Foods considered “grains” are defined as the edible seeds of plants which belong to the grass family, and include wheat, oats, rye, barley, rice and maize. Though they do not fit the specific definition, buckwheat and flax are also generally considered grain foods. Grain foods generally contribute the highest portion of “complex” carbohydrates to the average diet. This food group also referred to as “cereals”, are well known to make up the largest portion of most food pyramids, largely because they are rich sources of carbohydrate, the body’s preferred fuel source. Unfortunately however, many people may fail to realise that the recommended high intake of cereal foods proposed by the healthy eating pyramids, refers to that of wholegrain foods, as apposed to refined grains. [1]
The anatomy of the grain consists of an outer layer referred to as the “bran”, a middle layer called the “endosperm” which makes up the majority of the grains mass, and a small inner portion called the “germ”. Wholegrain foods/cereals are made using the entire grain. Such foods include wholemeal bread, brown pasta, brown rice etc. (Oats and Rye are generally always made using the “whole-grain”) During the milling process, the outer “bran” layer is stripped, leaving only the inner layers. This happens in the production of “refined grain” foods/cereals, such as white bread, white rice, white pasta etc. Unfortunately however, the bran is a very rich source of a plethora of vitamins, minerals, fibres, sterols, phytates, lignans, antioxidant phenolic compounds and other beneficial phytochemicals such as avenanthramides and avenalumic acid. [2]
The endosperm however contains relatively poor levels of these substances, instead being rich in starch (complex carbohydrate). Consequently, foods made from refined grains have an overall higher carbohydrate content and lower levels of the beneficial substances lost during the refining process. Furthermore, they have a higher Glycemic Index (GI) and Glycemic Load; references which describe the rate at which carbohydrates are broken down into sugars and released into the blood stream. [3,4]
As a result, population-based studies have found that the risk of developing diabetes and cardiovascular disease (heart disease and stroke) [5] among people with higher intakes of refined grains is significantly increased. Additionally, studies have also revealed significantly lower risks of developing these diseases [6,7] as well as various cancers [8] and other chronic health problems [9] among people whose wholegrain intakes are higher (generally about 3 serves per day). Unfortunately, whilst the average daily cereal/grain intake among adults is estimated to be approx 6-7 serves per day, the average daily wholegrain intake is no greater than 1 serve per day, [10,11] and even less in children and teenagers. [12]
This article reviews and discusses the results of population based studies which have examined the correlation between wholegrain intake and chronic disease, as well as briefly outlining some of the mechanisms thought to be responsible for these effects.
Sub Headings:
* Wholegrain Foods and Cancer: Epidemiology
* Chemo-protective mechanisms of wholegrain foods
* Wholegrain foods and cardiovascular disease: Epidemiology
* Cardio-protective mechanisms of wholegrain foods
*Wholegrain foods and Diabetes: Epidemiology
* What is Diabetes, insulin and the Glycaemic Index (G.I.)
* Wholegrains, G.I, G.L and insulin resistance
* References
Wholegrain Foods and Cancer: Epidemiology
It has been suspected that wholegrain / cereal fibre consumption may prevent colon cancer since it was identified as the only protective food among men in 38 countries in a study published in 1984. [13] More recent evidence has supported this theory as well, however new evidence suggests a protective effect on various cancers.
In 1995, professor of epidemiology at the University of Minnesota , Dr David Jacobs and his colleagues reviewed 14 case-control and prospective studies which examined the association between wholegrain intake and the risk of digestive cancers. [14] They reported that these studies found:
“…… a striking consistency in reduced risk for colorectal and gastric cancers associated with intake of whole grain, also found in isolated studies of endometrial cancer and coronary heart disease ”
In 1998, Prof Jacobs and colleagues expanded their review to investigate the association between wholegrain consumption and the risk of other cancers not included in the previous paper. They reviewed 40 case-control studies of 20 different cancers, nearly all of which reported a protective association. Together, these studies compared the diets of over fourteen and a half thousand cancer patients (cases), with over 35 thousand cancer-free people (controls). When the results were pooled together, they showed that compared with lower intakes, higher consumption of wholegrain foods decreased the risk of all cancers by an average of 31%. When they removed several unreliable studies with design or reporting flaws, the results found a 34% protection among all cancers. Specifically, the results found that preference for wholemeal bread over white bread reduced the risk of cancer by 33%, that more frequent intake of whole grains reduced the risk by 49%, and that even consuming 1 wholegrain serving per day reduced the risk by 22%. [14]
Table 1: Results from Case-Control Studies Reviewed by Jacobs et al (1988) [14]
Colon Cancer
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [15] 1992, Italy | 123 | 699 | Wholegrain Bread | 30% Reduced Risk |
| [16] 1988, Belgium | 438 | 2,851 | Wholegrain Bread | 21% Reduced Risk |
| [17] 1988, Italy | 339 | 778 | Wholegrain Bread & Pasta | 28% Reduced Risk |
| [18] 1997, USA | 1,993 | 2,410 | Wholegrain Foods | 20% Reduced Risk |
Rectal Cancer
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [15] 1992, Italy | 125 | 699 | Wholegrain Bread | 70% Reduced Risk |
| [16] 1988, Belgium | 365 | 2,851 | Wholegrain Bread | 22% Reduced Risk |
| [17] 1988, Italy | 236 | 778 | Wholegrain Bread & Pasta | 12% Reduced RIsk |
Colorectal Cancer
( Studies which did not distinguish between the two )
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [19] 1989, USA | 147 | 147 | Wholegrain Bread | 32% Reduced Risk |
| [20] 1994, Italy | 119 | 119 | Wholemeal Bread | 3% Increased Risk |
| [21] 1984, USA | 86 | 176 | Wholegrains | Colon =48% IR, Rectal = 39% RR |
Gastric Cancer
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [22] 1990, USA | 137 | 137 | Wholegrain Bread | 56% Reduced Risk |
| [23] 1987, Italy | 206 | 474 | Wholegrain Bread & Pasta | 60% Reduced Risk |
| [24] 1992, Belgium | 449 | 3,524 | Wholemeal Bread | 38% Reduced Risk |
| [25] 1991, Germany | 143 | 579 | Wholemeal Bread | 63% Reduced Risk |
| [26] 1993, Sweden | 338 | 679 | Wholemeal Bread | 30% Reduced Risk |
| [27] 1991, Poland | 741 | 741 | Non-White Bread | 38% Reduced Risk |
| [28] 1985, Greece | 110 | 100 | Brown Bread | 69% Reduced Risk |
Pancreatic Cancer
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [29] 1989, USA | 212 | 220 | Whole wheat Bread | 56% Reduced Risk |
| [30] 1985, USA | 201 | 402 | Wholegrain Bread | No Difference |
| [31]1986, USA | 490 | 490 | Wholegrain Bread | 30% Reduced Risk |
| [32] 1991, Netherlands | 164 | 480 | High Fibre Cereal Foods | 16% Reduced Risk |
Breast Cancer
| Reference, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [33] 1987, Italy | 1,108 | 1,281 | Wholegrain Bread & Pasta | 10% Reduced Risk |
| [34] 1993, Switzerland | 107 | 318 | Wholegrain Bread & Pasta | 40% Reduced Risk |
Brain Cancer
| Ref, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [35] 1994, Australia | 416 | 406 | Wholegrain CerealsWholegrain BreadWholegrain Pasta | 14% IR (f) 34% RR (m)32% IR (f) 46% RR (m)49% IR (f) 40% RR (m) |
| [36] 1993, Germany | 206 | 418 | Brown Bread | 40% Decreased Risk |
Endometrial Cancer
| Ref, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [37]1993, Switzerland | 274 | 572 | Wholegrain Bread & Pasta | 57% Reduced Risk |
| [38] 1986, Italy | 206 | 206 | Wholegrain Bread & Pasta | 39% Reduced Risk |
| [39] 1990, USA | 332 | 511 | Wholegrain CerealsWholegrain Foods | 41% Reduced Risk35% Reduced Risk |
Oral Cancers
| Ref, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [40] 1992, Italy | 102 Tongue104 Mouth | 726 | Wholegrain Bread & Pasta | 90% Reduced Risk50% Reduced Risk |
| [41] 1988, USA | 871 oral/ pharynx | 979 | Whole-wheat Bread | 30% RR (m) 50% RR (f) |
