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January 2002, Volume 56, Number 1, Pages 1-14
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Cereal grains and coronary heart disease
A S Truswell

Biochemistry Department, University of Sydney, Sydney, New South Wales, Australia

Correspondence to: A S Truswell, Biochemistry Department, University of Sydney, Sydney, NSW 2006, Australia

Guarantor: AS Truswell.

Contributors: AS Truswell.


Cereal grains and their products provide around 30% of total energy intake in British adults, (much more than any of the other major food groups). Coronary heart disease (CHD) is the largest single cause of death in Britain and many other Western countries. This review examines the question whether there is a relation between cereal consumption and CHD.

Several of the nutrients in cereals have known potential for reducing risk factors for CHD: the linoleic acid, fibre, vitamin E, selenium and folate. Cereals also contain phytoestrogens of the lignan family and several phenolic acids with antioxidant properties. Processing generally reduces the content of these nutrients and bioprotective substances. Although cereals at the farm gate are very low in salt, processed cereal foods, eg bread and some breakfast cereals, are high-salt foods and thus could contribute to raising blood pressure.

Human experiments have clearly shown that oat fibre tends to lower plasma total and LDL cholesterol but wheat fibre does not. Rice bran and barley may also lower cholesterol but most people do not eat enough barley to have an effect. Cereal foods with low glycaemic index such as pasta and oats are beneficial for people with diabetes and might lower plasma lipids.

Between 1996 and 2001 an accumulation of five very large cohort studies in the USA, Finland and Norway have all reported that subjects consuming relatively large amounts of whole grain cereals have significantly lower rates of CHD. This confirms an earlier report from a small British cohort. The protective effect does not seem to be due to cholesterol-lowering. While cohort studies have shown this consistent protective effect of whole grain cereals, there has been (only one) randomised controlled secondary prevention trial of advice to eat more cereal fibre. In this there was no reduction of the rate of reinfarction. The trial had some weaknesses, eg there were eight different diets, compliance was not checked objectively, and duration was for only 2 y.

It appears valid to make health claims (as now permitted by the US FDA) that whole grain cereal foods and oat meal or bran may reduce the risk of CHD.

European Journal of Clinical Nutrition (2002) 56, 1-14. DOI: 10.1038/sj/ejcn/1601283


cereal grains; dietary fibre; coronary heart disease; plasma cholesterol; prospective cohort studies


Cereals are grasses, monocotyledonous plants. Cereal grains occupy the largest box (USA) or most of the equal largest box (Australia) in pictorial food guides for nutrition education. 'Eat plenty of cereal foods, preferably wholegrain and without added fat, salt or sugar' can be found in several sets of national dietary guidelines. Coronary heart disease (CHD; ICD 410-414) is still the disease that causes more deaths than any other in Europe. The question of the relation between the cereal food group and CHD is therefore important for public health nutrition. Is there evidence that all or some of the cereals group affect the risk of CHD? If there is, then it follows that if people increase their intake of this (these) cereal food(s) it would be a contribution to further reducing the national burden of CHD.

Cereal foods can be subdivided in several ways:

into cereals and cereal products OR cereal-based products or dishes;
into botanical species¾wheat, rice, maize, barley, oats, rye, etc;
into whole grain cereals (and products) or refined cereals;
into the many different ways of eating cereals and products¾for wheat these include bread, breakfast cereals, pasta, biscuits, cakes, muffins, pancakes, pizza, as thickener, etc; rice is mostly eaten boiled, as are oats (which are also eaten raw in muesli). Maize is mostly eaten as popcorn or cornflakes; sweet corn is also eaten as a vegetbl Rye makes a less common bread, and most of the barley is used to make beer or whisky.

When cereal is mixed with other foods its components are diluted and their effects on health become very difficult to discern.

This review considers cereals and CHD in three sections:

  1. What food composition analysis suggests;
  2. Experiments to see the effect of cereals or concentrated cereal components on risk factors for CHD; and
  3. Epidemiological studies, relating intake of cereals to outcome of coronary heart disease.

(A) Components of cereals¾nutrients, fibre and phytochemicals


As an important part of a balanced diet (ie one that provides all the food groups in the nutrition education pyramid or plate and all the recommended dietary intakes) the cereal group provides important amounts of most nutrients (Table 1)¾but not all. 'Man cannot live by bread alone'. Against human requirements cereals are naturally lacking in calcium, vitamin A, vitamin C and vitamin B12 (and also in sodium before processing; Table 1). An example of the contribution to the diet of major nutrients in cereals is illustrated by Figure 1 from Hansen (1973).

Several of these nutrients in cereals have the known potential, if in adequate amounts, for reducing risk factors for CHD. The predominantly polyunsaturated oil (50% linoleic acid) and possibly some of the fibre could lower plasma LDL-cholesterol, the vitamin E and selenium are antioxidants, and folic acid might lower plasma homocysteine.

Processing can make large changes in the composition of cereal products. Refining reduces many of the nutrients which are concentrated in the germ, aleurone layer, scutellum or outer coat. Table 2 compares the content of important nutrients in wholemeal wheatflour and white flour. All the nutrients which could be protective against CHD are reduced, linoleic acid and fibre and folate by about half and selenium and vitamin E by much more. The other way in which processing affects composition is by addition of micronutrients when breakfast cereals, bread, etc are fortified with some vitamins or minerals. The added nutrients are usually calcium or iron, and several B vitamins (thiamin, riboflavin, niacin, folic acid).


