Chapter 5 - Carbohydrates.docx

Chapter 5: Carbohydrates Carbohydrates are organic molecules whose primary role is to provide energy. There are three main types of car- bohydrates: sugars, starches and fibres. The word carbohydrate tells us the three atoms that make up these nutrients – carbon (carbo) and hydrogen and oxygen (hydr...

Chapter 5: Carbohydrates Carbohydrates are organic molecules whose primary role is to provide energy. There are three main types of car- bohydrates: sugars, starches and fibres. The word carbohydrate tells us the three atoms that make up these nutrients – carbon (carbo) and hydrogen and oxygen (hydrate). These atoms bond to form ring-like structures called saccharides, or sugars. These saccharides can then from single-, double- or multiple-unit chains. A carbohydrate’s structure affects how quickly it is digested and absorbed, as well as its impacts on health. By the end of this chapter, you will be able to: Outline the structure and function of different carbohydrates. Differentiate between refined and unrefined carbohydrates. Outline how carbohydrates are digested and absorbed. Give an overview of diabetes and outline its symptoms, risk factors and treatment. Give an overview of the roles of carbohydrates in both health and disease. All carbohydrates are made up of monosaccharides, or single sugars. Carbohydrates vary in the types and num- ber of monosaccharides they have in their structure. Unlike other carbohydrates, fibre has monosaccharides bonded together in a way that humans cannot digest. The word sugar refers to molecules that have a single (monosaccharide) or double (disaccharide) unit of sugar in their structure. Sugars are found naturally in many foods including fruits and milk. These are known as intrinsic sugars. Sugars are also added to foods by the food industry to enhance the flavour of processed foods. These are known as extrinsic sugars or added sugars. Sugars are sweet tasting and absorbed quickly from foods. There are many monosaccharides. However, three main ones exist in the foods we eat (Figure 5.1). Glucose is the most common monosaccharide. It is the building block of most other longer carbohydrates like starch and fibre. It is also the main monosaccharide found in the blood. As such, the terms blood sugar and blood glucose are often used interchangeably. Glucose can fuel the needs of all cells in the body, including brain cells and red blood cells, which both have an absolute requirement for glucose. Glucose can be metabolized into ATP, the body’s main energy currency. Figure 5.1: Monosaccharides. Fructose is often referred to as fruit sugar because it is found in many fruits as well as some vegetables and honey. It is significantly sweeter than glucose and most other sugars. It is therefore added to a lot of processed foods in order to increase perceived sweetness. Galactose is often called milk sugar because it is found in milk. It is similar in sweetness to glucose. The three dietary monosaccharides just described are used to make up the three most common disaccharides in the diet: sucrose, maltose and lactose (Figure 5.2). Disaccharides are sugars with two monosaccharide units. Figure 5.2: Disaccharides. Sucrose, or table sugar, is what most people think of when they think of sugar. It is what we put in our coffee and use in baking. It is typically white or brown (Box 5.1). Sucrose is made up of a glucose molecule bound to a molecule of fructose. The enzyme sucrase breaks down sucrose into its respective two sugars, which can then be absorbed at the villi of the small intestine. Maltose, or malt sugar, is the reason bread tastes sweeter as it is chewed. One of the main nutrients found in bread is starch, which is formed from a long chain of glucose molecules. As the mouth’s enzymes break down longer starch chains, the sweet-tasting glucose-glucose disaccharide maltose is formed. Once in the small intestine, the enzyme maltase breaks down maltose into glucose molecules, which can then be absorbed. Lactose, or milk sugar, is the main sugar found in milk, which is why coffee tastes sweeter when milk is added. Lactose is composed of a glucose and a galactose molecule. Note that galactose is also referred to as milk sugar, howev- er, this term is most often used to refer to lactose. Some people lack the enzyme lactase that helps separate these two monosaccharides. This condition, known as lactose intolerance, will be discussed in more detail later. In addition to the intrinsic sugars originally found in certain foods, extrinsic sugars are also added in to improve the flavour of foods. Table 5.1 lists some of the various sugars and sugar sources that are added into foods. If an ingredi- ent from a whole food naturally has sugar in it (ex. apples), the sugar in this ingredient will not be listed separately on the label. Thus, only added sugars are listed on an ingredients list. Table 5.1: Types of added sugar. According to the new Canadian food labelling requirements, manufacturers must now list all types of sugars together under the sugar heading