| [42] 1984 USA | 227 oral/pharynx | 405 | Wholegrain Bread & Cereal | 30% Reduced Risk |
| [43] 1988, USA | 275 esophagus | 275 | Wholegrain Bread | 29% Reduced Risk |
| [44] 1999 Italy | 110 larynx | 843 | Whole-meal Bread & Pasta | 40% Reduced Risk |
| [45] 1987 Italy | 105 esophagus | 348 | Wholegrain Bread & Pasta | 80% Reduced Risk |
Lymphomas
| Ref, Year & Country | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [46] 1989, Italy | 208 non-Hodgkins | 401 | Wholegrain Bread & Pasta | 56% Reduced Risk |
| [47] 1997 Italy | 158 Hodgkins429 non-Hodgkins141 myelomas101 soft tissue | 1,157 | Wholegrain foods | 40% Reduced Risk60% Reduced Risk50% Reduced Risk80% Reduced Risk |
Other Cancers
| Ref, Year & Country | Cancer | Number of Cases | Number of Controls | Food | Risk: High vs Low Intake |
| [48] 1991 Italy | Soft Tissue Sarcoma | 88 | 610 | Wholegrain Bread & Pasta | 60% Reduced Risk |
| [49] 1987 Italy | Ovarian Cancer | 455 | 1,385 | Wholegrain Bread & Pasta | 37% Reduced Risk |
| [50] 1988 Italy | Liver Cancer | 151 | 1051 | Wholegrain Bread & Pasta | 42% Reduced Risk |
| [51] 1992 Italy | Prostate | 271 | 685 | Whole-meal Bread | 10% Reduced Risk |
| [52] 1991 Italy | Thyroid | 385 | 798 | Wholegrain Bread & Pasta | 40% Reduced Risk |
| [53] 1989 Italy | Bladder | 163 | 181 | Wholegrain Bread & Pasta | 54% Reduced Risk |
Subsequent case-control studies have also reported significantly protective effects of wholegrain consumption against the risk of oral, oesophageal and laryngeal cancer. [54,55]
Several prospective cohort studies have also found that higher intakes of whole grain foods are protective against certain cancers. The results of a recent cohort study in Sweden which followed 61,433 women for nearly 15 years, found that higher intake (4.5 serves per day) of whole grain food reduced the risk of colon cancer by 33% compared with lower intakes (<1.5 serves per day). [56]
Wholegrain intake was also found to be protective against stomach cancer in the Cancer Prevention Study (CPS) II which followed 1.2 million American men and women over 14 years. After age adjustments, moderate and high wholegrain intake reduced the risk by 13 and 23% respectively in men, whilst in women, a higher intake reduced the risk by 17%; however these findings were less significant after multivariate adjustments. [57] No association between whole grains and stomach cancer was found in a smaller cohort called the 7 countries study in Europe, [58] however this study did find a strong inverse relationship with colorectal cancer and total dietary fibre, which wholegrain foods contributed to more that any other single food group. This study found that an increase of 10 grams of daily fibre intake was associated with a 33% lower 25-year colorectal-cancer mortality risk. [59]
The Cancer Prevention Study II Nutrition cohort also found that after age adjustment, 11 or more serves/per of week of wholegrain foods decreased the risk of colon cancer in men by 29%, and between 8-11 serves per week decreased the risk by 25% in women, however after multivariate adjustments, these findings were less significant. [60]
Wholegrain intake was shown to decrease the risk of endometrial cancer by 37% in a cohort following 23,014 women in Iowa for 12 years; however this association was only found among women who had never used Hormone Replacement Therapy (HRT) [61] This same cohort study found a 17% lower rate in all causes of death among women who consumed the most wholegrain fibre (4.7g/day).[62]
Chemo-protective Mechanisms of Wholegrain Foods
Wholegrain foods are especially rich sources of a plethora of important nutrients and beneficial anti-nutrients and non-nutrients such as B vitamins, vitamin E, Magnesium, selenium, soluble and insoluble fibre, plant sterols, lignans and other phytoestrogens, phytic acid, protease inhibitors, hemagglutinins, tannins, phenolic compounds and various other phytochemicals.
The following table [click to enlarge] lists some of the beneficial effects from various components found in wholegrain foods. The table was taken from a paper published in the American Journal of Clinical Nutrition by Professor Joanne Slavin and her colleagues at the university of Minnesota . [63]
Although they are a particularly rich source of these substances, many of which have been found have anti-cancer effects in animal studies, [64-71] wholegrain foods seem to afford protection that has not been found by any of these individual, isolated ingredients.[63] Consequently, ensuring adequate wholegrain intake from a variety of sources would be far more protective than simply looking to identify specific “nutritional magic bullets” so to speak. [72]
There are several theories on why whole grains may protect against cancer, other than being rich sources of these beneficial substances. Because of their complex nature, it has been suggested that there may be many potential mechanisms responsible for the protective properties of whole grain foods, including their ability to bind carcinogens, thus limiting their absorption or contact with the intestinal lining. [73]
One prominent theory to explain their protective effect on colon cancer is due to their fibre content. High fibre foods tend to speed the passage of stools through the colon, thus decreasing the amount of time that any potentially carcinogenic substances would have to be exposed to the colon wall. This decrease in transit is especially true for insoluble fibre, such as that found in wheat bran. [74]
Another possible mechanism may be the effect that fermented fibre has on bile acids Fermented fibres tend to increase the acidity of the colon which inhibits primary bile acids from converting to secondary bile acids. This is thought to be significant because these secondary bile acids may promote cell proliferation, which would enhance the ability for mutations to occur and for tumour cells to replicate; thus allowing cancers to spread. Furthermore, a particular product of fermented fibre is a short chain fatty acid called butyrate, which has been found to protect against colon cancer in laboratory studies. [75]
An inverse association has been found between fibre intake, particularly from cereal/ grain foods, and the risk of colon cancer in population studies. One of the most evident associations was found in the European Prospective Investigation into Cancer and Nutrition (EPIC), which examined the incidence of bowel cancer among half a million Europeans, and found fibre, particularly cereal fibre to be protective. [76]
The Wheat Bran Fiber Study however found no difference in the reoccurrence of colon polyps in 1,429 men who were given either a high wheat bran fiber cereal supplement (13.5 grams of fiber in 2/3 cup cereal per day) or a low wheat bran fiber cereal supplement (2 grams of fiber in 2/3 cup cereal per day) for 3 years. [77]
There have been several criticisms of this study however. The first is that it examined colon polyps, not malignant cancer. Polyps may or may not become cancerous, but this study did not prove that wheat bran could not prevent cancer altogether. The second problem was that it involved men who were already at a high risk, as they had already been found to have colon polyps. Consequently, there may have still been some abnormal tissue remaining in their colon to begin with. Therefore, it does not prove that a more protective effect may have been found among people with healthy colon tissue to begin with. Thirdly, 13.5 grams of fiber may not have necessarily been adequate, as the results from population studies such as EPIC have found fibre intakes in excess of 30g/day to offer the most protection. Furthermore, the men in this trial were given “cups” of wheat bran. Presumably, this meant that the bran was finely ground; however finely ground wheat bran does not have the same stool-bulking effect that course wheat bran does, even at the same dosage, [78] which suggests that the particle size of the whole grain is an important factor in determining the physiologic effect. [79] Another problem was that it lasted only 3 years, whereas the protective effect seen in population studies has been consumption of high fibre diets over many years, between 6-12. Lastly, this study only examined one specific food (wheat bran) as apposed to a variety of fibrous foods. Although wheat bran has been shown to be the most protective fibre source in animal studies [80] the anti-cancer effect of whole grains may come from components other than that found solely in wheat bran.
