Nutrition 331 Nutrition for Health

Study Guide

Unit 11: Introduction to Chronic Diseases of Lifestyle, Obesity, and Diabetes

Introduction

In Canada and other affluent countries, some health problems such as cancer, diabetes, heart disease, and obesity are so common, it is hard to imagine a community or country with low rates of these conditions. However, barely 100 years ago during the First World War, a physician could graduate from medical school without ever having seen a case of coronary heart disease or lung cancer!

In this unit, we will explore the relationship between affluent lifestyles in developed countries and chronic diseases and negative health conditions. Then we will explore a major cause of and contributor to chronic diseases of lifestyle—excess weight and obesity. Finally, we will discuss type 2 diabetes.

Chronic, lifestyle-related diseases have been known by different names, including Western diseases and non-communicable diseases. In this unit, we will use the most common name: chronic diseases of lifestyle.

Objectives

After completing this unit, you should be able to

1. identify and discuss chronic diseases associated with affluent lifestyles in developed countries, including the roles of lifestyle and genetics.
2. discuss evidence from historical and population studies on the roles of lifestyle and genetics in the development of chronic diseases of lifestyle and discuss the limitations of these studies.
3. discuss obesity trends and the factors contributing to obesity in Canada, including overeating and the roles of fat, sugar, and fibre.
4. discuss the health risks associated with obesity.
5. discuss the three main strategies that promote healthy weight loss, including the dietary strategies.
6. discuss the roles of fibre, overweight or obesity, and exercise in causing or preventing type 2 diabetes.
7. describe the glycemic index and glycemic response and their roles in type 2 diabetes; identify foods with higher and lower glycemic indices.

Section 1: Causes of Chronic Diseases of Lifestyle

Chronic diseases of lifestyle (CDL) are long-term health problems caused by unhealthy lifestyle choices in areas such as diet, exercise, or substance use (tobacco, alcohol, etc.). The causes of death (mortality) tell part of the story of CDL. Studying Canadians who live with chronic diseases (morbidity) is also useful. The major nutrition concerns observed in many Canadians are diets too high in trans fats, sodium, and calories and too low in dietary fibre. This leads to metabolic diseases such as metabolic syndrome, type 2 diabetes, gallstones, and osteoporosis; cardiovascular diseases (CVD) such as atherosclerosis, heart attack, angina, and heart arrhythmias; and gastrointestinal disorders including constipation, hiatus hernia, appendicitis, diverticular diseases, and hemorrhoids.

Table 11.1: Leading causes of death in Canadians. Adapted from Leading Causes of Death in Canadians, 2011 (Statistics Canada, 2015)

As you can see from Table 11.1, cardiovascular diseases (heart disease plus stroke) cause about 25.2 percent of all deaths in Canada. However, cancer is the single largest cause of death. Of cancer deaths in men, the following are the leading types: lung (28.3% of all cancer deaths), colon (12.5%), prostate (10.2%), and pancreas (4.7%). The leading types of cancer death for women are lung (26.7% of all cancer deaths), breast (14.4%), colon (11.1%), and pancreas (5.6%) (Canadian Cancer Society, 2011).

While genetics has some influence on the development of CDL, an unhealthy environment where overeating and underexercising are the norm allows the genes for obesity, type 2 diabetes, heart disease, and cancers to be expressed. There is an enormous weight of research evidence that supports this statement. The following cases represent a few examples.

Historical epidemiological studies offer clues about the causes of some CDL. During World War II, several European countries had widespread food shortages, especially for foods of animal origin (eggs, meat, cheese). This food shortage was followed by pronounced drops in the incidences of chronic diseases, including CHD and type 2 diabetes, as well as dental cavities and appendicitis. People ate proportionately more grain products and vegetables than before. In Britain, the only bread sold was whole wheat bread. Meat, sugar, and butter were rationed. After the war ended, disease rates climbed again as these items became more plentiful.