in the ingredi- ents list (Figure 5.3), meaning that the types and total sugar content are now displayed more prominently. Figure 5.3: Canada’s Healthy Eating Strategy mandates that Oligosaccharide have a few monosaccharides in their chains – between 3 and 10. The main oligosaccharides found in the diet are considered fibres because humans lack the enzymes needed to break them down. These are fruc- tooligosaccharides (FOSs) and galactooligosaccharides (GOSs) – both named based on the monosaccharides that make up their chains. While they cannot be broken down by enzymes in the small intestine, bacteria in the large intestine can ferment them. Accordingly, both are prebiotics because bacteria use them for food and growth. Polysaccharides are chains of monosaccharides greater than 10 units in length. We can further divide these into two categories – starches and fibre. The human body has enzymes that can break down starches but lacks those that break down fibre. Starch Starch is composed of long chains of glucose molecules in either a straight-chain (amylose) or branched-chain (amylopectin) formation (Figure 5.4). Amylopectin is the most common carbohydrate in the human diet. Most foods that contain starch have a greater degree of amylopectin than amylose. During digestion, starch is first broken down into oligosac- charides, then into disaccharides and eventually into the monosaccharide glucose, which is then absorbed. Accordingly, eating foods high in only starch increases blood sugar rapidly. Figure 5.4: Amylose and amylopectin. We get starch from eating plant foods. Photosynthesis allows plants to take carbon out of the atmosphere and incorporate it into glucose, which is then packaged into starch. When we eat plants, we get this starch as well as the fibre that is typically found in their outer casing. Compared to animal products, plants are more economical to grow and har- vest. Accordingly, starch is found in many staple foods such as potatoes, rice, maize, corn and wheat. Dietary fibre is a collective term for plant substances such as cellulose, dextrin and inulin that human enzymes cannot break down. These carbohydrates are mainly in the rougher parts of plants, such as their outer casing. Vegeta- bles, fruits, whole grains and legumes are all good sources of fibre. Animal products do not contain fibre; it is only found in plant products. Like starch, fibre is composed of long chains of glucose molecules. However, the bonds that hold adjacent glu- cose molecules together in fibre are different than those in starch and the human body lacks the enzymes needed to break these bonds (Figure 5.5). Accordingly, these fibres reach the large intestine predominantly undigested. Here, bacte- ria can ferment certain fibres into short-chain fatty acids. These short-chain fatty acids are then absorbed and contribute to our energy intake. Even though fibres are predominantly composed of glucose, fibre is not a source of glucose to the body. Instead, it is potentially a source of short chain fatty acids. Whether fibre can or cannot be fermented into short chain fatty acids primarily depends on whether it is soluble or insoluble fibre. Figure 5.5: Amylose vs. fibre. Soluble fibre dissolves in water to form a gelatinous solution, which adds bulk and viscosity to ingested food. Oats, apples, beans, peas, citrus fruits, barley and psyllium are all good sources of soluble fibre. Bacteria in the large intestine can ferment soluble fibre to produce short-chain fatty acids (Figure 5.6). Each gram of soluble fibre provides around 2–3 kcal of energy. Soluble fibre consumption may improve cardiovascular health. Indeed, consumption of sol- uble fibre is associated with a decrease in blood glucose. It also helps to trap cholesterol-containing compounds in the body and is associated with a decrease in total cholesterol in the blood (McRae, 2017). Figure 5.6: Bacterial fermentation of fibre. Insoluble fibre does not dissolve readily in water and is best known for its ability to facilitate the passage of food material through the digestive track. This contributes to the health of the digestive system. High sources of insoluble fibre include wheat, bran and beans, as well as various vegetables such as potatoes and cauliflower. Insoluble fibre is not fermented by bacteria in the large intestine and passes through the digestive tract mostly unchanged. Glycogen, like amylose, is a large, unbranched chain of glucose units. Unlike amylose, it is found in negligible amounts in the human diet. In the body, we make glycogen by synthesizing chains of glucose molecules with the aim of storing them. Small pockets of glycogen are found around our liver and our muscle (Figure 5.7). This reservoir provides a quick source of glucose when needed. Maximum glycogen storage capacity is around 15 g/kg body weight (Acheson et al., 1988). In a 70-kg person, that equates to around 1050 g, or about 1 kg of stored carbohydrate. Converse- ly, our fat cells have the theoretical potential to store hundreds of kilograms. Thus, fat is our main long-term