Guidelines Dietary - Eat For Health

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3.1.2 The evidence for ‘limit intake of foods high in saturated fat’The early work on dietary fats and heart disease focused on the type of fat in the overall diet, with the fat beingcontributed by a wide range of foods. The evidence that replacing saturated fats with polyunsaturated fats affectsserum cholesterol levels has been accumulating for the last 60 years, 36,666 and the relationship has been confirmedin a recent review of human intervention trials and other studies. 94,667-670The intake of trans fats is low in Australia and consequently there is no specific recommendation to limit theirintake compared to current intake. 671 However, it is important to ensure that intake remains at its current low level.The evidence for associations between foods high in fat and the development of type 2 diabetes, hypertension,cancer and poor mental health has been reviewed in detail.The Guidelines recommend some caution in choosing foods high in fat (in particular saturated fat) because ofthe implications for weight management and cardiovascular disease risk. Fat-rich foods are energy (kilojoule)dense, heightening the risk of excess energy intake 672 as shown by dietary modelling. 9 Additionally, there is ampleevidence of the relationship between dietary patterns and disease risk at the population level. 94 Fat content is animportant component of dietary quality and it may be that the evidence for limiting saturated fat in the diet is bestconsidered from a whole-of-diet perspective, with additional reference to overall nutritional quality.Scientific evidence on the effect of dietary fat on health comes from studies that address dietary variables in anumber of ways. These include whole-of-diet studies examining the proportion of fat in the diet (relative to proteinand carbohydrate), the type of fat in the diet (relative to other types of fat), the effects of specific fatty acids inthe diet, and the effects of individual foods in which fat is a significant component. For example, studies couldexamine the effects of:• a low fat diet• a diet with a modified dietary fat ratio – for example, a high polyunsaturated:saturated fat ratio• a diet enriched with specific fatty acids (e.g. omega-3 fatty acids)• oils and fats (e.g. olive oil, spreads) in a defined dietary pattern.Methodological issues arise when considering the effects of fats and of dietary fat in the total diet. The difficultyin designing studies that address the effect of dietary fat on disease risk is reflected in several recent reviewson the topic. 94,667-670 It is important to note that inconsistency in results affects the strength of the evidencestatements below.Guideline 3Table 3.1: Evidence statements for ‘limit intake of foods high in saturated fat’Established evidenceSaturated fat is the strongest dietary determinant of plasma LDL concentration.Replacing saturated fat with polyunsaturated and monounsaturated fats is associated with improved blood lipids related tocardiovascular disease.Evidence statementHigher consumption of omega-3 LCPUFA fat (intake amount not specified) is associated with reduced risk of dementia.GradeCNotes: Grades – A: convincing association, B: probable association, C: suggestive associationIncludes evidence statements and gradings from the Evidence Report (literature from years 2002–2009). Does not include evidence fromother sources, such as the 2003 edition of the dietary guidelines (in which individual studies were classified according to their design aslevel I, II or III but overall grades for relationships were not derived), although these sources have been used to inform these Guidelines.Grade C evidence statements showing no association and all Grade D statements can be found in Appendix E.Limit intake of foods containing saturated fat, added salt, added sugars and alcoholNational Health and Medical Research Council69
Cardiovascular disease, type 2 diabetes and excess weight• Cardiovascular disease: Of the systematic reviews addressing the risk of cardiovascular disease andconsumption of fats and oils, 664,673-681 only one review 664 focused on the proportions of dietary fatty acids inthe overall diet rather than the effects of omega-3 fatty acids on markers of cardiovascular health. This reviewconfirmed that replacing SFAs with unsaturated fatty acids may reduce the risk of coronary heart disease,and that replacing trans fats with unsaturated fats improves blood cholesterol levels. From a whole-of-dietperspective, this review found that reducing the risk of cardiovascular disease by replacing SFAs withcarbohydrate (as is the case in some low fat diets) depends on the effects on body weight. 664The Joint FAO/WHO Expert consultation on fats and fatty acids in human nutrition 2010 682 reported convincingevidence that replacing SFAs with PUFAs decreases the risk of coronary heart disease. The Dietary Guidelinesfor Americans, 2010 drew similar conclusions, finding: 198––strong evidence that dietary SFAs are positively associated with increased serum cholesterol and LDLcholesterol, with increased risk of cardiovascular disease––an association between replacing dietary SFAs or trans fats with PUFAs with improved blood lipid profilesand reductions in levels of numerous markers of inflammation––strong evidence that replacing dietary SFAs with MUFAs and/or PUFAs is associated with improved bloodlipids related to cardiovascular disease––moderate evidence that 250 mg of omega-3 LCPUFAs delivered from two servings of seafood per weekis associated with reduced cardiac mortality from coronary heart disease and reduced risk of suddendeath from cardiovascular disease.