China is an excellent example of the influence of lifestyle on rates of diseases. Chinese people are purchasing more animal foods, more fast food, more restaurant food, and fewer cereals. Fat intakes jumped from 19 percent of calories from fat (1989) to 27 percent of calories (1997). At the same time, physical activity in the workplace declined. In recent years, these dietary changes have been followed by a dramatic surge in rates of overweight and obesity (Popkin, 2010).

In developing countries, the emergence of CDL follows a consistent pattern as the average income increases. Obesity and dental cavities appear fairly quickly; type 2 diabetes after about 20 years; and CHD after about 30 years.

Studies of migrants also support the significance of lifestyle choices relative to genetics. A well-documented case is that of Japanese migrants to Hawaii and California. Since arriving in the early part of the twentieth century, they adopted the lifestyle of their new home. Subsequently, their disease pattern shifted from a Japanese pattern to an American one, featuring a dramatic rise in colon and breast cancer and a sharp decline in stomach cancer (very common in Japan) (Dunn, 1975; Robertson et al., 1977).

The health problems of people from South Asia also shift when they emigrate to Europe or North America. In affluent countries, their caloric intake increases and their physical activity decreases. This lifestyle, along with a genetic predisposition to insulin resistance (discussed later in this unit), translates into higher rates of type 2 diabetes. Canadians with South Asian roots also have higher rates of CHD than Canadians of European descent (Sheth et al., 1999).

These historic and population studies are important clues to sorting out genetic versus lifestyle influences on chronic disease rates. Recall from our discussion in Unit 2 that confounding variables must also be considered in epidemiological research. While we are presenting the argument for lifestyle choices that lead to chronic diseases, it is possible that confounding variables not explored in the research are responsible for increases in CDL. For example, watching television could be a confounding factor in epidemiological studies on affluent populations.

Based on these diverse lines of evidence, we can conclude that CDL are closely associated with a Western lifestyle. The major conditions linked to a Western lifestyle are as follows:

• cardiovascular diseases (heart disease plus stroke)
• obesity
• type 2 diabetes
• several types of cancer (lung, colon, and breast)
• gallstones
• osteoporosis
• several gastrointestinal conditions (such as constipation, diverticular disease, and hemorrhoids)

We can therefore state confidently that the dominant causes of the above conditions are diet, smoking, and lack of exercise, though the relative importance of each of these factors varies greatly from one condition to the next.

Several common chronic diseases are not included here as they are not clearly associated with the Western lifestyle. These diseases include type 1 diabetes and cancer of the prostate and pancreas.

While we often discuss the prevention of CDL, risk reduction or lower-risk lifestyle are more applicable terms. Prevention implies that a disease will never develop—something that cannot be guaranteed for a chronic disease. Another view of prevention is that it delays the onset of a disease by years or even decades. For example, someone with a family history of type 2 diabetes (genetic predisposition) may delay its onset by 10 to 20 years by adopting a healthy lifestyle. This represents quite an improvement in quality of life. Risk reduction adds both years to life and life to years.

Section 2: Health Consequences of Obesity

“They are as sick that surfeit with too much as they that starve with nothing.”
—Shakespeare, The Merchant of Venice (act 1, scene 2)

Like people in much of the world, Canadians are facing an epidemic of obesity. We are growing into a nation of fat people, living in an environment that supports overeating and limited physical activity. Figure 9-1: The Increasing Prevalence of Obesity among Canadian Adults (2000–2014) (p. 371) shows the rise in prevalence of obesity in Canada from 2000 to 2014.

Health professionals recognize that overweight and obesity contribute to or aggravate many health problems. The disorders most closely associated with being overweight are gallstones, diabetes, and hypertension. Overweight is a common precursor of stroke, almost certainly because of its effect on blood pressure. Other conditions more common in overweight people than in those of a healthy weight are kidney stones, infertility (in women), varicose veins, gout, respiratory problems, arthritis, rheumatism, and backache. Extra weight also increases the risk for certain cancers, notably those of the gallbladder, colon, and uterus, and in post-menopausal women, breast. Obesity is clearly linked to heart disease, mainly because of its association with increases in both blood pressure and blood cholesterol. Obesity also increases a person’s risk of accidents and carries social disadvantages.