Wholegrain Foods and Cardiovascular Disease: Epidemiology
Whole grains are among the foods most proven to decrease the risk of cardiovascular disease according to epidemiological investigations. Several large cohort studies have found that intakes of approximately 3 serves per day or more have a significantly protective effect.
Results from the Adventist Health Study revealed that among the 31 thousand adults involved, the risk of non fatal and fatal heart disease was 44% and 11% lower respectively among those who usually consumed whole wheat bread. [81] Similarly, every 10-g increase in cereal fiber per day decreased the risk of heart attacks in the U.S. Male health professionals study which followed 43,757 older men for 6 years.[82]
The Iowa Womens Health Study followed 34,492 postmenopausal women for 9 years after which time 438 had died from heart disease. Consuming 1.2 servings of wholegrain food per day was associated with a 29% reduced risk whilst 1.9 servings decreased the risk by 36%. [83] An inverse association between wholegrain intake and heart disease was also found in the Nurses Health Study which recorded 761 cases of CHD throughout the 10 years that 75,521 women were studied. The results demonstrated a 25% reduction in CHD risk among women who consumed 3 wholegrain servings per day.[84]
After following 16,933 men and 16,915 women for over 11 years, The Norwegian County Study recorded a 25% reduction in the risk of heart disease among those who consumed 9 slices (5.4 servings) of wholegrain bread per day compared with those who consumed only 1 or less sliced pre day. [85]
Compared with those who rarely or never consumed whole-grain cereal, men whose intake was greater than or equal to 1 serving per day, had a 17% lower risk of death from all causes and a 20% lower risk of death from Cardiovascular Disease (Both CHD and Stroke) in a 5 and a half year long cohort study of 86,190 US male physicians aged between 40 – 84 years. [86] In fact, wholegrain intake has also been found to decrease the risk of ischemic stroke in several population-based studies.
Among the 15, 792 adults followed for 11 years in the Atherosclerosis Risk in Communities (ARIC) cohort, those whose daily wholegrain intake was 1.5 servings had an 11%, 27% and 13% lower risk of ischemic stroke, coronary artery disease and all cause mortality respectively, whilst 3 serves per day decreased the risk by 28%, 25% and 23% respectively. [87] In the Nurses Health Study, an average daily intake of 3 servings of whole grains reduced the risk of ischemic stroke by 31% among the 75,521 US women aged 38 to 63 years studied for 12 years. [88] In a similar cohort of over 71,768 women, compared with the typical “Western” diet high in red and processed meats, refined grains and desserts, diets characterized by higher intakes of fruits, vegetables, legumes, fish, and whole grains reduced the risk of all strokes by 22% and ischemic strokes by 26%.[89]
A daily cereal fibre intake of 6.3g or more decreased the risk of cardiovascular disease by 21% in an 8-year long cohort that studied 3,588 American men and women aged 65 years. [90] The authors also noted that
“… higher cereal fiber intake was associated with lower risk of total stroke and ischemic stroke and a trend toward lower risk of ischemic heart disease death .”
Cardio-protective Mechanisms of Wholegrain Foods
It is not entirely certain how wholegrain foods exert their protective effect on the cardiovascular system, however there are several theories which include the fact that they are a rich source of beneficial nutrients and non-nutrient substances such as Folate, tocotrienols (a form of Vitamin E), Magnesium, Potassium, Selenium, and certain phenolic phytochemicals, all of which are associated with a decreased risk of cardiovascular disease. [91]
Whole grains such as wheat bran also possess significant antioxidant activity, due to their considerable phenolic content. In the colon, bacterial enzymes release these phenolic acids thus allowing them to be absorbed, offering antioxidant protection. [92] Plant sterols such as beta-sitosterol are another component of whole grains, which are known to be able to lower serum cholesterol levels by inhibiting cholesterol absorption in the gut. [93,94]
Oats in particular, can improve gastro-intestinal function, improve glucose metabolism, [95] and are rich in a substance called beta-glucan, which reduces serum cholesterol levels. [96] Consumption of barley was also found to reduce total cholesterol, LDL-Cholesterol and triglyceride levels as well as increase HLD “good” cholesterol levels, in a recent trial conducted by researchers at the United States Department of Agriculture. [97]
Furthermore, whole grains are especially high in dietary fibre, resistant starches and oligosaccharides, which are fermented by bacteria in the gut to produce short chain fatty acids which are also known to lower cholesterol synthesis in the liver, [98] thus improving serum cholesterol levels. [99]
Other than their antioxidant and hypocholesterolaemic characteristics, wholegrain foods provide a good source of both macronutrients (such as carbohydrate and protein) and micronutrients (vitamins and minerals) with a relatively low Glycemic Index (GI) and a low Glycaemic Load ( which is [the GI of a food multiplied by the amount of carbohydrate] ÷ 100), thus improving insulin function. Diets with a low GL are associated with a reduction in the risk of heart disease and diabetes. [100]
Wholegrain foods and Diabetes: Epidemiology
In 2000, researchers from the University of Minnesota published the results of the Iowa Women’s Health Study; a prospective cohort which studied the diets of nearly 36 thousand women between 55 and 69 years old, all of whom were initially free of diabetes. Throughout a 6 year follow up, 1,141 of these women had been diagnosed with diabetes. After studying their dietary intakes, it was found that wholegrain intake was inversely related to the risk of diabetes; that is, the greater the wholegrain intake, the lower the risk. There were 21% fewer cases of diabetes among those who consumed the most wholegrain foods (3 serves or more per day) compared to those who consumed the least. This study also found that total dietary fibre as well as dietary magnesium had a protective association. [101]
In the same year, researchers at the Harvard Medical School published the results of another cohort study which followed 75,521 women for 10 years, after which time 1,879 cases of diabetes were reported. Once again, wholegrain consumption decreased the risk of diabetes. Compared to those who had the least wholegrain intake, a higher intake reduced the risk by 38%. This study also found that a high intake of refined-grain cereals increased the risk by 31%. Moreover, those who had the highest ratio of refined grain to wholegrain intake had a 57% greater risk. These associations were particularly strong among overweight women. This study found no protective association between total fibre, magnesium or vitamin E intake. [102]
Similar results were obtained in a more recently published cohort study which followed both men and women for 10 years, after which time a 35% reduction in the risk of diabetes was observed among those with a higher wholegrain intake. [103]
A higher whole-grain intake was associated with a 42% reduced risk of diabetes in the Health Professionals follow-up study, which had followed almost 43 thousand men, 1,197 of whom were diagnosed as diabetic throughout the 12 years they were studied. [104]
What is Diabetes, Insulin and the Glycaemic Index?