energy storage location. Figure 5.7: Glycogen stores. Foods that are high in carbohydrates, such as grains, are sold either refined or unrefined. Unrefined sources of carbohydrates are those consumed in their entire form; the main edible parts of the plant have not been changed or removed (Figure 5.8). These are often called whole sources, such as whole grain wheat and whole grain oats. Conversely, refined sources of carbohydrates have part of the plant – typically the bran and germ layer – removed. This usually low- ers the nutrient density of that plant. Figure 5.8: Parts of a whole grain. In our food system, wheat is found in both its whole form and its refined form. When we eat whole or unrefined wheat, we are getting all the main parts of the grain, including the bran, endosperm and germ. The bran layer is the outer, waxy cover on the grain. It tends to be high in fibre and has calcium, iron and B vitamins. Most of the grain is the endosperm layer. It is mainly composed of starch and tends to be lower in other nutrients. The germ layer, or embryo, is the smaller inner part of the grain. It has the highest protein content of the three. It also contains more fibre than the endosperm, as well as B vitamins and vitamin E. A diet that is higher in refined grains tends to be lower in fibre and phytochemicals and therefore lacks their associated benefits. Canada’s Food Guide recommends checking the ingredients list for the words whole grain followed by the grain’s name (Health Canada, 2019). Note that whole wheat is not the same as whole grain wheat; it is not fully whole grain. However, it still contains more fibre than a more refined grain. The stages of carbohydrate digestion are outlined in Figure 5.9. Only a small percentage (5–10%) of carbohydrate digestion occurs in the mouth. Salivary amylase begins the digestion of starch by breaking down amylose and amylopec- tin into maltose and glucose. Accordingly, the more we chew a starch, the sweeter it might seem. A small amount of car- bohydrate is absorbed orally, but most moves on to the esophagus. The esophagus does not secrete any carbohydrate-di- gesting enzymes, so no active digestion occurs here. However, the amylase that was secreted by the mouth continues to act on the starch. Figure 5.9: Carbohydrate digestion. Since amylase is sensitive to high acidity, it is inactivated in the stomach, where there are no carbohydrate-di- gesting enzymes to take up its role. There is therefore no chemical digestion of carbohydrate in the stomach. Most carbohydrate digestion occurs in the small intestine. Once carbohydrates are detected here, the hormone cholecystokinin (CCK) is released from duodenum cells. This hormone acts on receptors in the pancreas to promote the release of pancreatic juice into the small intestine. Pancreatic juice contains pancreatic amylase, which further digests starch into shorter and shorter saccharide chains. The microvilli provide another source of carbohydrate-digesting enzymes. Recall that these very tiny finger-like projections on the membranes of intestinal cells are collectively referred to as the brush border. The brush border con- tains an essential set of carbohydrate-digesting enzymes that are released by intestinal cells to finish off the digesting job that the amylases started. Lactase, maltase and sucrase, which respectively break down lactose, maltose, and sucrose are all brush border enzymes. These enzymes are conveniently located within the cells that line the villi of the small in- testine, so once carbohydrates have been digested into monosaccharides they can then be absorbed immediately (Figure 5.10). Some individuals have a compromised secretion of lactase, leading to a condition known as lactose intolerance (Box 5.2). Figure 5.10: Digestion and absorption of carbohydrates at the small intestine villi. Glucose, fructose and galactose are absorbed across the walls of small intestine cells into blood capillaries. They then go to the liver, where fructose and galactose are metabolized. Some glucose is also stored in the liver as glycogen. Since glucose is not metabolized in the liver, whatever is not stored as glycogen enters the general circulation. This leads to an increase in blood glucose. Box 5.2: Carbohydrate digestion: lactose intolerance. Individuals who are lactose intolerant may experience symptoms such as cramps, bloating, diarrhea and pain in the abdomen when they consume the lactose found in milk products (Vesa et al., 2000). Lactose intolerance is caused by insufficient secretion of the brush border enzyme lactase. This leads to an inabil- ity to digest lactose and absorb its glucose and galactose components. These sugars pass on to the large intestine, where bacteria can ferment them. This process leads to the production of methane gas, which is responsible for many of the symptoms noted above. While the actual rates of lactose intolerance are unknown, approximately 16% of Canadians believe they have the condition (Barr, 2013). There is no cure for lactose intolerance, but symptoms can be limited by