In Unit 8, we discussed evidence for fat distribution patterns as a health risk indicator. Abdominal fat poses a greater risk to health than fat on the hips or extremities. A larger waist circumference poses a greater health risk than a smaller one.

Section 3: Causes of Obesity

The control of eating is quite complex and it involves psychological, cultural, and behavioural factors.

Many factors contribute to increasing obesity rates. Canadians are exposed to an environment fraught with labour-saving devices, reliance on vehicles, large restaurant meals or fast food meals, and the availability of food and snacks virtually anywhere in an urban setting.

Another factor that contributes to the current epidemic of obesity is portion sizes. Over the last few decades, portion sizes have grown considerably. Bottles of cola are now far larger than was usual in the 1950s. Movie theatres sell jumbo-sized containers of popcorn. Dinner plates are significantly larger than they were 40 years ago. One expression says it all: Supersize it.

This section discusses the reasons why low-fibre, high-sugar, and high-fat diets contribute to excessive caloric intakes and therefore, obesity. The discussion focuses on adults, although similar problems are observed in children and teens. Note that hormonal causes of obesity (e.g., hypothyroidism or polycystic ovarian disease) account for a very small percentage of obese individuals. Overconsumption of foods and inadequate activity levels account for the vast majority of people who are overweight or obese.

A strong clue to the cause of obesity is its worldwide distribution pattern. Obesity is a disease that appears when people adopt an affluent lifestyle. The pattern of development demonstrates that lifestyle, not genetics, is the true cause. If genetics were the true cause, then obesity would be associated with all lifestyles. Nevertheless, like other chronic diseases, obesity runs in families, a fact that indicates a genetic susceptibility.

The significance of lifestyle over genetics to the development of obesity is supported by studies on animals. In the wild, animals do not become obese.

Deer and rabbits do not overeat vegetation and become fat. Lions do not overeat their prey. Animals become obese only when they are fed an unnatural diet.

The key aspect of an affluent lifestyle that is responsible for the development of obesity is diet rather than inactivity. Animals in the wild are often quite sedentary. Lions, for example, spend only a small part of their day hunting, providing game is plentiful. Similarly, animals in captivity maintain normal weight when fed their natural diets but may become obese on unnatural diets. Household pets often demonstrate this correlation. This argument does not dismiss the role of inactivity, however—quite the opposite. Many studies have indicated that overweight people, especially children, exercise less rather than eat more than those of normal weight. Nevertheless, population and animal studies strongly indicate that inactivity does not cause overweight in absence of a modern diet. Once such a diet is available, everyone becomes vulnerable to overweight. Who actually becomes overweight is then influenced by such factors as genes and exercise.

Humans and animals have a remarkable system for regulating the appetite. The following example indicates just how accurate this system is. If a man who normally eats 2500 kilocalories per day had an error in his appetite and overconsumed by a mere 1 percent, he could accumulate 25 pounds of fat in a decade. In actual fact, people in non-developed countries eating a traditional diet are able to maintain a stable weight for decades. The question we need to ask is this: What causes this system to break down on a modern diet? In this section, we will focus on three aspects of the modern diet (dietary fibre, sugar, and fat) and on the satiety they provide. To review the definition of satiety, see page 167 of the eText.

Dietary Fibre and Obesity

The refining of carbohydrate-rich foods, such as cereals, results in products that are low in fibre. This lack of fibre is thought to encourage overconsumption of energy. First, refined foods are easier and faster to eat than unrefined foods. Second, consumption of refined foods produces less satiety (appetite satisfaction) than unrefined carbohydrates.

