Listy 2005, 106(6-7), 231

26) Morales, A; Toxicol Appl Pharmacol 2006, 210(1-2), 128

27) Krajcovicova-Kudlackova, M; Oncol Rep 1996, 3, 1119

60. Majchrzak, D.; Singer, I.; Maenner, M.; Rust, P.; Genser, D.; Wagner, K.-H.; Elmadfa, I. B-vitamin status and concentrations of homocysteine in Austrian omnivores, vegetarians and vegans. Annals of Nutrition & Metabolism (2006), 50(6), 485-491.

Abstract

A vegetarian diet is considered to promote health and longevity and reduce the risk of cardiovascular diseases and cancer. However, a vegetarian diet may be deficient in some nutrients. Exclusion of animal products in vegetarian diets may affect the status of certain B-vitamins, and further cause the rise of plasma homocysteine concn. The nutritional status of various B-vitamins (B1, B2, B6, B12, folic acid) and the concn. of homocysteine in blood plasma of omnivores (n = 40), vegetarians (n = 36) and vegans (n = 42) in Austria was evaluated. The evaluation was done using the functional parameters erythrocyte transketolase (ETK), glutathione reductase (EGR) and glutamic oxaloacetic transaminase (EGOT) activation coeffs. Enzyme activity was measured photometrically. The quantity of vitamins B1, B2 and B6 in urine and the concns. of vitamin B6 and homocysteine in plasma were detd. by HPLC methods with fluorescence detection. Plasma concn. of vitamin B12 and folic acid were measured with RIA. Most of the subjects showed a satisfying vitamin B1 status. Vegans presented a significantly lower mean plasma vitamin B12 concn. than omnivores and vegetarians and deficiency in 2.4% of the volunteers but the highest mean value of plasma folate among the investigated groups. A deficient status of folate was found in 18% of omnivores and in approx. 10% of vegans and vegetarians. The status of riboflavin is considered to be deficient in about 10% of omnivores and vegetarians and in over 30% of vegans. According to the activation coeff. of GOT, approx. one third of all subjects showed vitamin B6 deficiency. Elevated homocysteine concn. in plasma was obsd. in 66% of the vegans and about 45-50% of the omnivores and vegetarians. Vegan subjects had significantly higher mean plasma homocysteine levels than omnivores. Thiamin and folate need not be a problem in a well-planned vegan diet. Vitamins B12 and B2 may need attention in the strict vegan diet, esp. regarding elevated homocysteine levels in plasma.

Pyridoxine status appeared to be independent of the diet.

Indexing -- Section 18-2 (Animal Nutrition)

Blood plasma

Erythrocyte

Human

Urine

(B-vitamins and homocysteine in Austrian omnivores, vegetarians and vegans)

Vitamins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(B-vitamins and homocysteine in Austrian omnivores, vegetarians and vegans)

Diet

(vegetarian; B-vitamins and homocysteine in Austrian omnivores, vegetarians and vegans)

54-47-7, Pyridoxal phosphate

59-30-3, Folic acid, biological studies

59-43-8, Vitamin B1, biological studies

68-19-9, Vitamin B12

82-82-6, 4-Pyridoxic acid

83-88-5, Vitamin B2, biological studies

6027-13-0, L-Homocysteine

8059-24-3, Vitamin B6

9000-97-9

9001-48-3, Glutathione reductase

9014-48-6, Transketolase

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(B-vitamins and homocysteine in Austrian omnivores, vegetarians and vegans)

Supplementary Terms

omnivore vegetarian vegan diet B vitamin folate homocysteine

Citations

1) European Vegetarian Union; http://www.european-vegetarian.org/lang/en/info/howmany.php 2005

2) Anon; J Am Diet Assoc 2003, 103, 748

3) Waldmann, A; Eur J Clin Nutr 2003, 57, 947

4) Dwyer, J; Am J Clin Nutr 1999, 70(suppl), 620S

5) Antony, A; Am J Clin Nutr 2003, 78, 3

6) Appleby, P; Am J Clin Nutr 1999, 70(suppl), 525S

7) Larsson, C; Am J Clin Nutr 2002, 76, 100

8) Millet, P; Am J Clin Nutr 1989, 50, 718

9) Huang, Y; Eur J Nutr 2003, 42, 84

10) Gamble, M; Am J Clin Nutr 2005, 81, 1372

11) McNulty, H; Am J Clin Nutr 2002, 76, 436

12) Powers, H; Am J Clin Nutr 2003, 77, 1352

13) Talwar, D; Clin Chem 2000, 46, 704

14) Capo-Chichi, C; J Chromatogr B 2000, 739, 219

15) Bitsch, R; Nutritional Status Assessment 1991, 1, 233

16) Sauberlich, H; Am J Clin Nutr 1972, 25, 629

17) Ubbink, J; J Chromatogr 1991, 565, 441

18) Sauberlich, H; Laboratory Tests for the Assessment of Nutritional Status, ed 2 1999