• Hypertension: The evidence suggests that consumption of fat, irrespective of amount or type, is notassociated with hypertension in the short term (Grade C; Evidence Report, Section 12.4). 683-691Guideline 3• Type 2 diabetes: While overweight and obesity increase the risk of type 2 diabetes, 88 recent studies ofshort-term interventions are inconclusive and may not adequately reflect the nature of the effect of dietaryfat on type 2 diabetes. The evidence suggests that consuming omega-3 LCPUFAs (0.4 –6 g/day) and dietsof varying fat content are not associated with fasting plasma glucose or insulin concentrations (Grade C;Evidence Report, Section 12.3). 674,681,691-701In the longer term, the review conducted for the Dietary Guidelines for Americans 2010 found strong evidencethat dietary SFAs were positively associated with increased markers of insulin resistance and increased risk oftype 2 diabetes. In addition, it found that decreasing dietary SFAs and replacing them with PUFAs or MUFAsdecreases the risk of type 2 diabetes in healthy adults and improves insulin responsiveness in insulin resistant andtype 2 diabetes subjects. PUFA intake was associated with a significant decrease in the risk of type 2 diabetes. 198• Excess weight: Dietary fat provides a substantial amount of energy (kilojoules) per gram but total dietary energyis the variable that affects weight. Reducing the amount of dietary fat will not necessarily reduce dietaryenergy, but it is prudent to choose low fat and low energy-density foods in a total dietary pattern that seeks tocontrol overall energy intake. Because of this total energy effect, there are difficulties in appraising researchinto the effect of dietary fat alone on weight gain 672 (see Chapter 1).Cancer• All-cause: The evidence suggests there is no association between consumption of omega-3 LCPUFAs withtotal all-cause cancer incidence or mortality (Grade C; Evidence Report, Section 12.5). 677,702• Other cancers: Evidence of an association between total fat consumption across a range of intakes and breastor endometrial cancer is inconclusive (Evidence Report, Sections 12.6 and 12.7). However, the WCRF reportstates there is suggestive evidence that total fat consumption increases the risk of post-menopausal breastcancer (see Appendix F). 43Other conditions• Dementia: The evidence suggests that higher consumption of omega-3 LCPUFAs is associated with a reducedrisk of dementia (Grade C; Evidence Report, Section 12.8). 517,529,703-70670EAT FOR HEALTH – australian dietary guidelinesNational Health and Medical Research Council
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EAT FOR HEALTHAustralianDietaryGuid
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© Commonwealth of Australia 2013Pa
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Australian Dietary GuidelinesGuidel
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GUIDELINE 2• Enjoy a wide variety
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guideline 5• Food safety 975.1 Se
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Table A2: Mean daily intakes of ene
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More recent evidence from Western s
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Relationship between the documents
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In this way, the Evidence Report wa
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Challenges for adoption of the Guid
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Australian Guide to Healthy EatingA
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Guideline 11.1 Setting the sceneA h
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Guideline 1UnderweightWhile the gre
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Guideline 1Figure 1.2: Mean energy
Page 32 and 33: Evidence statementBabies born to mo
Page 34 and 35: • Childhood weight gain: There is
Page 36 and 37: Given the scope of the Guidelines,
Page 38 and 39: Appropriate steady weight gain duri
Page 40 and 41: Dietary restriction beyond prudent
Page 42: 1.5 Practice guide for Guideline 1T
Page 45 and 46: 2.1 Enjoy a wide variety of nutriti
Page 47 and 48: Pregnant and breastfeeding womenCon
Page 49 and 50: 2.2 Enjoy plenty of vegetables, inc
Page 51 and 52: • Prostate cancer: The evidence s
Page 53 and 54: The following studies relate primar
Page 55 and 56: Dietary fibre from vegetables and f
Page 57 and 58: Children and adolescentsThe recomme
Page 59 and 60: Cancer• Colorectal cancer: There
Page 61 and 62: Based on current consumption data,
Page 63 and 64: disaggregate possibly different eff
Page 65 and 66: CancerNo recent studies investigati
Page 67 and 68: Based on most recent consumption da
Page 69 and 70: 2.5 Enjoy milk, yoghurt, cheese and
Page 71 and 72: Other conditionsThe traditional nut
Page 73 and 74: The 1995 National Nutrition Survey
Page 75 and 76: Reviews have also shown an associat
Page 77 and 78: 2.7 Practice guide for Guideline 2T
Page 80 and 81: GUIDELINE 3Limit intake of foods co
Page 84 and 85: 3.1.3 How limiting intake of foods
Page 86 and 87: InfantsFor infants under the age of
