Coronary heart disease (CHD) is a significant cause of morbidity and mortality in Australia, New Zealand and many affluent and developing countries. It is a much-studied subject with a voluminous body of literature describing the disease process, the genetic and environmental factors involved in increasing and decreasing risk and the routes to prevention and treatment. Coronary events are the key outcomes of the condition and include myocardial infarction (MI), ischaemia and (sudden) cardiac death as the major outcomes for the disease. Atherosclerosis is the underlying process for CHD and involves the occlusion of the coronary arteries through the accumulation of lipids in the intima. Ischaemia results from a loss of tissue perfusion leading to inadequate oxygenation and nutrient supply.
MI is a major loss of blood flow resulting from arterial occlusion while sudden cardiac death can result from instability of cardiac contraction (arrhythmia). CHD has a complex multifactorial aetiology and there is an inherited element in risk (e.g. apolipoprotein phenotype) and also those which cannot be changed (e.g. age). There is also a strong modifiable component including lifestyle factors. Factors which contribute to increased risk include high blood pressure (hypertension), obesity, diabetes, cigarette smoking and lack of exercise. Obesity (especially abdominal obesity) is an independent risk factor but also predisposes to diabetes, another independent risk factor. However, there is an interaction between these two and hypertension leading to the so-called “metabolic syndrome” which predisposes to early-onset CHD.
Plasma lipids are extremely important contributors to CHD risk through atherosclerosis. Raised plasma total and low density lipoprotein (LDL) cholesterol are positive risk factors. The significance of LDL can be understood readily as cholesterol is a significant component of intimal atherosclerotic plaques. Plasma high density lipoprotein (HDL) is a negative risk factor and raised concentrations appear to confer protection through promoting cholesterol efflux from tissues. There is a general negative relationship between plasma HDL and triacylglycerols (TAG) and raised plasma TAG may increase risk through this mechanism and also independently. It has been established quite convincingly that drug therapy to lower plasma cholesterol lowers CHD risk to the point where a statin is available as an over the counter item in British pharmacies for that purpose (Anon, 2005). However, diet and lifestyle changes to modify risk factors remain the first line of attack in primary prevention strategies (Kendall & Jekins, 2004).
Recommendations to lower risk involve a portfolio of changes including limitations in the intakes of saturated and trans (unsaturated) fatty acids, both of which raise LDL cholesterol. n-6 polyunsaturated fatty acids (PUFA) lower LDL cholesterol but long chain n-3 PUFA do not. The latter appear to lower CHD risk by promoting myocardial function and altering blood clotting parameters. As will be discussed in this review, some dietary fibre components lower plasma cholesterol and so could lower risk. Other dietary components also appear to protect against CHD but through other mechanisms which
remain to be defined. Folate is one such factor.
Raised plasma homocysteine is correlated with increased risk of CHD and concentrations are lowered by increased folate intake (Shai et al., 2004). However, the mechanisms whereby homocysteine acts remains unknown but may involve changes in arterial endothelial function, possibly through inflammatory mediators. Folate is found in whole grain foods while soluble fibre is also found in a limited number of cereals (principally oats and barley) and it is thought that these might contribute to lowered risk. However, whole grains in general are believed to protect against CHD and it is the purpose of this review to assess the
strength of the evidence of the relationship between their intake and lowered risk of CHD.
1.0 INTRODUCTION
2.0 DEFINITIONS
3.0 SCOPE OF THE REVIEW
4.0 THE HEALTH CANADA EXTERNAL REVIEW PAPERS
4.1 Scope of the appraisal
4.2 Assessment of the Health Canada Scientific Survey
4.2.1 The selection and assessment of evidence in the review
4.2.2 Re-analysis of pivotal studies cited in the review
5.0 UPDATE OF EVIDENCE SINCE THE CANADIAN REVIEW WAS PUBLISHED
5.1 Overview
5.2 Literature Collection
5.3 Assessment
5.4 Overall conclusions
6.0. DETERMINING THE RELATIONSHIP BETWEEN REPORTED WHOLE GRAIN INTAKES AND CHD RISK
6.1 Analytical methodologies
6.2 Cereals and cereal foods which qualify for whole grain status
6.3 Robustness of self-reported intakes of whole grain foods and the importance of semantics
7.0 RELEVANCE TO AUSTRALIA AND NEW ZEALAND
7.1 Whole grains and general dietary recommendations
7.2 Whole grains, dietary fibre and starch in Australia and New Zealand
8.0 RELATIONSHIP OF WHOLE GRAIN INTAKES WITH RELEVANT BIOMARKERS OF DISEASE OUTCOME
8.1 Criteria
8.1 Whole grains and other health outcomes relevant to CHD
8.2 Whole grain consumption and biomarkers
8.3 Whole grain starch digestibility
9.0 FUTURE ISSUES
10.0 REFERENCES
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