minimizing the consumption of lactose-containing milk products. There are several lactose-free dairy prod- ucts including lactose-free milk and ice cream. Butter, yogurt and cheese often have lower levels of lactose and may be tolerated well by those who have milder symptoms. Another option is to take lactase tablets. There are various options on the market, with varying degrees of lactose digestion. Too much stomach acid could inactivate the enzymes found in these tablets, so they tend to work more effectively in some people compared to others (O’Connell & Walsh, 2006). The glycemic response is the spike in blood glucose that follows a meal once glucose enters the general circula- tion (Figure 5.11). Diets that produce a lower glycemic response are associated with improved insulin sensitivity, lower body weight and may decrease the risk of diabetes, cardiovascular disease (CVD) and obesity (Livesey et al., 2008). Accordingly, Diabetes Canada recommends that individuals with both type 1 and type 2 diabetes choose foods that produce a lower glycemic response to help control blood sugar levels (Diabetes Canada, n.d.). The glycemic index and glycemic load can help us determine the glycemic response of foods. Figure 5.11: The glycemic response. The glycemic index (GI) was invented by Dr. Thomas Wolever and Dr David Jenkins at the University of Toronto to help people manage blood sugar levels. It is the relative ranking of a food’s potential to spike blood sugar on a 100-point scale. Pure sugar, glucose, is given a score of 100 as a benchmark. Low-GI foods score 55 or less, mid-GI foods score between 56 and 69 and high-GI foods score above 70 (Table 5.2). Individuals with diabetes may choose to consume more low GI foods to help them regulate their blood sugar. Table 5.2: Glycemic index of common foods. Compared to the glycemic index, glycemic load (GL) is believed to be a more accurate assessment of how much blood glucose will spike since it considers the food’s GI plus the actual amount of carbohydrate within the food. Some foods may have a high GI, but because the food contains low levels of carbohydrate, the GL is much lower. Watermelon illustrates the difference between GI and GL. The GI of watermelon is 72 – which makes it a high GI food. However, since a serving of watermelon contains only a small amount of carbohydrate, its glycemic load is 7. Low-GL foods score less than 10, moderate-GL foods score 10–20, and high-GL foods score above 20. Our bodies strive for glucose homeostasis, which is when there is neither too much nor too little glucose is in the blood. Low blood glucose levels result in a state known as hypoglycemia, in which an individual may experience tiredness, lethargy and irritability. Conversely, chronic hyperglycemia, or elevated blood sugar levels, can damage blood vessels and the kidneys and promote diabetes. There are two main hormones involved in regulating blood glucose level: insulin and glucagon. Both are secreted by the pancreas (Box 5.3). Box 5.3: The endocrine and exocrine pancreas. The pancreas has two very important yet very different functions. Dif- ferent cells and parts of the pancreas are involved in these two functions These are sometimes referred to as the pancreas’ exocrine and endo- crine roles. Exocrine means outside of the body and typically refers to secretions that occur into the digestive tract. The digestive tract is technically out- side of the body since it is a long tube that runs through us. In Chapter 3 we learned that the pancreas secretes enzyme-containing pancreatic juice into the small intestine. Pancreatic amylase, lipase and protease promote the digestion of carbohydrates, lipids and proteins, respectively. Endocrine refers to the secretion of substances into the bloodstream, specifically hormones. The secretion of the hormones insulin and gluca- gon into the blood to regulate blood glucose is the main endocrine role of the pancreas. Figure 5.12 summarizes how insulin regulates blood glucose levels. When blood glucose levels spike after a meal, insulin secretion from the pancreas also rises. Most cells require insulin in order to take up glucose from the bloodstream and into the cell. Once insulin allows glucose to enter the cell, blood glucose levels normalize. Once in the cell, glucose can then be stored, converted into fat or used for energy, depending on the body’s needs. Figure 5.12: Insulin lowers blood glucose levels. Insulin is like a key that unlocks a door allowing glucose to enter the cell. When insulin binds to its receptors on the cell surface, a response occurs that brings glucose transporters to the cell’s surface. These channels provide a pas- sage for glucose to enter the cell. If insulin cannot open this door, glucose remains in the blood and blood glucose levels remain high. This can occur if insulin is not being secreted (insulin deficiency) or if the cell’s response to insulin is compro- mised (insulin resistance). These are the hallmarks of type 1 and type 2 diabetes, respectively. When blood glucose levels are too low, the pancreas