Page 88 and 89: Bone healthEvidence suggesting an a
Page 90 and 91: 3.3.2 The evidence for ‘limit int
Page 92 and 93: 3.3.4 Practical considerations: lim
Page 94 and 95: 3.4.2 The evidence for ‘limit int
Page 96 and 97: 3.4.3 How limiting intake of alcoho
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Page 101 and 102: 4.1 Setting the sceneThe World Heal
Page 103 and 104: 4.2.1 Breastfeeding incidence and d
Page 105 and 106: 4.2.3 Cardiovascular disease and ex
Page 107 and 108: Lower socioeconomic status mothersW
Page 109 and 110: 4.4 Practice guide for Guideline 4T
Page 111 and 112: 5.1 Setting the sceneFoodborne illn
Page 113 and 114: 5.4.2 InfantsThe immune system of i
Page 115 and 116: A1Social distribution of diet-relat
Page 117 and 118: • Consumption of milk and milk pr
Page 119 and 120: Food intake, diet and nutritional s
Page 121 and 122: The prevalence of health risk facto
Page 123 and 124: Table B2: Members of the Working Co
Page 125 and 126: The evidence was assessed according
Page 127 and 128: As part of the consultation process
Page 129 and 130: Expert reviewThe Guidelines underwe
Page 131 and 132: 1995 - The Core Food GroupsThe Core
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Appendix DQuestions for the literat
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Umbrella review questions1. What di
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Appendix ESummary of evidence state
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Evidence statementGradeFruitThe eff
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Limited - no conclusionEvidence is
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Appendix GFood, nutrition and envir
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Figure G1: Examples of environmenta
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G4Australia’s progress toward a s
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It is suggested that by 2011, 125 c
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Appendix IPhysical activity guideli
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Appendix JStudies examining the hea
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Appendix KAlcohol and energy intake
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Cholesterol: Cholesterol, chemicall
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Limit: Limit is used to emphasise t
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Salt: Dietary salt is an inorganic
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Acronyms and abbreviationsADHDAIDSA
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References1. Rayner M, Scarborough
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37. National Health and Medical Res
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75. Taveras EM, Berkey CS, Rifas-Sh
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112. Olds TS, Tomkinson GR, Ferrar
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153. Rangan AM, Schindeler S, Hecto
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192. Stookey JD, Constant F, Gardne
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231. Hyson DA, Schneeman BO, Davis
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271. Marks GC, Coyne C, Pang G. Typ
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312. Cunningham J, O’Dea K, Dunba
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355. Burns C, Inglis A. Measuring f
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392. Harland JI, Haffner TA. System
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433. Northern Territory Government.
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473. Aune D, Chan DSM, Lau R, Vieir
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512. Ness A, Maynard M, Frankel S,
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550. Vislocky LM, Pikosky MA, Rubin
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588. Sellers TA, Vierkant RA, Djeu
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628. Rosner SA, Åkesson A, Stampfe
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669. Siri-Tarino PW, Sun Q, Hu FB,
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705. Mamalakis G, Kiriakakis M, Tsi
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743. Cook NR, Cutler JA, Obarzanek
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782. Balakrishnan M, Simmonds RS, T
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820. Newcomb PA, Nichols HB, Beasle
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862. Australian Institute of Health
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903. Romero-Gutiérrez G, Vaca-Orti
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942. Käferstein F, Abdussalam M. F
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985. Centre for Epidemiology and Re
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1025. Lee A, Bonson A, Yarmirr D, O
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1066. Natural Resource Management M
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1106. Liu Y, Sobue T, Otani T, Tsug
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Notes
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www.nhmrc.gov.auwww.eatforhealth.go
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Guidelines Dietary - Eat For Health

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