The importance of fibre can be further illustrated by comparing whole wheat and white bread. The latter needs less chewing, is more quickly eaten, and produces much less satiation. Each of these differences, particularly the question of satiation, makes it easy to see why white bread is easy to overeat. Try making this comparison yourself.

Intervention studies indicate that adding dietary fibre to the diet reduces energy intake. Moreover, epidemiological evidence shows that people who consume more fibre are less likely to gain weight and become obese than people who consume less fibre (Slavin, 2005).

Sugar and Obesity

Table sugar is a carbohydrate food that is so highly refined that all its fibre has been removed. Its consumption inevitably means a reduced daily intake of fibre. Sugar can therefore be seen as the nutritional opposite of fibre.

Compare a slice of whole wheat bread and 170 millilitres (6 oz.) of a soft drink (about half a can). Each contains 70 kilocalories. The soft drink can be swallowed in seconds and provides minimal satiation. The differences in speed of consumption between a soft drink and whole wheat bread is much greater than the differences between white bread and whole wheat bread.

It is therefore predictable that sugar will induce an increased energy intake. This relationship has been demonstrated in various studies (Malik et al., 2013; Te Morenga et al., 2014). In some experiments, subjects were fed soft drinks sweetened either with sugar or synthetic sweetener. Soft drinks sweetened with sugar lead to higher energy intake and more weight gain. Likewise, when people reduce their intake of these drinks, some weight loss is often seen. Cohort studies are consistent with these findings: people who drink more sugar-sweetened drinks tend to gain more weight.

Fat and Obesity

The view has been widespread for many years that the Western diet contains an excessive amount of fat and that this is a major cause of obesity. However, the evidence concerning the relationship between dietary fat and obesity is far from clear. Considerations of human metabolism point to a good reason why fat may be fattening: converting dietary fat to body fat uses only 3 percent of the ingested energy. By contrast, converting dietary carbohydrate to body fat requires an energy expenditure of 23 percent of energy intake. Studies on experimental studies (rats and mice) have repeatedly demonstrated that a high-fat diet induces obesity. But there is no solid evidence that what happens to rats and mice also happens with humans. Do foods rich in fat induce excessive energy intake in humans and hence weight gain? Our most reliable evidence on this question comes from long-term cohort studies and these show little association between the fat in a person’s diet and their risk of weight gain (Mozaffarian, 2016). For example, milk, both low fat and whole, has little association with weight gain. Nuts are a high-fat food but have no association with increased risk of weight gain.

But there is one major argument in support of a role for dietary fat in causing excessive weight gain. Foods with concentrated energy (more calories per gram) have less satiating power and are therefore more likely to be consumed in excess (Drewnowski, 1998). Fat has more than twice as many calories per gram than either protein or carbohydrate; that is, fat-rich foods tend to be energy dense. The eText discusses energy density (final paragraph on p. 400 to first paragraph on p. 402).

We can illustrate the importance of this by comparing the following foods. Fruit and soup have high water content and therefore low energy density. For example, an apple provides 70 kilocalories while a bowl of tomato-vegetable soup (250 mL) has only 55 kilocalories. By contrast, pizza consists mainly of fat and carbohydrate but with little water; a slice of pizza delivers 250 kilocalories. The energy-dense food (pizza) facilitates a large energy intake before the appetite has been satiated, whereas foods with a low energy density, such as apples and soup, will create a feeling of fullness after relatively little energy has been consumed. To burn the 250 kilocalories from a slice of pizza requires a 70-kilogram person to walk about 4.5 kilometres.

Knowing which foods are higher or lower in fat and sugar will guide most people in estimating which foods have a high or low energy density. Calculations are not necessary. In short, no one ever became overweight by eating too many carrots or by drinking too much tomato juice!

Just as high-fibre and low-fat intakes are two sides of the same coin in decreasing energy intake, high-sugar and high-fat intakes work synergistically to increase energy intake. This relationship was described well in a letter to the medical journal Lancet (Bradley, 1993):

The author also points out that foods commonly used to induce obesity in animals are high in sugar and fat; for example, chocolate chip cookies.