Cereals contain phytoestrogens of the lignan family (Figure 2). Plant lignans are changed by intestinal bacteria to mammalian lignans. They include: secoisolariciresinol diglycosideright arrowenterdiol; matairesinolright arrowenterolactone. In people who consume relatively large amounts of whole grain cereals these phytoestrogens in adults may have a protective effect against hormone-related cancers (the structure of enterodiol is similar to that of tamoxifen). It is possible that, via a hormonal effect on HDL, there could be some influence on risk of CHD (Thompson, 1993), but there is no clear evidence for this at present.

Other likely candidates for some protective potential against CHD are phenolic acids, found in the outer layers of cereal grains, which are antioxidants in vitro (Thompson, 1993). The most abundant are ferulic acid, vanillic acid, p-coumaric acid, protocatechuic acid and caffeic acid (Figure 3). While vitamin E, another antioxidant, is fairly well absorbed in humans, these phenolic acids in cereal brans would not benefit the circulatory system unless they could be absorbed in adequate amounts.

(B) Experiments on effects of cereal foods or fractions on risk factors for CHD

It is very unlikely that a randomised controlled human trial could be achieved in which CHD outcomes are recorded after people have taken either a high cereal diet or a low cereal diet in a randomised controlled trial for years, with all other dietary and other variables kept similar. It is, however, relatively simple to give a particular food, or fraction of it, to subjects under controlled conditions for a few weeks and measure if there is an effect on, say, plasma cholesterol, one of the major risk factors for CHD. If the particular food consistently and significantly lowers plasma LDL-cholesterol, it is reasonable to expect that the food may help to reduce the risk of CHD. It is on the basis of such short-term, safe and comfortable human experiments that the US FDA (but no other country at present) allows a health claim that oatmeal or oat bran (as part of a healthy diet) may reduce the risk of CHD.

Wheat fibre and plasma cholesterol*

For researchers setting out to test the dietary fibre hypothesis in the early 1970s this was the obvious type of fibre to experiment with. Hugh Trowell (1975) had reasoned that wheat fibre would lower plasma cholesterol. It is available in concentrated, fairly reproducible yet natural form as bran or whole grain wheat breads, which can be readily compared in controlled experiments with isocaloric low-fibre white bread.

There are at least 34 published reports of controlled human experiments in which plasma cholesterol was measured when subjects ate extra wheat fibre (Table 3). In 27 of these experiments plasma total cholesterol did not go down¾it even rose significantly in two trials (van Dokkum, 1978; Stasse-Wolthuis, 1979). Most of these 27 experiments were well designed, with control-test-control or crossover design or parallel control groups, and some were of long duration. In some studies all food was provided for the subjects in a metabolic unit (Jenkins et al, 1975; Kay & Truswell, 1977; Raymond et al, 1977; Stasse-Wolthuis et al, 1980). In the best of these reports with negative results, frequent measurements were made of plasma cholesterol concentrations. Five of the researchers in Table 3 who could not demonstrate an effect of wheat fibre on plasma cholesterol did find a cholesterol-lowering effect with pectin, using similar methods.

By contrast, in the seven papers reporting lower plasma cholesterol on wheat fibre the subjects total less than one-quarter of those in the 27 negative reports. Several used only one-way designs (control-test) and only one plasma cholesterol per feeding period. The subjects were outpatients, and in some trials, they ate ad libitum. In some trials the plasma cholesterols were measured in the routine hospital clinical biochemistry laboratory. In one interesting paper in Table 3, Munoz et al (1979) reported reduced plasma cholesterol when subjects ate bran from hard red spring wheat but not with ordinary soft white wheat bran.

Except for the possibility this raises¾that there might be some reproducible 'super bran'¾it is clear that wheat fibre does not have a cholesterol-lowering effect. In recent years wheat bran has been used as the placebo control in trials on the effect of guar gum and of oat bran on plasma cholesterol.

It was still possible that wheat fibre might raise plasma HDL-cholesterol, even if it does not lower total cholesterol. This had been reported by O'Moore et al (1978) and Lindgärde and Larsson (1984). In the earlier trials with wheat fibre only total cholesterol was measured, not lipoprotein fractions. However in most papers that do report HDL-cholesterol it has not been changed significantly by wheat fibre (McDougall et al, 1978; Dixon, 1978; Stasse-Wolthuis et al, 1979; Flanagan et al, 1980; Gariot et al, 1986; Kestin et al, 1990) and wheat fibre has no consistent effect on fasting plasma triglycerides (Truswell & Kay, 1976).

Oat 'fibre' and plasma cholesterol

In nice contrast to wheat fibre, most researchers who have tried the effect of eating increased oat fibre, either as rolled oats or as oat bran have found reductions of plasma total and LDL-cholesterol.