releases glucagon into the blood. This can occur during times of fasting. Glucagon increases blood glucose by promoting three main processes: Glycogenolysis: the conversion of glycogen to glucose. Gluconeogenesis: the conversion of certain amino acids into glucose. Lipolysis: the breakdown of stored lipids. Glycerol from triglycerides can then be used to make glucose. Carbohydrates have one main role in the body – to provide a source of energy. Glucose is the main carbohydrate in the body and is used as a source of energy by all body tissues. While some tissues can use fat for energy as well, the brain and red blood cells preferentially use glucose. In Chapter 3 we learned that cells can metabolize glucose and cap- ture its energy as ATP. ATP can then be used to fuel the needs of that cell. Since our bodies preferentially use glucose for energy, if we do not consume enough carbohydrates in the diet, we must get glucose from somewhere else. Certain amino acids are used to make glucose through gluconeogenesis. However, this leads to the breakdown of body protein to provide these amino acids. This can occur during periods of carbohydrate and/or caloric restriction. Getting enough carbohydrates in the diet spares this from happening and helps maintain protein in tissues such as the muscles. Carbohydrates are involved in the metabolism of lipids. Recall that the metabolism of the glycerol and fatty acids that make up a triglyceride molecule leads to the production of acetyl CoA. Acetyl CoA can only enter the next stage, the citric acid cycle, if there is enough oxaloacetate present. Sufficient carbohydrate is required to maintain oxaloacetate lev- els. This concept is referred to as fat burning in a carbohydrate flame. A high-fat, low-carbohydrate diet will not provide enough carbohydrates to metabolize fats this way. Instead, acetyl-CoA is used to form molecules called ketone bodies, which are used to fuel the body’s needs. These will be discussed in greater depth in Chapter 6. Throughout the day, our blood glucose fluctuates based on how much we have eaten and how much we have used up energy. Our bodies work hard to make sure these fluctuations are short and that an adequate amount of blood glucose is maintained. Diabetes is a disease characterized by chronically elevated blood glucose levels, due to the body’s inability to regulate them. Elevated blood glucose levels can have a wide range of negative health effects. In the acute, or earlier, stages of diabetes a range of symptoms are seen. These are outlined in Figure 5.13a. Figure 5.13: Symptoms of diabetes. In later stages, diabetes negatively effects several important body structures and functions and increases mor- tality rate (Figure 5.14b). In 2017, diabetes ranked seventh in the leading causes of death in Canada (Statistics Canada, 2018). The high mortality rate seen in diabetes is related to its tendency to increase risk of CVD (Matheus et al., 2013). The link between these two diseases is two-fold. First, diabetes and CVD share many common risk factors such as obesity, high blood pressure and irregular blood lipids. Secondly, diabetes may itself have negative effects on the cardiovascular system, for instance by promoting cardiomyopathy, a condition in which the heart has difficulty pumping blood (Asghar et al., 2009). Once diabetes is established, care must be taken to manage blood glucose levels to minimize these nega- tive effects. Individuals with lower socioeconomic status are at increased risk for the negative effects of diabetes. It also disproportionally affects Indigenous individuals (Box 5.4). Box 5.4: An Indigenous lens: Diabetes and colonialization. Oral history suggests that before colonization, Indigenous people reg- ularly participated in an active lifestyle and enjoyed traditional diets that had a healthy balance of nutrients. This was associated with their low rates of chronic disease, good health and longevity (First Nations Health Authority, n.d.; Hackett, 2005). Today, a shift has occurred, and chronic diseases such as diabetes disproportionally affect the health and wellbeing of Indigenous individuals. In Canada, First Nations living off-reserve and on-reserve have a diabetes incidence of 10% and 17%, respectively (Public Health Agency of Canada, 2011). This is two to three times higher than the non-aboriginal population in Canada. This striking difference has led to examinations as to why the disparity exists and how to reduce it. Cultural loss has been suggested as one of the main drivers of the increased incidence of diabetes and other chronic diseases in Indigenous populations. The Believing we can Reduce Aboriginal Incidence of Diabe- tes (BRAID) research group investigated this relationship by interviewing 10 Cree and Blackfoot Elders as well as reviewing health and cultural data across 31 First Nations communities in Alberta. Interestingly, they found that First Nations people who retained their culture through language were significantly less likely to develop diabetes (Oster et al., 2014). In fact, communities