19) Edwards, P; Clin Chem 1989, 35, 241

20) Chrisley, B; J Chromatogr 1991, 563, 369

21) Stanger, O; J Kardiol 2003, 5, 190

22) Singer, I; Ann Nutr Metab 2005, 49(suppl 1), 260

23) Bissoli, L; Ann Nutr Metab 2002, 46, 73

24) Krajcovicova-Kudlackova, M; Ann Nutr Metab 2000, 44, 135

25) Haddad, E; Am J Clin Nutr 1999, 70(suppl), 586S

61. Son, Kum Hee; Choue, Ryowon. A study for comparison of dietary quality and vitamin K intake of vegetarians with carnivores. Hanguk Yongyang Hakhoechi (2006), 39(6), 529-538.

Abstract

The prevalence of chronic diseases have been rising in the developing countries because of their increased animal foods consumption and Western lifestyle. Lately, vegetarian diet that exclude animal products get public attention. The purpose of this study was to evaluate the nutritional status and dietary quality of vegetarians, and their consumption of vitamin K and was also assessed. Vegetarians including strict vegan and lacto-ovo-vegetarian consumed their diet at least over 6 mo. Carnivores were gender and age matched with vegetarians and they consumed over 50% of protein and fat from animal sources. Current nutrient intakes and dietary quality were assessed using 3-day food records and intake of vitamin K was calcd. from the data base of "Provisional Table on the vitamin K contents of foods, USA". Blood sample were collected and biochem. parameters and plasma phylloquinone concns. were analyzed. Anthropometric data from vegetarian and carnivore were not significantly different. The intake of calories, protein, vitamin B2, Ca and Zn of the vegetarians were remarkably lower than RDA for each nutrient. Moreover, index of nutritional quality and nutrient adequacy ratio of vegetarians were lower than those of carnivore. Vegetarian consumed less fat and the ratio of n-6/n-3 fatty acid was lower in vegetarian. The intake of essential amino acids in vegetarian was significantly lower than that of carnivore. The vitamin K consumption and plasma phylloquinone concn. of vegetarian were significantly higher than those of carnivore (p < 0.05). The dietary vitamin K consumption was pos. correlated with plasma phylloquinone levels in vegetarian (p < 0.01).

Indexing -- Section 18-2 (Animal Nutrition)

Glycerides, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

Dietary energy

Dietary fiber

Nutrients

Nutrition, animal

(comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

Fats and Glyceridic oils, biological studies

Lipoproteins

Proteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

Amino acids, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(essential; comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

Diet

(vegetarian; comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

50-99-7, D-Glucose, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(blood; comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

50-81-7, Vitamin C, biological studies

56-87-1, L-Lysine, biological studies

57-88-5, Cholesterol, biological studies

59-30-3, Folic acid, biological studies

59-43-8, Vitamin B1, biological studies

59-67-6, Niacin, biological studies

61-90-5, L-Leucine, biological studies

63-68-3, L-Methionine, biological studies

63-91-2, L-Phenylalanine, biological studies

68-19-9, Vitamin B12

71-00-1, L-Histidine, biological studies

72-18-4, L-Valine, biological studies

72-19-5, L-Threonine, biological studies

73-22-3, L-Tryptophan, biological studies

73-32-5, L-Isoleucine, biological studies

83-88-5, Riboflavin, biological studies

84-80-0, Phylloquinone

1406-18-4, Vitamin E

6027-13-0, Homocysteine

7439-89-6, Iron, biological studies

7440-66-6, Zinc, biological studies

7440-70-2, Calcium, biological studies

7723-14-0, Phosphorus, biological studies

8059-24-3, Vitamin B6

11103-57-4, Vitamin A

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(comparison of dietary quality and vitamin K intake of vegetarians with carnivores)

Supplementary Terms

vegetarian diet nutrient nutrition vitamin K

62. Barnard, Neal D.; Cohen, Joshua; Jenkins, David J. A.; Turner-Mcgrievy, Gabrielle; Gloede, Lise; Jaster, Brent; Seidl, Kim; Green, Amber A.; Talpers, Stanley. A low-fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. Diabetes Care (2006), 29(8), 1777-1783.