Table 4 shows that the percentage reductions of total cholesterol have ranged from -18% to 0 in subjects receiving rolled oats (oatmeal) or oat bran. In 28 of the 38 studies there was a significant reduction of total cholesterol, with a similar percentage reduction of LDL-cholesterol. HDL-cholesterol and triglycerides did not change. In 10 studies, however, there was no significant change in total or LDL-cholesterol. Most of the trials showing no effect were conducted with free-living out patients. In the most publicised trial with no effect (Swain et al, 1990) the subjects had quite low plasma cholesterols (4.40 mmol/l), their fat and energy intakes were higher in the oat bran period and, although total cholesterols were only 3% lower on oat bran than on the comparison low-fibre diet, the ratio of LDL/HDL was actually 9% lower (statistical significance not reported). It is also remarkable that all four of the trials in New Zealand (Auckland, Christchurch and Dunedin) found no effect. This raises the possibility that the oat bran used in that country was atypical (? low in beta-glucan). Very few of all the published trials reported the fibre composition of the oat bran.

On the other hand the trials with the most optimistic results (Anderson et al, 1984a and 1984b; Storch et al, 1984) had very small subject numbers and a suboptimal one-way design (control-oat bran). Another question is whether the predominantly polyunsaturated oil in oats (7-10 g/100) contributes to the cholesterol-lowering effect. In a number of the trials wheat bran or refined wheat or corn cereal were used in contrasting periods but they contain less oil. Judd & Truswell (1981) gave a balanced amount of polyunsaturated oil in the control period. Some of the later trials have used more concentrated oat gum, presumably low in oil.

A further difficulty in interpreting these results is that some authors (eg Keenan et al, 1991; Kashtan et al, 1992) report the difference between oat fibre and start (day 0) as the effect, whereas a different result is seen if plasma cholesterol on oat fibre is compared with that in the synchronous (control) wheat fibre period.

In the majority of reports (Table 4) there appears to be a tendency to a dose-response effect, though even in the best-designed trial (Davidson et al, 1991) this was rather inconsistent. Two estimates have been published of the size of the average cholesterol-lowering effect. Truswell (1995) noted that the unweighted mean plasma cholesterol reduction in 30 trials was 5.5%, with daily intakes of around 50 g oat bran. Brown et al (1999) calculated from 25 trials they accepted for meta-analysis that plasma cholesterol falls by -0.04 mmol/l per gram of soluble oats fibre consumed. The trouble with this estimate is that the soluble fibre content was not actually measured in most of the trials. But if we take the soluble fibre in rolled oats at 4.5 g/100 g and in oat bran 7 g/100 g, then 50 g oatmeal should lower cholesterol by 0.09 mmol/l and 50 g of oat bran by 0.14 mmol/l. The latter is 3% of a starting plasma cholesterol of 5.0 mmol/l.

The active part of oats total fibre is the beta-glucan. This is soluble 'fibre', not fibrous, and it is the main component of oat gum. Concentrated oat gum lowers plasma cholesterol in humans (Braaten et al, 1994) and animals (Welch et al, 1988). Treatment of oat bran with a beta-glucanase increased its free sugars, decreased its viscosity and abolished the cholesterol-lowering action in rats (Tietyen et al, 1990). Hot extrusion of oat bran or flour has been reported to increase the solubility of its beta-glucan (Hamilton et al, 1989). This may explain the 7 and 4% plasma cholesterol falls in well-controlled experiments with oat bran 'breakfast' cereals taken two or three times a day (Hamilton et al, 1989; Reynolds et al, 1989).

The most plausible mechanism of action of oats beta-glucan is by its viscosity interfering with reabsorption of bile acids and hence producing a negative sterol balance (cholestyramine effect). In oat fibre periods increased bile acids have been reported in faeces (Judd & Truswell; 1981; Kirby et al, 1981) and in ileostomy effluent (Zhang et al, 1993).

Other cereal fibres and plasma cholesterol

Rice bran at intakes of 100 g/day reduced plasma total cholesterol by 7% (no significant effect on other plasma lipids) (Hegsted et al, 1993). Sixty g/day of rice bran reduced LDL-cholesterol slightly, increased HDL-cholesterol slightly, increased the total cholesterol/HDL-cholesterol ratio significantly and lowered triglycerides (Kestin et al, 1990). Fifteen and 30 g/day rice bran reduced plasma triglycerides but not other lipids (Sanders & Reddy, 1991). In this latter experiment the lipids in rice bran were balanced with oil of similar fatty acid pattern in the control (wheat bran) period. Rice bran does not contain beta-glucan; its soluble fibre content (hemicellulose) is about half that of oat bran. The oil, and particularly gamma-oryzanol in its unsaponifiable fraction (Yoshino et al, 1989) may be a major reason for cholesterol reduction by large intakes of rice bran. The hemicelluloses of rice bran have been shown to bind bile acids (Normand et al, 1987). The properties of its bran, are unlikely to apply to rice as it is usually eaten, ie polished and white, unlike oats, which is eaten wholegrain. It is not only the vitamins in rice grain that are lost when it is refined and polished.