In conclusion, the exact role of fat in causing obesity is still not clear. While foods with a high energy density (which often means high in fat) seem to induce an excessive energy intake, there is little strong evidence that the fat content of food is directly related to long-term weight gain.

Section 4: Treatment of Obesity

A waist is a terrible thing to mind.

As discussed in Unit 8, it is easy to advise people to eat less and exercise more, but it is much more complex to implement this advice successfully. Weight-loss treatments have a very low success rate: most people who try to lose weight fail, and most who succeed, regain it. The old saying, “An ounce of prevention is worth a pound of cure,” is especially true with respect to obesity.

This section addresses strategies for eating a healthy diet that promotes weight loss, summarizes why physical activity is a key component in a weight-loss strategy, and discusses behaviour modification. The behaviour modification section addresses some of the reasons why people select certain foods when eating for reasons other than nutrition.

Obesity should not be seen as a temporary problem but rather as a lifestyle disease. Adults who are successful at losing weight and maintaining weight loss realize that they have a lifelong health concern, much like people with type 1 diabetes or debilitating arthritis. Accordingly, they realize that permanent changes in lifestyle will be the solution. A permanent change in lifestyle not only helps individuals to lose excess weight, it also helps to prevent other chronic, obesity-related diseases.

The first component of a healthy weight-loss strategy is to lower caloric intake. A healthy weight-loss diet will be based on Canada’s Food Guide and will meet the DRIs for vitamins and minerals. Foods should be chosen to counteract the primary causes of obesity: too much fat and sugar and too little fibre. The eText, pages 397–402, describes many strategies that can be helpful for choosing appropriate foods and portion sizes. It suggests 1200 kilocalories (Table 9-9, p. 399) as a minimum reasonable number of calories per day. Note that diets providing fewer than 1600 kilocalories per day may be inadequate in nutrients such as iron, zinc, folate, vitamin E, calcium, and vitamin D. A diet with fewer than 1600 kilocalories per day should be planned by a dietitian.

The second important component of healthy weight loss is exercise. Studies have generally demonstrated that people who incorporate exercise as part of a weight-loss program are more successful than non-exercisers. Exercise helps in weight loss by burning calories, speeding up metabolism, and reducing stress (people often eat inappropriately in relation to stress); exercise may also help with appetite control (see pp. 402–404).

The third main component, behaviour modification, addresses feelings and emotions that may contribute to overeating and considers when and why an individual is eating. In brief, behaviour modification seeks to change cues that may lead to overeating. For example, if a person observes that they eat most of their high-calorie foods while watching television, they may choose to eat food only at the kitchen table (presuming that isn’t where they watch television). Other behavioural triggers and possible solutions are discussed on pages 409–411. (You will not be tested on this section.)

There are many commercially available treatments for obesity. Some are safe and effective. However, many are not. Treatments that are unsafe, ineffective, or both are regularly advertised in the press. Books on weight loss frequently become bestsellers. Criteria for evaluating weight-reduction diets are listed in Table 9-9: Rating Sound and Unsound Weight-Loss Schemes (p. 399, optional).

As the eText indicates, the dramatic weight loss that occurs early in fasting or in quick-weight-loss schemes, such as low-carbohydrate diets or fasting, results primarily from loss of lean tissues, glycogen, and water (pp. 391–393). At best, only a minor portion of the weight lost is fat. These diets have a low long-term success rate, one reason being that eliminating carbohydrate sources in the diet eliminates most foods (e.g., fruit, vegetables, bread, and cereals). The diets are therefore monotonous and often bring a feeling of deprivation. Dieters tend to binge often on foods undesirable for weight control. Once eating is resumed, water weight is soon regained as glycogen stores are replenished.