Insulin is a hormone produced by the pancrease which allows glucose in the blood to be taken up by the bodies’ cells and used for energy, as well as preventing blood glucose levels from rising too high. The most common form of diabetes, accounting for approximately 85% of all cases, [105] is Type II, also known as “late” or “adult onset diabetes”. In Type II diabetes, the pancreas produces insulin, however the insulin does not function properly. This leads to excessively high levels of glucose in the blood, which, over a long period of time, can lead to a multitude of serious health problems such as an increase in the risk of heart disease, stroke, glaucoma & blindness, as well as amputations [106] and even a reduced lifespan. [107] The risk increases progressively with age, in fact it is thought that in excess of 20% of the population aged over 60 have type II diabetes [108].
When we eat, depending on what we eat, our blood glucose levels will rise over a period of 1-2 hours, before falling again back to normal levels. In diabetics, glucose levels are abnormally high to begin with (fasting levels), rise way too far upon food consumption, and take longer than normal to return to fasting levels again. [109]
High fasting glucose levels are often an indicator of diabetes, however a more accurate diagnosis can be made by monitoring the rise of glucose after a high glucose meal/drink, and then monitoring how long it takes to return to fasting levels; a test known as a “ glucose tolerance test ”.
If we consumed a food high in pure glucose, our blood glucose levels would rise very sharply, peak, and then plummet very rapidly. The rise and fall of blood glucose levels that occurs after a specific reference glucose intake, was given a score of 100 on the “glycaemic index”. [110] The glycaemic index values of other foods, were then given a number that correspond to how similar their effect is on blood glucose by comparison with this reference intake. [111]
For example, certain foods such as white bread, potatoes and a lot of “junk foods” cause our blood insulin to rise sharply, similar to the way in which the glucose reference value does, because once they are in our gut, we absorb their sugars very quickly. These foods are said to have a high Glycaemic Index, or high “GI”. [112]
Other foods such as nuts, legumes and oats, release their energy very slowly, so that our blood glucose rise slowly, and fall slowly. These foods are said to have a low GI. Foods with a GI value of about 70 or higher, are generally considered high. Those with a GI of around 40 or lower are generally considered low, whilst those in between are considered moderate. More importantly however is the GI of the entire meal. For example, if you combined a high GI food such as white rice, with a low GI foods such as legumes, the GI of the entire meal would be somewhere in between.
Additionally, another important issue is the “Glycaemic Load” (GL), which is an indicator of glucose response or insulin demand that is induced by total carbohydrate intake. It is calculated by multiplying the GI of a food/meal, by the total number of carbohydrates, and then dividing that number by 100. [113]
The problem with high GI foods is not only that they provide only very short lasting energy followed by rapid declines, but they put a lot of strain so to speak, on our insulin. When our glucose levels “spike”, or rise very rapidly, our insulin has to work extra hard to try to modulate blood levels. If this happens constantly, it is thought that our insulin can start to become resistant. This decline in the ability of insulin to function properly may lead to type II diabetes.
One of the most prominent causes of insulin resistance is having excess body fat, which is why obesity is the most serious risk factor for developing diabetes. [114] Furthermore, obese type II diabetics who lose weight and maintain a healthy body weight can generally gain far better control over their condition, and expect a decrease in the risk of many of the more severe complications associated with the disease. [115]
Other than obesity, is the most strongly correlated risk factor for developing insulin resistance is a diet with a relatively high GI and more importantly, a high GL. [116] The importance of the GL is the ability to obtain adequate carbohydrate without having a high GI. For example, foods such as lean meat may have a low GI, but we need adequate sources of carbohydrate as well, which meat does not provide. Refined grain foods such as white bread are a good source of carbohydrate; however they have a very high GI. Foods such as whole grains however also provide a good source of carbohydrate, but do so without the high GI; thus they have a favourable GL. Therefore, obtaining our primary source of carbohydrates through whole grains (which provide excellent sources of other nutrients as well) ensures adequate intake without the high GI. This is important because low GL diets are associated with a decreased risk of heart disease and type II diabetes, as a low GL diet provides enough energy without causing insulin resistance. Several important studies have confirmed that whole-grain intake may prevent diabetes by protection against insulin resistance. [117]
Whole grains, GI, GL & Insulin Resistance
In a randomized crossover trial conducted by the Harvard Medical School in 2002, insulin levels were significantly improved in overweight insulin resistant adults who consumed a wholegrain rich diet compared to those receiving a refined-grain rich diet, even though both contained the same percentage of fat and carbohydrate. [118]
These findings were supported by the results of the Framingham Offspring study, which revealed that wholegrain intake was inversely associated with fasting insulin levels among 2, 941 people. Furthermore, wholegrain intake was also inversely associated with body mass index (BMI), waist-to-hip ratio, Total Cholesterol (TC) and LDL “bad” cholesterol – all factors known to increase the risk of diabetes, as well as heart disease. These results shed further insight into the mechanisms by which wholegrain intake protects against diabetes. [119]
In 1997, researchers from the Harvard School of Public Health published the results of a prospective study which followed 42,759 men aged 40-75 years who were free of diabetes of cardiovascular disease to begin with. During 6-years of follow-up, 523 of these men had been diagnosed with type II diabetes. An analysis of their diets revealed that even after multivariate adjustments, compared to lower GI diets, those with the highest GI diets had a 37% greater risk of diabetes. Moreover, those with the greatest cereal fibre intake had 30% reduction in risk. [120]
The same researchers published the results of another prospective cohort study which followed 65, 173 US women, 915 of which were diagnosed with diabetes throughout the 6 year follow up. Once again, high GI diets increased the risk by 37%. Moreover, high GL diets increased the risk by 47%, whilst higher cereal fibre intakes decreased the risk by 28%. Most importantly, the combination of a high GL and a low cereal fiber intake increased the risk by a massive 150%. [121] More recently, the results of a cohort study following 91, 249 younger women for 8 years found a 59% greater risk for developing diabetes among those with a higher GI diet, whereas higher intakes of cereal fibre decreased the risk by 36%. [122]
The most recent study to support these findings found a 32% greater risk among the 31,641 men and women followed for 4 years who had the highest GI diets, despite greater intakes of total carbohydrates having a decreased risk. Higher intakes of white bread and other starchy foods however increased the risk by 37% and 47% respectively. [123]
It is commonly thought that foods containing “complex” carbohydrates or starches, are good and produce slow burning energy, whilst food with “simple carbohydrates” or sugars, have the opposite effect and increase the risk of diabetes. This is often not the case, as we can see in the case of foods such refined grains which have a very high GI, despite being high in complex carbohydrates. [124] Conversely, some foods high in sugars such as fruit and fruit juices, actually have a relatively low GI as they contain soluble fibres that delay the release of sugar into the blood.