Barley contains soluble fibre as beta-glucan. In a well controlled 11 week crossover trial with 21 mildly hypercholesterolaemic men in Adelaide (McIntosh et al, 1991), a diet high in barley fibre gave 6% lower plasma total and LDL-cholesterol than a control diet with the same 38 g/day of fibre from wheat. The subjects in this trial ate 170 g/day of barley foods, including barley bran and barley flakes. There is at least one other report of a cholesterol-lowering effect of barley in humans (Newman et al, 1989). Barley, in western countries is nearly all used for brewing. As human food it is only a minor cereal. Its consumption is unlikely to make a substantial contribution to plasma cholesterol-lowering.

Cereal foods with low glycaemic index

Whole grain cereal products: whole grain wheat breads¾not wholemeal (Jenkins et al, 1988)¾oatmeal, pasta, high amylose maize and rye bread have low glycaemic indices (Foster-Powell & Brand Miller, 1995). When they are eaten the rise of blood glucose is lower than after the same amount of carbohydrate from most breads, most breakfast cereals and most boiled rice. Diets with low glycaemic index foods predominating have fairly clear health advantages for people with diabetes (Brand Miller, 1994). As well as improved glycaemic control, plasma cholesterol declined in some of the controlled dietary trials (Brand Miller, 1994). Reductions of plasma cholesterol have also been reported in non-diabetic subjects on low, compared with high glycaemic index diets (Brand Miller, 1994).

Cereal foods with disproportionately high salt

Australian and other countries' dietary guidelines recommend people to 'choose low salt foods and use salt sparingly' (eg, National Health & Medical Research Council, 1992). This is mainly as a contribution to reducing the prevalence of high blood pressure. The salt intake that many humans consume produces hypertension in chimpanzees. The chimpanzee experiment (Denton et al, 1995) is the nearest we can get to a controlled human experiment. The Nutrition Research Foundation at the University of Sydney held a symposium in December 1993 to consider whether and to what extent the dietary guideline to 'choose low salt foods' is compatible with the guideline to 'eat plenty of breads and cereals ¼'

The paradox is that cereals are very low in sodium when they are harvested but after processing and as eaten some of them are among our highest sodium foods. An objective approach to grading the sodium content of cereal foods would be to use RG Hansen's index of nutritional quality method (Hansen et al, 1979) and compare sodium content numbers against 2300 mg/day (100 mmol) as the upper end of desirable intake for adults (National Health & Medical Research Council, 1992).

Two slices of bread weigh (approx) 60 g. This much bread contains (Mugford et al, 1996) 636 kJ=6.4% of standard 10 MJ energy intake day. Its sodium content, 312 mg is 13.6% of standard 2300 mg. Bread is therefore a donor of sodium to the diet. 13.6/6.4=sodium (% standard) is 2.12´energy (% standard).

Again, 'All Bran' even in its new formulation contains 190 mg sodium in a 50 g standard serving (Salt Skip News, 1994): 190/2300=8%. The energy in this serving is 554 kJ which is 5.5% of 10 MJ. The sodium is still higher against the daily reference than the energy content: 8/5.5=1.45x.

The sodium content at which bread's sodium would equal its per cent energy contribution is 243 mg/100 g. Similarly the sodium content at which the sodium would equal the energy contribution of a breakfast cereal (with 1500 kJ per 100 g) is 345 mg sodium. There are a few breads and a number of breakfast cereals with sodium content lower than this, ie not disproportionately high relative to energy content, some as low as 1 mg/100 g. Sodium levels are tending to be brought down in breakfast cereals.

(C) Epidemiological studies relating cereal grains to CHD

Cohort studies

Professor Jerry Morris of London, the epidemiologist who first clearly demonstrated that exercise protects against CHD (Morris et al, 1953), published with Jean Marr (an expert on food intake methodology (Marr, 1971)) the results of a cohort of 337 men working for London Transport or banks, followed for 10 to 20 y (Morris et al, 1977). CHD incidence was lower in these who ate more food energy (could be related to physical activity), and independently CHD was strikingly lower in those who were originally eating more cereal fibre. When these results were first presented at the Royal Society of Medicine, the audience was puzzled. The reliability of the investigators could hardly be doubted but fibre of wheat (the main British cereal) does not reduce plasma cholesterol (Truswell et al, 1978).

Perhaps people who eat plenty of cereal fibre are more health conscious in a variety of ways. Morris did note that they were less likely to smoke (Morris et al, 1977). Burr and Sweetnam (1982) identified a cohort of 11 000 who shopped at 'health foods' shops or subscribed to health food magazines and followed them up for 5 y. There was no evidence that their fibre intake made any difference to the heart disease mortality.

Some prospective studies that report a negative (protective) association of total dietary fibre with CHD incidence have not been corrected for energy intake (Kromhout et al, 1982; Fehily et al, 1993). If people eat more megajoules per day (being better reporters or having larger energy expenditure) they are likely to eat more fibre (and other food components). Other studies report negative association for total dietary fibres (vegetable+fruit+cereal) (Khaw & Barrett-Connor, 1987) or for grain intake only in women (Knekt et al, 1994).