Abstract

Objective: We sought to investigate whether a low-fat vegan diet improves glycemic control and cardiovascular risk factors in individuals with type 2 diabetes. Research Design and Methods: Individuals with type 2 diabetes (n = 99) were randomly assigned to a low-fat vegan diet (n = 49) or a diet following the American Diabetes Assocn. (ADA) guidelines (n = 50). Participants were evaluated at baseline and 22 wk. Results: Forty-three percent (21 of 49) of the vegan group and 26% (13 of 50) of the ADA group participants reduced diabetes medications. Including all participants, HbA1c (A1C) decreased 0.96 percentage points in the vegan group and 0.56 points in the ADA group (P = 0.089). Excluding those who changed medications, A1C fell 1.23 points in the vegan group compared with 0.38 points in the ADA group (P = 0.01). Body wt. decreased 6.5 kg in the vegan group and 3.1 kg in the ADA group (P < 0.001). Body wt. change correlated with A1C change (r = 0.51, n = 57, P < 0.0001). Among those who did not change lipid-lowering medications, LDL cholesterol fell 21.2% in the vegan group and 10.7% in the ADA group (P = 0.02). After adjustment for baseline values, urinary albumin redns. were greater in the vegan group (15.9 mg/24 h) than in the ADA group (10.9 mg/24 h) (P = 0.013). Conclusions: Both a low-fat vegan diet and a diet based on ADA guidelines improved glycemic and lipid control in type 2 diabetic patients. These improvements were greater with a low-fat vegan diet.

Indexing -- Section 18-7 (Animal Nutrition)

Body weight

(low-fat vegan diet improved body wt. in type 2 diabetes patient)

Diet

Human

(low-fat vegan diet improved glycemic control, body wt. and cardiovascular risk factors in type 2 diabetes patient)

Fats and Glyceridic oils, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved glycemic control, body wt. and cardiovascular risk factors in type 2 diabetes patient)

High-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved high-d. lipoprotein cholesterol in type 2 diabetes patient)

Low-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved low-d. lipoprotein cholesterol in type 2 diabetes patient)

Glycerides, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved triglyceride in type 2 diabetes patient)

Very-low-density lipoproteins

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved very low-d. lipoprotein cholesterol in type 2 diabetes patient)

Albumins, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet reduced urinary albumin in type 2 diabetes patient)

Diabetes mellitus

(non-insulin-dependent; low-fat vegan diet improved glycemic control, body wt. and cardiovascular risk factors in type 2 diabetes patient)

62572-11-6, Hemoglobin A1c

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved HbA1c in type 2 diabetes patient)

57-88-5, Cholesterol, biological studies

Role: BSU (Biological study, unclassified); BIOL (Biological study)

(low-fat vegan diet improved total cholesterol in type 2 diabetes patient)

Supplementary Terms

glycemic control vegan diet cardiovascular risk diabetes

Citations

1) Jenkins, D; Am J Clin Nutr 2003, 78, 610S

2) Fraser, G; Diet, Life Expectancy, and Chronic Disease 2003, 129

3) Nicholson, A; Prev Med 1999, 29, 87

4) Barnard, N; Am J Med 2005, 118, 991

5) Wilson, D; Clin Chem 1993, 39, 2090

6) American Diabetes Association; Diabetes Care 2003, 26(Suppl 1), S51

7) Schakel, S; J Am Diet Assoc 1988, 88, 1268

8) Barthelmai, W; Klin Wochenschr [in German] 1962, 40, 585

9) Allain, C; Clin Chem 1974, 20, 470

10) Wieland, H; J Lipid Res 1983, 24, 904

11) Finley, P; Clin Chem 1978, 24, 931

12) Friedewald, W; Clin Chem 1972, 18, 499

13) Corcoran, R; Clin Chem 1977, 23, 765

14) Bouchard, C; Am J Clin Nutr 1983, 37, 461

15) Krentz, A; Drugs 2005, 65, 385

16) Kendall, A; Am J Clin Nutr 1991, 53, 1124

17) Howarth, N; Nutr Rev 2001, 59, 129

18) Lovejoy, J; Metabolism 1998, 47, 1520

19) Hua, N; Br J Nutr 2001, 86, 515

20) Petersen, K; N Engl J Med 2004, 350, 664

21) Sparks, L; Diabetes 2005, 54, 1926

22) Goff, L; Eur J Clin Nutr 2005, 59, 291

23) Jenkins, D; JAMA 2003, 290, 502

24) Jenkins, D; Am J Clin Nutr 1987, 46, 66

25) Laitinen, J; J Am Diet Assoc 1993, 93, 276

26) Franz, M; J Am Diet Assoc 1995, 95, 1018

27) Barnard, N; J Cardiopulm Rehabil 2004, 24, 229

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