This is a table which compares the GI and GL values of a variety of common Australian foods, particularly those which may cause confusion due their relatively high carbohydrate levels. Full list of the International Table of Glycemic Index and Glycemic Load Values can be downloaded here: http://www.ajcn.org/cgi/content/full/76/1/5/T1
Table derived from: http://www.biohealthinfo.com/html/resources/articles/article_archive/fatbelly.html
I’d like to thank the following people who contributed towards helping me write this article by supplying input and or data. Your assistance is much appreciated.
Dr David Jacobs – Professor of Epidemiology: University of Minnesota
Dr Joanne Slavin – Professor of Nutrition: University of Minnesota
[1] Dixon LB, Cronin FJ, Krebs-Smith SM. Let the pyramid guide your food choices: capturing the total diet concept. J Nutr. 2001 Feb;131(2S-1):461S-472S.
[2] Miller G, Prakash A & Decker E (2002) Whole-grain micronutrients. In Whole-Grain Foods in Health and Disease , pp. 243–258 [L Marquart, JL Slavin and RG Fulcher, editors]. St Paul , MN : Eagan Press.
[3] Hallfrisch J , Facn , Behall KM . Mechanisms of the effects of grains on insulin and glucose responses. J Am Coll Nutr. 2000 Jun;19(3 Suppl):320S-325S.
[4] Slavin J , Jacobs D , Marquart L . Whole-grain consumption and chronic disease: protective mechanisms. Nutr Cancer. 1997;27(1):14-21.
[5] Liu, S. Intake of refined carbohydrates and whole grain foods in relation to risk of type 2 diabetes mellitus and coronary heart disease . J Am Coll Nutr. 2002 Aug;21(4):298-306.
[6] Murtaugh MA, Jacobs DR Jr, Jacob B, Steffen LM, Marquart L. Epidemiological support for the protection of whole grains against diabetes. Proc Nutr Soc. 2003 Feb;62(1):143-9.
[7] Truswell AS. Cereal grains and coronary heart disease . Eur J Clin Nutr. 2002;56(1):1-14.
[8] Jacobs, D. R., Slavin, J., and L. Marquart, ” Whole grain intake and cancer: A review of the literature .” Nutr Cancer 24, 221-299, 1995. ‘
[9] Jacobs DR Jr , Meyer HE , Solvoll K . Consumption of whole grain foods and chronic disease Tidsskr Nor Laegeforen. 2004 May 20;124(10):1399-401.
[10] Cleveland LE, Moshfegh AJ, Albertson AM, Goldman JD. Dietary intake of whole grains.
J Am Coll Nutr. 2000 Jun;19(3 Suppl):331S-338S.
[11] Kantor LS, Variyam JN, Allshouse JE, Putnam JJ & Lin B (2002) Dietary intake of whole grains: a challenge for consumers. In Whole-Grain Foods in Health and Disease , pp. 301–325 [L Marquart, JL Slavin and RG Fulcher, editors]. St Paul , MN : Eagan Press ]
[12] Harnack L, Walters S & Jacobs JR (2003) Dietary intake and food sources of whole grains among US children and adolescents: data from the 1994–1996 continuing survey of food intakes by individuals . Journal of the American Dietetic Association 103 , 1015–1019.
[13] McKeown-Eyssen GE , Bright-See E . Dietary factors in colon cancer: international relationships . Nutr Cancer. 1984;6(3):160-70.
[14] Jacobs, D. R., Slavin, J., and L. Marquart, ” Whole grain intake and cancer: A review of the literature .” Nutr Cancer 24, 221-299, 1995. ‘
[15] Bidoli, E., Franceschi, S., Talamini, R., Barra, S., and C. LaVecchia, “Food Consumption and Cancer of the Colon and Rectum in North-Eastern Italy .” Int J Cancer 50, 223-229, 1992.
[16] Tuyns, J. A., Kaaks, R., and M. Haelterman, “Colorectal Cancer and the Consumption of Foods: A Case-Control Study in Belgium .” Nutr Cancer 11, 189-204, 1988.
[17] LaVecchia, C., Negri, E., DeCarli, A., D’Avanzo, B., Gallotti, L., and S. Franceschi, “A Case- Control Study of Diet and Colorectal Cancer in Northern Italy .” Int J Cancer 41, 492-498, 1988.
[18] Slattery, M. L., Potter, J. D., Coates, A., Ma, K.-N., Berry, T. D., Duncan, D. M., and B. J. Caan, “Plant Foods and Colon Cancer: An Assessment of Specific Foods and Their Related Nutrients (United States)” Cancer Causes Control 8, 575-590, 1997
[19] Peters, R. K., Garabrant, D. H., Yu, M. C., and T. M. Mack, “A Case Control Study of Occupational and Dietary Factors in Colorectal Cancer in Young Men by Subsite.” Cancer Res 49, 5459-5468, 1989.
[20] Centonze, S., Boeing, H., Leoci, C., Guerra, V., and G. Misciagna, “Dietary Habits and Colorectal Cancer in a Low-Risk Area. Results from a Population-Based Case-Control Study in Southern Italy .” Nutr Cancer 21, 233-246, 1994.
[21] Pickle, L. W., Greene, M. H., Ziegler, R. G., Toledo , A., Hoover R., Lynch H. T., and J. F. Fraumeni, Jr., “Colorectal Cancer in Rural Nebraska .” Cancer Res 44, 363-369, 1984.
[22] Wu-Williams, H. A. Yu, C. M., and T. M. Mack, “Life-Style, Workplace and Stomach Cancer by Subsite in Young Men of Los Angeles County .” Cancer Res 50, 2569-2576, 1990.
[23] LaVecchia, C., Negri, E., Decarli, A., D’Avanzo, B., and S. Franceschi, “A Case-Control Study of Diet and Gastric Cancer in Northern Italy .” Int J Cancer 40: 484- 498, 1987.
[24] Tuyns, J. A., Kaaks, R., Haelterman, M., and E. Riboli, “Diet and Gastric Cancer. A Case-Control Study in Belgium .” Int J Cancer 51, 1-6, 1992.
[25] Boeing, H., Frentzel-Byme, R., Berger, M., Berndt, V., Gores, W., et al., “Case-Control Study of Stomach Cancer in Germany .” Int J Cancer 47, 858-864, 1991.