Between 1996 and 1999, however, an accumulation of very large prospective studies (Table 5) have been reported that all confirm and extend the finding of Morris et al (1977). Rimm et al (1996) reported from the Health Professionals Follow-up Study. The cohort consisted of male dentists, veterinarians, pharmacists, optometrists, osteopaths and podiatrists. After exclusions there were 43 757 men. Their diets at the start were assessed with a 131 item food frequency questionnaire. Fibre intake was adjusted for energy intake by regression analysis. During 6 y of follow-up there were 511 non fatal cases of myocardial infarction and 229 coronary deaths (total 734 events). Relative risk of CHD for the top quintile (fifth) of total dietary fibre was 0.64 compared with 1.00 in the lowest fibre quintile. On further analysis insoluble fibre was found to be protective but (surprisingly) not soluble fibre. A separate multivariate analysis was conducted for fibre from cereals, vegetables and fruit. The negative association for cereal fibre was the strongest relative risk for highest intake quintile 0.71 (95% confidence interval 0.55 to 0.91). This relative risk did not appear to be much changed by adjustments for several micronutrients.

Rimm et al made further calculations, eg they checked their results with fibre calculated both by Southgate's method and by Englyst's. They concluded that they could not completely exclude the possibility that some unknown factor, associated with high fibre intake is responsible, but it would need to have a strong influence. 'The lack of any substantial confounding by known predictors of cardiovascular disease and by other dietary factors, together with demonstrated benefits in metabolic studies, suggests that higher intake of dietary fibre, particularly from cereal and grain sources can reduce substantially the risk of coronary heart disease' (Rimm et al, 1996).

Pietinen et al (1996) in Finland gave a 276 food item dietary questionnaire to most of the participants at the start of the Alpha-Tocopherol, Beta Carotene (ATBC) Cancer Prevention Study. They were men, all smokers 50 to 60 y of age at entry. The ATBC study was a randomised prevention trial: alpha-tocopherol or beta-carotene or both or neither were given and subjects followed up for 6 y. The dietary questionnaire was taken home to be filled in, brought back two weeks later and checked by a nurse. The 21 930 subjects with good dietary data experienced 1399 CHD events (581 of which were deaths). In the analysis of association of dietary components with CHD events, adjustment had to be made for vitamin treatment groups (there were fewer coronary deaths in the vitamin E group and more in the beta-carotene group). Intake of dietary fibre ranged two-fold between the highest quintile (mean 34.8 g/day) and the lowest (16.1 g/day). Higher fibre intake was associated with lower intakes of saturated fat, cholesterol and alcohol and higher intakes of rye products, dietary beta-carotene, vitamins C and E. It was also associated with more physical activity but there were no differences in age, body mass index (BMI), smoking or serum cholesterol or blood pressure across quintiles of dietary fibre intake.

In age and treatment group-adjusted analysis, water soluble fibre, cellulose and vegetable and fruit fibre were significantly inversely associated with risk of CHD events (fatal and non-fatal). For total dietary fibre (energy adjusted) quintiles the relative risks were 1.00, 0.91, 0.88. 0.86. 0.84 (P for trend 0.03). Coronary deaths were more strongly negatively associated with total dietary fibre. They were also significantly inversely associated with soluble and insoluble fibre and with cereal fibre (RR 0.77). Simultaneous adjustment for each of the main food group sources showed that only the inverse association between cereal fibre and CHD mortality remained significant. Food groups inversely associated with CHD deaths were rye products, potatoes, vegetables and fruits and berries.

An unusual feature of this study, apart from its huge size and statistical power is the relatively large range of fibre intakes. A major contributor of cereal fibre in Finland is rye. Those in the highest quintiles of total dietary fibre consumed 161 g/day of rye. The overall mean daily intake of fibre in the ATBC study was 18.9 insoluble fibre and 5.4 g soluble fibre. Adjustment for serum cholesterol did not change the results, so the cholesterol-lowering effect of soluble fibre cannot be the explanation. Pietinen et al could only speculate that dietary fibre may influence risk of coronary disease via postprandial lipid response or glucose and insulin responses or haemostatic factors.

DR Jacobs et al have published two papers about the Iowa Women's Health Study, relating the risk of death to whole grain intake. 'Whole grain cereals' are clearly much the same as 'high fibre cereals'. The main difference is one of emphasis. Jacobs et al are thinking about other components in whole cereal grains as possibly beneficial, not just the fibre. In their first paper (Jacobs et al, 1998) postmenopausal women were followed for 9 y. Food intake at the start was assessed with a 127 item food frequency questionnaire. The questionnaire was sent by mail to a random sample of all women 55-69 y of age who had an Iowa driver's licence. After exclusions there were 34 492 in the cohort. Disease outcomes were ascertained from state and national health registers. 3320 women died, including 438 from CHD. The authors found a striking inverse association of whole grain intake with risk of death from CHD. Age and energy-adjusted relative risks from lowest to highest quintiles of whole grain intake were 1.0, 0.84, 0.58, 0.45 and 0.60- (P for trend 0.0002). For total refined grain intake, on the other hand, there was a small positive, non significant association; relative risks (multivariable adjusted) were 1.0, 0.99, 1.14, 1.04 and 1.12 (P=0.57) from lowest to highest intake quintile. The responsible types of whole grain cereal were mainly dark bread and whole-grain breakfast cereals. The inverse association of whole-grain intake with risk of CHD death was somewhat weakened after adjustment for various typical constituents such as dietary fibre, phytic acid and vitamin E. The authors concede that in this study dietary assessment was made once, by a mailed, self-administered questionnaire and non-fatal CHD events were not collected.