Although many studies have been carried out to investigate which diet produces the best weight-loss results (low carbohydrate, low fat, high protein), we still do not have a clear answer. Indeed, there is little evidence that one diet has any significant advantage diet over another (Freedhoff & Hall, 2016). It is especially noteworthy that there is little evidence that a low-fat diet has any advantage (Tobias et al., 2015). In one especially informative, two-year study, overweight subjects were fed diets with widely varying amounts of fat (20% vs. 40%), protein (15% vs. 25%), or carbohydrate (35% vs. 65%) (Sacks et al., 2009). The investigators saw no evidence that varying the amounts of macronutrients had an appreciable effect on weight loss. What they did observe was that the persons who attended most sessions were the ones who achieved the most weight loss. While the average subject had lost 4 kilograms after two years, those who attended at least two-thirds of the sessions lost 9 kilograms. The investigators interpret this to mean that subjects who were well motivated to lose weight (as indicated by turning up for most sessions) were most successful. In other words, while weight-loss efforts have a poor rate of success, some people do achieve long-term success. What are their secrets?

The National Weight Control Registry (USA) collects information on more than 4000 adults who have lost at least 13.6 kilograms and kept it off for at least one year (Wing & Phelan, 2005). The members have lost an average of 33 kilograms each and have maintained the minimum weight loss (13.6 kg) for an average of more than five years. These people therefore represent the small minority who have both lost weight and kept it off. Members report engaging in high levels of physical activity (approximately one hour per day), eating a low-calorie and low-fat diet, eating breakfast regularly, self-monitoring weight, and maintaining a consistent eating pattern across weekdays and weekends. Moreover, weight-loss maintenance may get easier over time; after individuals have successfully maintained their weight loss for two to five years, the chance of longer-term success greatly increases.

A safe, manageable goal for weight loss is to reduce energy intake and increase exercise enough to lose 0.5 to 1 kilogram (1 to 2 lb) per week. This requires a calorie deficit of 500 to 1000 kilocalories per day. Rapid weight loss can be dangerous to health. Many low energy diets are nutritionally unbalanced and unsafe. Diets too low in energy can also cause a loss of lean tissue, especially muscle.

The root causes of obesity can be summarized as a hyperactive fork and hypoactive feet. The solution is to change these lifestyle factors.

Obesity: A Summary

Despite decades of intensive research, it is clear that there is still a great deal to be learned on the subject of obesity. But some things are perfectly clear. First, obesity is a preventable disease. Treatment of overweight and obesity has a low success rate, which highlights the vital importance of prevention of excess weight gain as the dominant goal. This can be accomplished by a lifestyle that includes adequate exercise and a healthy diet. The diet should centre on foods that have a high fibre content and a low energy density, especially fruit, vegetables, and whole grains. Intake of foods rich in sugar, such as cola drinks, should be limited, as should large food portions. There is only weak evidence that the fat content of the diet plays a major role in the causation of obesity.

As stressed in the e-Text (p. 394), when an obese person loses even a modest degree of weight, say 2.5 to 5 kilograms, this may be enough to bring about significant improvements in both their health and quality of life. Unfortunately, obese persons often have unrealistic expectations of the degree of weight loss that can be achieved and are often disappointed when they fail to reach their dream weight.

Section 5: The Causes of Diabetes

Diabetes (or diabetes mellitus as it is more properly known) appears in three types. Type 1 usually first begins in childhood or young adulthood. Type 2 is most common in the middle-aged and elderly. In the 1990s, health professionals started to diagnose type 2 diabetes in adolescents. This worrisome development will have many implications on our health system. Obesity is a major risk factor for type 2 diabetes: 80 percent of sufferers are obese. The third type of diabetes is gestational diabetes (diabetes during pregnancy), which is attributable to weight gain and pregnancy hormone levels. In this unit, we are concerned almost exclusively with type 2. This disease is especially common in people of North American Indigenous origin.