[26] Hansson, L. E., Nyren, O., Bergstrom, R., Wolk, A., Lindgren, A., Baron, J., and H. O. Adami, “Diet and Risk of Gastric Cancer. a Population-Based Case-Control Study in Sweden .” Int J Cancer 55, 181-189, 1993.
[27] Boeing, H., Jedrychowski, W., Wahrendorf, J., Popiela, T., Tobiasz-Adamczyk, B., and A. Kulig, “Dietary Risk Factors in Intestinal and Diffuse Types of Stomach Cancer: A Multicenter Case-Control Study in Poland .” Cancer Causes Control 2, 227-233, 1991.
[28] Trichopoulos, D., Ouranos, G., Day, N. E., Tzonou, A., Manousos, O., Papadimitriou, C., and A. Trichopoulos, “Diet and Cancer of the Stomach: A Case-Control Study in Greece .” Int J Cancer 36, 291-297, 1985.
[29] Olsen, G. W., Mandel, J. S., Gibson, R. W., Wattenberg, L. W., and L. M. Schuman, “A Case-Control Study of Pancreatic Cancer and Cigarettes, Alcohol, Coffee and Diet.” Am J Public Health 79, 1016-1019, 1989.
[30] Gold, E. B., Gordis, L., Diener, M. D., Seltser, R., Boitnott, J. K., Bynum, T. E., and D. F. Hutcheon, “Diet and Other Risk Factors for Cancer of the Pancreas.” Cancer 55:460-467, 1985.
[31] Mack, T. M., Yu, M. C., Hanisch, R., and B. E. Henderson, “Pancreas Cancer and Smoking, Beverage Consumption, and Past Medical History.” JNCI 76, 49-60, 1986.
[32] Bueno de Mesquita, H. B., Maisonneuve, P., Runia, S., and C. J. Moerman, ” Intake of Foods and Nutrients and Cancer of the Exocrine Pancreas: A Population Based Case-Control Study in the Netherlands .” Int J Cancer 48, 540-549, 1991.
[33] LaVecchia, C., Negri, E., Decarli, A., D’Avanzo, B., and S. Franceschi, “A Case-Control Study of Diet and Gastric Cancer in Northern Italy .” Int J Cancer 40: 484- 498, 1987.
[34] Levi, F., LaVecchia, C., Gulie, C., and E. Negri, “Dietary Factors and Breast Cancer Risk in Vaud , Switzerland .” Nutr Cancer 19, 327-335, 1993.
[35] Giles, G. G., McNeil, J. J., Donnan, G., Webley, C., Staples, M. P., Ireland, P. D., Hurley, S. F., and M. Salzberg “Dietary Factors and the Risk of Glioma in Adults: Results of a Case-Control Study in Melbourne, Australia.” Int J Cancer 59, 357-362, 1994.
[36] Boeing, H., Schlehofer, B., Blettner, M., and J. Wahrendorf, “Dietary Carcinogens and the Risk for Glioma and Meningioma in Germany .” Int J Cancer 53, 561-565, 1993
[37] Levi, F, Franceschi, S, Negri, E, and C. LaVecchia, “Dietary Factors and the Risk of Endometrial Cancer.” Cancer 71, 3575-81, 1993.
[38] LaVecchia, C., DeCarli, A., Fasoli, M., and A. Gentile, “Nutrition and Diet in the Etiology of Endometrial Cancer.” Cancer 57, 1248-1253, 1986.
[39] Goodman, M. T., Wilkens, L. R., Hankin, J., Lyu, L., WU, AH, Kolonel, LN. “Association of Soy and Fiber Consumption with the Risk of Endometrial Cancer.” Am J Epidemiol 146, 294-306, 1997.
[40] Franceschi, S., Barra, S., LaVecchia, C., Bidoli, E., Negri, E., and R. Talamini, “Risk factors for cancer of the tongue and mouth.” Cancer 70, 2227-2233, 1992.
[41] McLaughlin, J. K., Gridley, G., Block, G., Winn, D. M., Preston-Martin, S., Schoenberg, J. B., Greenberg, R. S., Stemhagen, A., Austin, D. F., Ershow, A. G., Blot, W. J., Fraumeni, J. F. Jr., “Dietary factors in oral and pharyngeal cancer.” JNCI 80, 1237-1243, 1988.
[42] Winn, D. M., Ziegler, R. G., Pickle, L. W., Gridley, G., Blot, W. J. and R. N. Hoover, “Diet in the etiology of oral and pharyngeal cancer among women from the Southern United States.” Cancer Res 44,1216-1222, 1984.
[43] Yu, M. C., Garabrant, D. H., Peters, J. M., and T. M. Mack, “Tobacco, alcohol, diet, occupation, and cacinoma of the esophagus.” Cancer Res 48, 3843-3848, 1988.
[44] LaVecchia, C., Negri, E., D’Avanzo, B., Franceschi, S., Decarli, A., and P. Boyle, “Dietary indicators of laryngeal cancer risk.” Cancer Res 50, 4497-4500, 1990.
[45] Decarli, A., Liati, P., Negri, E., Franceschi, S., and C. LaVecchia, “Vitamin A and other dietary factors in the etiology of esophageal cancer.” Nutr Cancer 10, 29-37, 1987.
[46] Franceschi, S., Serraino, D., Carbone, A., Talamini, R., and C. LaVecchia, “Dietary Factors and Non-Hodgkins Lymphoma: A Case-Control Study in the Northeastern Part of Italy .” Nutr Cancer 12, 333-341, 1989.
[47] Tavani, A., Pregnolato, A., Negri, E., Franceschi, S., Serrnino, D., Carbone, A., and C. LaVecchia, “Diet and Risk of Lymphoid Neoplasms and Soft Tissue Sarcoma.” Nutr Cancer 27, 256-260, 1997.
[48] Serraino, D., Franceschi, S., Talamini, R., Frustaci, S., and C. LaVecchia, “Non-occupational Risk for Adult Soft-Tissue Sarcoma in Northern Italy .” Cancer Causes Control 2, 157-164, 1991.
[49] LaVecchia, C., DeCarli, A., Negri, E., Parazzini, F. Gentile, A., Cecchetti, G., Fasoli, M., and S. Franceschi, “Dietary Factors and the Risk of Epithelial Ovarian Cancer.” JNCI 79, 663-669, 1987.
[50] LaVecchia, C., Negri, E., Decarli, A., D’Avanzo, B., and S. Franceschi, “Risk factors for hepatocellular carcinoma in Northern Italy .” Int J Cancer 42, 872-876, 1988.
[51] Talamini, R., Franceschi, S., LaVecchia, C., Serranino, D., Barra, S., and E. Negri, “Diet and prostatic cancer: case-control study in Northern Italy .” Nutr Cancer 18, 277-286, 1992.
[52] Franceschi, S., Levi, F., Negri, E., Fassina, A., and C. LaVecchia, “Diet and thyroid cancer: a pooled analysis of four European case-controlled studies.” Int J Cancer 48,395-398, 1991.
[53] LaVecchia, C., Negri, E., Decarli, A., D’Avanzo, B., Liberati, C., and S. Franceschi, “Dietary factors in the risk of bladder cancer.” Nutr Cancer 12, 93-101, 1989.