In their second paper Jacobs et al (1999) show in tables the risks of 10 major causes of death, by quintiles of whole-grain and refined grain intake, adjusted for 23 other variables. Whereas Jacobs et al (1998) excluded women with CHD at baseline, in this 1999 article they were included. With the multiple adjustments the relative risks for CHD deaths by increasing quintiles of whole-grain intake were 1.0, 1.03, 0.86, 0.70, 0.82, (P=0.03). The foods classified as whole grain cereals were (% of total) dark bread (61%), whole grain breakfast cereal (18%), popcorn (13%), cooked oatmeal (7%), wheat germ (1.5%), brown rice (1.3%), bran (0.6%) and other grains: bulgar, couscous (0.3%).

Two reports by the Harvard epidemiology and nutrition group appeared in 1999 from the US Nurses cohort study. One is about dietary fibre, the other about whole-grain consumption in relation to CHD. In the paper by Wolk et al (1999) 68 782 women were followed up for 10 y from 1984. Dietary data were collected by mailed food frequency questionnaires in 1984, 1986 and 1990. The authors documented 591 major CHD events (429 non-fatal myocardial infarction and 162 deaths). They found a significant inverse association between total dietary fibre intake and risk of CHD. This was due to a significant inverse relation with cereal fibre, but not with vegetable or fruit fibre. Women in the highest quintile of cereal fibre intake had a 34% lower risk of CHD events, compared with those in the lowest quintile. Relative risks in ascending cereal fibre intake quintiles were 1.0, 1.06, 0.71, 0.76, 0.68 (P for trend 0.002). The inverse association was not explained by higher intakes of vitamin E, folate, vitamin B-6, magnesium, vegetables or fruit. Wolk et al (1999) speculate that cereal fibre might act via increased insulin sensitivity or perhaps favourable effects on plasminogen activator type 1.

In the other paper from the same group, Liu et al (1999) evidently conducted a separate analysis of data from the same large cohort of US nurses. Four of the authors of this paper are co-authors of Wolk et al (1999). In this second paper whole grain consumption (rather than cereal fibre) was assessed against CHD events. Seventy-five thousand, five hundred and twenty-one women subjects completed food frequency questionnaires in 1984, 1986 and 1990 and were followed up for 10 y. Whole-grain food included dark breads, whole-grain breakfast cereals, popcorn, cooked oatmeal, wheat germ, brown rice, bran and other less common grains (the same classification as used by Jacobs et al (1999) 'Refined grain' included sweet rolls, cake, desserts, white bread, pasta, muffins, biscuits, refined grain breakfast cereals, white rice, pancakes, waffles and pizza. (Breakfast cereals were classified as whole grain if they contained over 25% whole grain or bran by weight). Seven hundred and sixty one cases of CHD were documented, 208 of them fatal. After adjusting for age and smoking the relative risks of ascending quintiles of whole grain intake were 1.0, 0.86, 0.82, 0.72 and 0.67 (P for trend 0.001). Women with higher intakes of whole grain foods not only smoked less, they were more likely to exercise, to take hormone replacement or use supplements of multivitamins or vitamin E. After additional adjustment for these behaviours, as well as BMI, alcohol intake, aspirin use and type of fat intake, the relative risks of CHD events by quintile of wholegrain intake were 1.0, 0.92, 0.93, 0.83 and 0.75 (P for trend 0.001). The lower risk associated with higher whole-grain intake was partly but not fully explained by its contribution to intakes of dietary fibre, folate, vitamin B-6 and vitamin E. There was no significant association (negative or positive) between refined grain intake and CHD events.

DR Jacobs of the University of Minnesota School of Public Health has also been one of the leaders of a large prospective cohort of the general population (men and women 35-56 y) in three Norwegian counties (Finnmark, Sogn og Fjordane and Oppland). They were followed from between 1977 and 1983 to 1994 (for 17 to 11 y). The response rate was 79%. Diet was assessed with a 66 item food frequency questionnaire.

The authors combined self-report of number and type of bread slices (white, light whole grain, dense whole grain) to form a whole grain bread score. This could range from 0.05 (1 slice per day made with 5% whole grain flour) to 5.4 (9 slices per day, made with 60% whole grain flour).

These Norwegian whole grain bread eaters were less likely to be smokers, were more physically active, had lower serum cholesterol and blood pressure and ate less saturated fat than white bread eaters.

CHD deaths (expressed as hazard rate ratios went down stepwise with increasing whole grain quintiles (1, 0.92, 0.85, 0.75 and 0.63). When adjusted for smoking physical activity, use of cod liver oil and multivitamins, blood pressure, serum cholesterol and BMI, the hazard rate ratios were still inversely and stepwise related to whole grain intake quintiles (1, 0.99, 0.94, 0.88. 0.76; P for linear trend 0.04).

Cancer deaths were also inversely related to whole grain intake quintiles but adjusted hazard rate ratios did not show a significant trend. The authors did not estimate total vegetable and fruit intake in their food frequency questionnaire; they focussed strongly on intakes of bread, meat, fish, milk, coffee, oranges, potatoes, cakes and fat.