Type 1 diabetes is a disease in which the pancreas loses its ability to produce insulin. The insulin must therefore be delivered by injection once or twice daily. In type 2 diabetes, on the other hand, the pancreas is usually functioning well, but the tissues, such as visceral fat, are insulin resistant. Consequently, the pancreas must produce above normal amounts of insulin to control the blood glucose. Even then, there may still be severe hyperglycemia. After many years of hyperinsulinemia, the pancreas seems to lose its ability to produce sufficient insulin. The disease then truly resembles type 1 diabetes, and the sufferer may need insulin injections.

The most important recognized causes of insulin resistance are overweight (especially if there is a large waist circumference) and lack of exercise.

The exact means by which type 2 diabetes develops is not properly understood. One important factor is probably rapid digestion and absorption of starch. As a result, the blood glucose climbs too high too quickly; this rapid increase provokes the pancreas to oversecrete insulin, thereby causing postprandial hyperinsulinemia (i.e., high levels of blood insulin following a meal). Over time, the body adapts to these bouts of hyperinsulinemia by becoming insulin resistant. The eText describes an alternative explanation for hyperinsulinemia, which is based on the body’s inability to use insulin efficiently (Figure 4‑14, p. 140). In either case, an early sign that a person is on the road to diabetes is impaired glucose tolerance.

An important factor that allows starch and sugar to be rapidly digested and absorbed is lack of dietary fibre (Heaton, 1994). In clinical trials, viscous fibre has proven to be the type of fibre best at preventing an excessive rise in blood glucose and insulin. Fibre affects blood sugar positively because it slows the digestion and absorption of glucose from the small intestine.

Epidemiological cohort studies have strengthened the view that fibre plays an important role in diabetes. For example, in one study, 36 000 women were observed over the course of six years. During this time, 1140 of the women developed diabetes. Women with a relatively high intake of fibre demonstrated about 21 percent lower risk of developing diabetes than did women with a low fibre intake. The protective associations were stronger for cereal fibre (primarily nonviscous wheat fibre) than for other types of fibre (Meyer et al., 2000). This is a surprising discovery about type 2 diabetes. While we would expect viscous fibre to be the fibre type most potent at preventing the disease, cohort studies consistently show that cereal fibre is most protective (Temple & Steyn, 2012).

Another important dietary factor linked to an increased risk of diabetes is intake of sugar-sweetened beverages (Malik et al., 2010).

The glycemic index (GI) is a ranking measure of the rise in blood glucose caused by different foods (see pp. 136–137). As you can see in Figure 4-13: Glycemic Index of Selected Foods (p. 136), legumes have a low GI, producing about one-third to one-half the rise in blood glucose of white bread. Fruits have an intermediate GI ranking. Foods with a high GI include instant rice, baked or mashed potatoes, and cornflakes. It is also noteworthy that cereals are digested more rapidly—and evoke a greater insulin response—if finely milled than if coarsely ground. Some, but not all, low GI foods are high in fibre.

The relationship of GI to hyperinsulinemia and, ultimately, type 2 diabetes is still being investigated. However, research in recent years has added credibility to the view that a diet rich in foods with a high GI leads to high blood insulin levels and insulin resistance, setting the stage for diabetes. Evidence also suggests that foods with a high GI may be a factor in obesity (by inducing overeating) and heart disease (by increasing blood lipids) (Ludwig, 2002).

While research studies have strongly suggested that the GI of the diet is correlated with the risk of diabetes and heart disease, whether GI is of practical value in diet planning is quite controversial. The eText explains this well on pages 136–137.

Intervention studies have been conducted in which subjects with impaired glucose tolerance (i.e., predisposed to diabetes) were given preventive treatment in the form of lifestyle therapy for weight loss, more exercise, and a healthier diet (more fibre, less fat). These studies reported a 40 to 50 percent drop in the proportion of subjects becoming diabetics (Temple & Steyn, 2012).

In summary, the four key factors that determine the risk of type 2 diabetes are overweight/obesity, exercise, sugar-sweetened beverages, and fibre intake. Other factors such as the relative ingestion of foods high on the glycemic index and foods high in saturated fats may also contribute to one’s risk for the disease.