[54] Levi F, Pasche C, Lucchini F, Chatenoud L, Jacobs DR Jr, La Vecchia C. Refined and whole grain cereals and the risk of oral, oesophageal and laryngeal cancer . Eur J Clin Nutr. 2000 Jun;54(6):487-9.
[55] Bosetti C, Negri E, Franceschi S, Conti E, Levi F, Tomei F, La Vecchia C. Risk factors for oral and pharyngeal cancer in women: a study from Italy and Switzerland . Br J Cancer. 2000 Jan;82(1):204-7.
[56] Larsson SC , Giovannucci E , Bergkvist L , Wolk A . Whole grain consumption and risk of colorectal cancer: a population-based cohort of 60,000 women . Br J Cancer. 2005 May 9;92(9):1803-7.
[57] McCullough ML , Robertson AS , Jacobs EJ , Chao A , Calle EE , Thun MJ . A prospective study of diet and stomach cancer mortality in United States men and women . Cancer Epidemiol Biomarkers Prev. 2001 Nov;10(11):1201-5.
[58] Jansen MC, Bueno-de-Mesquita HB, Rasanen L, Fidanza F, Menotti A, Nissinen A, Feskens EJ, Kok FJ, Kromhout D. Consumption of plant foods and stomach cancer mortality in the seven countries study. Is grain consumption a risk factor? Seven Countries Study Research Group. Nutr Cancer. 1999;34(1):49-55.
[59] Jansen MC, Bueno-de-Mesquita HB, Buzina R, Fidanza F, Menotti A, Blackburn H, Nissinen AM, Kok FJ, Kromhout D. Dietary fiber and plant foods in relation to colorectal cancer mortality: The Seven Countries Study Int J Cancer. 1999 Apr 12;81(2):174-9.
[60] McCullough ML, Robertson AS, Chao A, Jacobs EJ, Stampfer MJ, Jacobs DR, Diver WR, Calle EE, Thun MJ. A prospective study of whole grains, fruits, vegetables and colon cancer risk. Cancer Causes Control. 2003 Dec;14(10):959-70
[61] Kasum CM, Nicodemus K, Harnack LJ, Jacobs DR Jr, Folsom AR; Iowa Women’s Health Study. Whole grain intake and incident endometrial cancer: the Iowa Women’s Health Study . Nutr Cancer. 2001;39(2):180-6.
[62] Jacobs DR , Pereira MA , Meyer KA , Kushi LH . Fiber from whole grains, but not refined grains, is inversely associated with all-cause mortality in older women: the Iowa women’s health study . J Am Coll Nutr. 2000 Jun;19(3 Suppl):326S-330S.
[63] Slavin JL, Martini MC, Jacobs DR Jr, Marquart L. Plausible mechanisms for the protectiveness of whole grains. Am J Clin Nutr. 1999 Sep;70(3 Suppl):459S-463S.
[64] Thompson LU. Antioxidants and hormone-mediated benefits of whole grains . Crit Rev Food Sci Nutr 1994;34:473–97
[65] Raicht RF, Cohen BI, Fazzini EP, Sarwal AN, Takahashi M. Protec tive effect of plant sterols against chemically induced colon tumors in rats . Cancer Res 1980;40:403–5
[66] Graf E, Eaton JW. Suppresion of colon cancer by dietary phytic acid . Nutr Cancer 1993;19:11–9
[67] Adlercreutz H. Does fiber-rich food containing animal lignan precursors protect against both colon and breast cancer? An extension of the “fiber hypothesis .” Gastroenterology 1984;86:761–6
[68] Adlercreutz H, Mazur W. Phyto -oestrogens and western diseases. Ann Med 1997;29:95–120
[69] Steinmetz KA, Potter JD. Vegetables, fruit, and cancer. II. Mechanisms. Cancer Causes Control 1991:2:427–42]
[70] Wattenberg LW. Chemoprevention of cancer . Cancer Res 1985;45:1–8
[71] Kohlmeier L, Simonsen N, Mohus K. Dietary modifiers of carcinogenesis . Environ Health Perspect 1995;103(suppl):177–84
[72] Potter JD. Food and phytochemicals, magic bullets and measurement error: a commentary. Am J Epidemiol 1997;144:1026–7
[73] Slavin JL, Martini MC, Jacobs DR Jr, Marquart L. Plausible mechanisms for the protectiveness of whole grains. Am J Clin Nutr. 1999 Sep;70(3 Suppl):459S-463S.
[74] McIntyre A, Vincent RM, Perkins AC, Spiller RC. Effect of bran, ispaghula, and inert plastic particles on gastric emptying and small bowel transit in humans: the role of physical factors. Gut 1997;40:223–7
[75] McIntyre A, Gibson PR, Young GP. Butyrate production from dietary fibre and protection against large bowel cancer in a rat model . Gut 1993;34:386–91
[76] Sheila A Bingham, Nicholas E Day, Robert Luben, Pietro Ferrari, et al. Dietary fibre in food and protection against colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC): An observational study The Lancet . London : May 3, 2003. Vol. 361, Iss. 9368; pg. 1496
[77] Alberts DS, Martinez ME , Roe DJ, et al. Lack of effect of a high-fiber cereal supplement on the recurrence of colorectal adenomas . N Engl J Med 2000:342:1156-62.
[78] Wrick K, Robertson JB, Van Soest PJ, et al. The influence of dietary fiber source on human intestinal transit and stool output. J Nutr 1983;113:1464–79
[79] Slavin JL, Martini MC, Jacobs DR Jr, Marquart L. Plausible mechanisms for the protectiveness of whole grains. Am J Clin Nutr. 1999 Sep;70(3 Suppl):459S-463S.
[80] Steinmetz KA, Potter JD. Vegetables, fruit, and cancer. II. Mechanisms. Cancer Causes Control 1991:2:427–42
[81] Fraser GE, Sabate J, Beeson WL, Strahan TM. A possible protective effect of nut consumption on risk of coronary heart disease. The Adventist Health Study . Arch Intern Med. 1992;152(7):1416-1424.
[82] Rimm EB, Ascherio A, Giovannucci E, Spiegelman D, Stampfer MJ, Willett WC. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men . JAMA. 1996;275(6):447-451
[83] Jacobs DR, Jr., Meyer KA, Kushi LH, Folsom AR. Whole-grain intake may reduce the risk of ischemic heart disease death in postmenopausal women: the Iowa Women’s Health Study . Am J Clin Nutr. 1998;68(2):248-257.
[84] Liu S, Stampfer MJ, Hu FB, et al. Whole-grain consumption and risk of coronary heart disease: results from the Nurses’ Health Study . Am J Clin Nutr. 1999;70(3):412-419.
[85] Jacobs DR, Jr., Meyer HE, Solvoll K. Reduced mortality among whole grain bread eaters in men and women in the Norwegian County Study . Eur J Clin Nutr. 2001;55(2):137-143.
[86] Liu S, Sesso HD, Manson JE, Willett WC, Buring JE. Is intake of breakfast cereals related to total and cause-specific mortality in men? Am J Clin Nutr. 2003;77(3):594-599.