A Single randomised controlled trial

The only randomised controlled trial in which people were asked to eat more cereal fibre was carried out in South Wales, UK and reported in 1989 (Burr et al, 1989). Two-thousand and thirty-three men who had recovered from a myocardial infarction were given dietary fat advice or not, and/or fatty fish advice or not, and/or cereal fibre advice or not. There were thus eight possible combinations of dietary advice and this was a secondary prevention trial for 2 y¾the diet and reinfarction trial (DART). According to a dietary questionnaire at 6 and 24 months the cereal fibre advice group were eating 19 and 17 g cereal fibre per day respectively, compared to 9 g cereal fibre/day in the 'no fibre advice group'. After 2 y there were significantly fewer CHD recurrences in the fish advice group but not in the fibre advice group or the fat advice group. Compliance with fat advice was checked objectively with plasma cholesterols, compliance and with fish advice was checked with plasma eicosapentaenoic acid (EPA). Twenty-two percent of the fish group took Maxepa fish oil capsules which helped ensure increased EPA intake. There was, however, no objective check of fibre intake.

The authors admit that compliance must have been variable. Having eight different dietary groups looks as if it could lead to confusion. Follow-up was short and this was a secondary prevention trial of CHD (in which influence of environmental factors on the pathological process is likely to be weaker than in a primary prevention trial). By contrast, people with a history of CHD were excluded from the Nurses and the Health Professionals cohorts described above (Rimm et al, 1996; Wolk et al, 1999; Lui et al, 1999). Although the DART trial had its weaknesses, the results of its fibre arm means that there has to be a question mark at the end of the results of the cohort studies (Jacobs et al, 1999).

An ecological between-countries study

Recently, household budget data from 10 European countries were related to national mortality statistics for CHD, breast cancer and colorectal cancer (Lagiou et al, 1999) (Table 6). Simple correlation between total cereals and CHD mortality gave a coefficient of +0.13, ie a small positive association. The countries represented were Belgium, Germany, Greece, Hungary, Ireland, Luxembourg, Norway, Poland, Spain and UK and the data is for the start of the 1990s. This epidemiological approach is of course less reliable than cohort studies with multivariate analysis. It is affected by multiple confounding factors but it gives a view of the real life situation.

This paper also showed that in the country with the lowest rate of CHD, cereal consumption was second highest. Beyond Europe CHD rates are low in countries with high cereal, consumption, in Japan, China and Africa.


  1. There is no clear association, negative or positive between total cereal consumption and CHD. The pattern of consumption of the different cereal species and products varies between communities.
  2. The majority of over 40 human trials of the effect of oatmeal or oat bran on plasma lipids have found a modest reduction of total and LDL cholesterol. The US Food & Drug Administration permits a health claim for rolled oats, whole oat flour or oat bran¾eligible sources of soluble fibre¾as possibly reducing the risk of CHD (Food & Drug Administration, 1999). However, four of the five trials of oat fibre conducted in Australasia did not show a significant effect. It is also likely that whole barley and rice bran share the cholesterol-lowering effect of oats if sufficiently large amounts are eaten. Barley and brown rice are not, however, eaten in large amounts in Europe. Wheat fibre does not lower plasma total or LDL-cholesterol.
  3. In the late 1990s an impressive set of five separate prospective (cohort) epidemiological studies were published from USA, Finland and Norway, based on over 98 000 men and 109 000 women. The five cohorts all showed a significant inverse association of cereal fibre or whole grains with CHD. Only a minor part of this apparent protective effect can be explained by the cholesterol lowering effect of soluble fibre. Part of the effect may be due to folate and/or vitamin E and/or effects on glucose/insulin responses and/or haemostatic factors. From the available evidence none of these can be singled out as the major mechanism for protection from CHD. It is more likely that cereal grains contain several protective factors.
    Because of these recent epidemiological findings, Professor Willett (senior investigator of the Health Professionals Study and the US Nurses Study) has called for revision of the dietary pyramid used for nutrition education in the USA, and Australasia (Willett, 1998). Willett thinks the pyramid's foundation is in need of repair: greater emphasis should be placed on the health benefits of whole grains, not 'complex carbohydrates' (Willett, 1998). 'Complex carbohydrates' is a term that the FAO/WHO Consultation (Joint FAO/ WHO Expert Consultation, 1998) advises against using.
    The US FDA now also permits a health claim (Food & Drug Administration, 1999) for whole grain foods (as defined) 'Diets rich in whole grain foods and other plant foods and low in total fat, saturated fat and cholesterol may reduce the risk of heart disease and some cancers'. For purposes of this health claim whole grain foods contain 51% or more whole grain ingredients by weight per reference amount with dietary fibre 2.3 g/50 g or 1.7 g per 35 g and the food low in fat.
    Note in passing that the FDA claim adds reduced risk of some cancers to the the heart disease claim for whole grain foods. In Australia meanwhile the NH & MRC in its 1999 clinical practice guidelines recommends poorly soluble cereal fibres (eg wheat bran) as one of the dietary measures for primary prevention of colorectal cancer that is better supported by the scientific evidence (National Health & Medical Research Council, 1999).
  4. There is another possible way in which cereal foods, refined or whole grain, have the potential to contribute to reduction of atherothrombotic vascular diseases. This is as carriers of folic acid fortification. A high plasma (total) homocysteine level appears to be an independent risk factor for CHD, stroke and venous thrombosis (ie atherothrombotic vascular diseases in general, including but not confined to CHD; Hankey & Eikelboom, 1999). Folic acid at intakes in the nutritional range is the most effective of the three B vitamins in lowering high plasma homocysteine (Homocysteine Lowering Trialists' Collaborative, 1998). In the USA folic acid fortification of cereal foods has been mandatory since 1996 and in one representative group of people (Framingham, MA, participants offspring) the prevalence of low plasma folate decreased from 22 to 2% and the prevalence of high plasma homocysteine dropped from 19 to 10% (Jacques et al, 1999). Voluntary fortification of cereals and some other staple foods is being encouraged by the Australian Commonwealth Department of Health and the ANZ Food Authority. Although the reason for folic acid fortification is officially stated to be reduction of neural tube defects in babies, it could in fact have a bigger public health impact on cardiovascular diseases.

Historical perspective

The nutritional evidence and considerations in this review about the relative merits of whole grain and refined cereals are the latest chapter in a very long story of opinions about brown vs white breads (McCance & Widdowson, 1956). Until recently white bread and refined breakfast cereals were regarded as nutritionally suboptimal because they had lost major nutrients in the refining process. Addition of thiamin and some other nutrients to white bread and of several vitamins and minerals to many breakfast cereals was thought to at least partly answer these concerns.

In 1974 Cleave (1974) argued that refined flour may be a cause of several chronic degenerative diseases. Cereals provide the bulk of our starch consumption. In the 1970s starch was regarded as poor quality food. Though starch may still have a lowly image among consumers, its nutritional benefits have become better known to nutritional scientists (Stephen et al, 1995), starting with the 1977 Dietary Goals for the United States (Select Committee on Nutrition, 1977).

The low fibre content of white bread and refined ready-to-eat cereals remained a disadvantage but except for Morris's paper (Morris et al, 1977) and oat bran this was not thought relevant to heart disease, and the discovery of resistant starch reduced the biological difference between brown and white breads.

The present nutritional position of cereal foods, mostly refined, often with added nutrients and mixed ingredients and providing some resistant starch is that they are unobjectionable staple components of our usual western diet. For example, cereal foods and products provided 30% of the energy intake in the Dietary and Nutritional Survey of Australia (McLennan & Podger, 1997). Within the total cereals food group, whole grain products, only a minority of all the cereal products, are now emerging as nutritionally beneficial, not only for large bowel health but also for prevention of CHD.


While most cereal foods provide a range of nutrients, without special effect on risks of CHD, it appears that claims could be made that whole grain cereal foods and oat meal or bran may reduce the risk of CHD. The scientific evidence would support such claims and they are permitted in the USA. In Australia health claims on individual foods are not at present permitted by ANZFA.

This is the big picture. Two minor considerations are that foods with lower glycaemic index and with lower salt (NaCl) content may be beneficial.

One priority for nutrition research on human cereal consumption is to increase understanding of the mechanisms for the protectiveness of whole grains (Slavin et al, 1999). Another priority is to organise, perhaps internationally, a second CHD prevention trial with added whole grain cereals having more rigorous design, and larger numbers and longer follow-up than the DART trial. The authors of that trial called for more randomised controlled trials of prevention of CHD (Elwood et al, 1992).

*All the references for this section are in Truswell and Beynen (1992).


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Figure 1 Nutrient density (as defined here) is the ratio of the content of a nutrient (expressed as % of recommended nutrient intake (or RDA)) to energy content of the food (expressed as % of a standard energy intake). Thus if one were to obtain all one's dietary energy from bread and cereals, requirements for protein and iron would be met but the diet would not supply enough calcium; vitamins A and C would be very inadequate while the vitamin B1 (thiamin) would be twice the requirement. (Ref Hansen, 1973).

Figure 2 LIGNANS, phytoestrogens found in cereals. Plant lignans on left and forms produced by intestinal bacteria on right.

Figure 3 Phenolic acids found in cereal brans.


Table 1 Nutrients which cereals provide in important amounts. (Figures in brackets are % total intake from cereals in Dietary and Nutritional Survey of British Adults (Gregory et al, 1990; Ministry of Agriculture, Fisheries & Food, 1994))

Table 2 Nutrients (per 100 g) compared in wholemeal and white flours, from McCance & Widdowson's The Composition of Foods, 5th edition (Holland et al, 1991)

Table 3 (References in Truswell & Beynen (1992)) Wheat fibre and plasma total cholesterol

Table 4 Human experiments on effect of oat (fibre) on plasma cholesterol

Table 5 Recent Prospective Epidemiological Studies

Table 6 CHD mortality and cereal consumption (early 1990s) in 10 European countries from Lagiou et al, (1999)

Received 13 February 2001; revised 30 May 2001; accepted 6 June 2001
January 2002, Volume 56, Number 1, Pages 1-14
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