[87] Steffen LM , Jacobs DR Jr , Stevens J , Shahar E , Carithers T , Folsom AR . Associations of whole-grain, refined-grain, and fruit and vegetable consumption with risks of all-cause mortality and incident coronary artery disease and ischemic stroke: the Atherosclerosis Risk in Communities (ARIC) Study. Am J Clin Nutr. 2003 Sep;78(3):383-90.
[88] Liu S, Manson JE, Stampfer MJ, et al. Whole grain consumption and risk of ischemic stroke in women: A prospective study . JAMA. 2000;284(12):1534-1540
[89] Fung TT , Stampfer MJ , Manson JE , Rexrode KM , Willett WC , Hu FB . Prospective study of major dietary patterns and stroke risk in women. Stroke. 2004 Sep;35(9):2014-9. Epub 2004 Jul 1.
[90] Mozaffarian D, Kumanyika SK , Lemaitre RN, Olson JL, Burke GL, Siscovick DS. Cereal, fruit, and vegetable fiber intake and the risk of cardiovascular disease in elderly individuals .
JAMA. 2003 Apr 2;289(13):1659-66.
[91] Slavin J. Why whole grains are protective: biological mechanisms . Proc Nutr Soc. 2003;62(1):129-134.
[92] Kroon PA, Faulds CB, Ryden P, Robertson JA & Williamson G (1997) Release of covalently bound ferulic acid from fiber in the human colon. Journal of Agricultural and Food Chemistry 45 , 661–667.
[93] Thompson GR , Grundy SM . History and development of plant sterol and stanol esters for cholesterol-lowering purposes . Am J Cardiol. 2005 Jul 4;96(1 Suppl):3-9.
[94] Ostlund RE Jr . Phytosterols and cholesterol metabolism . Curr Opin Lipidol. 2004 Feb;15(1):37-41.
[95] Welch RW . Can dietary oats promote health? Br J Biomed Sci. 1994 Sep;51(3):260-70.
[96] Bell S, Goldman VM, Bistrian BR, Arnold AH, Ostroff G, Forse RA. Effect of beta-glucan from oats and yeast on serum lipids. Crit Rev Food Sci Nutr. 1999 Mar;39(2):189-202.
[97] Behall KM , Scholfield DJ , Hallfrisch J . Lipids significantly reduced by diets containing barley in moderately hypercholesterolemic men . J Am Coll Nutr. 2004 Feb;23(1):55-62.
[98] Hara H, Haga S, Aoyama Y & Kiriyama S (1999) Short-chain fatty acids suppress cholesterol synthesis in rat liver and intestine . Journal of Nutrition 129 , 942–948.
[99] Wolever TM, Schrade KB, Vogt JA, Tsihlias EB, McBurney MI. Do colonic short-chain fatty acids contribute to the long-term adaptation of blood lipids in subjects with type 2 diabetes consuming a high-fiber diet? Am J Clin Nutr. 2002 Jun;75(6):1023-30.
[100] Liu S, Willett WC. Dietary glycemic load and atherothrombotic risk . Curr Atheroscler Rep. 2002;4(6):454-461
[101] Meyer KA, Kushi LH, Jacobs DR, Jr., Slavin J, Sellers TA, Folsom AR. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Am J Clin Nutr. 2000;71(4):921-930
[102] Liu S, Manson JE, Stampfer MJ, et al. A prospective study of whole-grain intake and risk of type 2 diabetes mellitus in US women . Am J Public Health. 2000;90(9):1409-1415
[103] Montonen J, Knekt P, Jarvinen R, Aromaa A, Reunanen A. Whole-grain and fiber intake and the incidence of type 2 diabetes . Am J Clin Nutr. 2003;77(3):622-629.
[104] Fung TT, Hu FB, Pereira MA, et al. Whole-grain intake and the risk of type 2 diabetes: a prospective study in men . Am J Clin Nutr. 2002;76(3):535-540
[105] Bate KL, Jerums G. 3: Preventing complications of diabetes. Med J Aust. 2003 Nov 3;179(9):498-503.
[106] Payne CB . Diabetes-related lower-limb amputations in Australia . Med J Aust. 2000 Oct 2;173(7):352-4.
[107] Zimmet P, Alberti K, Shaw J. Global and societal implications of the diabetes epidemic . Nature 2001; 414: 782-787.
[108] Dunstan D, Zimmet P, Welborn T, et al. The rising prevalence of diabetes and impaired glucose tolerance: the Australian Diabetes, Obesity and Lifestyle Study . Diabetes Care 2002; 25: 829-834.
[109] Jenkins DJ, Kendall CW, Augustin LS, Franceschi S, Hamidi M, Marchie A, Jenkins AL , Axelsen M. Glycemic index: overview of implications in health and disease . Am J Clin Nutr. 2002 Jul;76(1):266S-73S. Review.
[110] Wolever TM . The glycemic index . World Rev Nutr Diet. 1990;62:120-85.
[111] Foster-Powell K, Miller JB. International tables of glycemic index.Am J Clin Nutr . 1995 Oct;62(4):871S-890S.
[112] Jenkins D. Starchy foods and glycemic index . Diabetes Care 1988; 11:149–59.
[113] Bell SJ , Sears B . Low -glycemic-load diets: impact on obesity and chronic diseases. Crit Rev Food Sci Nutr. 2003;43(4):357-77.
[114] Goran MI, Ball GD, Cruz ML. Obesity and risk of type 2 diabetes and cardiovascular disease in children and adolescents. J Clin Endocrinol Metab 2003; 88: 1417-1427.
[115] Aucott L, Poobalan A, Smith WC, Avenell A, Jung R, Broom J, Grant AM. Weight loss in obese diabetic and non-diabetic individuals and long-term diabetes outcomes–a systematic review. Diabetes Obes Metab. 2004 Mar;6(2):85-94.
[116] Roberts SB , Pittas AG . The role of glycemic index in type 2 diabetes . Nutr Clin Care. 2003 May-Sep;6(2):73-8.
[117] McKeown NM . Whole grain intake and insulin sensitivity: evidence from observational studies . Nutr Rev. 2004 Jul;62(7 Pt 1):286-91.]
[118] Pereira MA , Jacobs DR , Jr., Pins JJ, et al. Effect of whole grains on insulin sensitivity in overweight hyperinsulinemic adults. Am J Clin Nutr. 2002;75(5):848-855
[119] McKeown NM, Meigs JB, Liu S, Wilson PW, Jacques PF. Whole-grain intake is favorably associated with metabolic risk factors for type 2 diabetes and cardiovascular disease in the Framingham Offspring Study . Am J Clin Nutr. 2002;76(2):390-398.
[120] Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care. 1997;20(4):545-550.
[121] Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL , Willett WC. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women . Jama. 1997;277(6):472-477.
[122] Schulze MB, Liu S, Rimm EB, Manson JE, Willett WC, Hu FB. Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women . Am J Clin Nutr. 2004 Aug;80(2):348-56.
[123] Hodge AM, English DR, O’Dea K, Giles GG. Glycemic index and dietary fiber and the risk of type 2 diabetes. Diabetes Care. 2004 Nov;27(11):2701-6.
[124] Jenkins D. Starchy foods and glycemic index. Diabetes Care 1988; 11:149–59