with the highest levels of language preservation had the lowest diabetes rates. Those interviewed described expressing their culture as, “Being who we are”, and used words like, “sacred,” “wellbeing,” “balance” and “respect” to describe it. In the interviews, the Elders repeatedly linked chronic dis- ease such as diabetes, cancer and CVD as being due to loss of culture. One Elder commented: Everybody has been gifted with the “how” (knowledge), to deal with themselves and we have to realize that. We have to get back to that. Every Nation in this country and in this world has been gifted with that ability. Even the animals know how to heal themselves... Indian people were like that. They healed themselves, but times have changed. Like many complex problems, sustainable change cannot happen over- night. Luckily, research is ongoing, and many Indigenous and non-Indige- nous leaders are working together to determine which culturally appro- priate, community-based interventions will best address these and other disparities. There are two main types of diabetes: type 1 and type 2. These both involve chronically elevated glucose levels but develop differently. Type 1 diabetes accounts for approximately 10% of diabetes cases. It was formerly known as juvenile diabetes or insulin-dependant diabetes, but these terms are now used less frequently. In type 1 diabetes, the immune system attacks the in- sulin-secreting cells of the pancreas (Figure 5.14). There is accord- ingly no insulin to promote glucose’s uptake into the cells and out of the blood. Presently, we are not entirely sure why our immune system attacks our own body. This is an active area of research. Regardless of the cause, individuals with type 1 diabetes develop toxic levels of blood glucose. Figure 5.14: In type 1 diabetes, immune cells damage the insulin-secreting cells of the pancreas. Type 2 diabetes accounts for the remainder of cases of diabetes. In type 2 diabetes, the pancreas still secretes insulin, but the cells lose their sensitivity to it – that is, they don’t respond to it as well as they should. This is another hot area of interest and research. It is unclear which part of the process is compromised: insulin binding to its receptor or the cell’s response to insulin – or both (Figure 5.15). In the initial stages of type 2 diabetes, insulin levels tend to be very high, as the body produces more of it to get the excess glucose into the cells. In later stages, insulin secretion by the pancreas may decrease, and an individual may also require insulin injections. Gestational diabetes is elevated blood glucose and impaired glucose management that first occurs during preg- nancy (Diabetes Canada, 2020). Of women who have given birth, approximately 5% developed gestational diabetes – a number that has risen over time (Diabetes Canada, 2020). It is more common in older mothers, perhaps due to higher weights at time of pregnancy. While glucose management typically improves after childbirth, women who develop ges- tational diabetes are at a higher risk for developing type 2 diabetes (Bellamy et al., 2009) and CVD (Kramer et al., 2019). To reduce the risk of gestational diabetes, a moderate diet and activity pattern that promotes a healthy weight is recom- mended. It is also important that mothers are screened for gestational diabetes during pregnancy, so it can be detected early and properly managed. The risk factors for type 1 diabetes are not fully established. Environmental factors, including early infection with pathogens such as rubella, have been suggested (Rewers & Ludvigsson, 2016). The disease is more common in people born by caesarean, or who had a higher birthweight, but the reason is not clear. There is also likely a genetic factor at play. Genetic studies of people with type 1 diabetes have found more than 40 changes in their DNA compared to people without this condition (Barrett et al., 2009). The implications of these findings and how they affect disease development are not fully clear. The risk factors for type 2 diabetes are more well established. Obesity, a lack of physical activity, family history and a previous case of gestational diabetes all increase risk. Again, there is also likely a genetic component. Genetic stud- ies have found more than 40 genetic mutations that occur more frequently in the DNA of individuals with type 2 diabetes (Wheeler & Barroso, 2011). More research is needed to understand the significance of these findings. Since the cause of type 1 diabetes is unclear, there is also no known way to prevent it. The main causes of type 2 diabetes are obesity and overweight. Therefore, strategies that aim at reducing these conditions are recommended. A renowned study called the Diabetes Prevention Program (DPP) showed that the risk of type 2 diabetes can be significantly reduced with intensive lifestyle modification or medication use (Box 5.5). Specifically, lifestyle factors such as a reduction in caloric intake and an increase in physical activity leading to a reduction in body weight were associated with a decrease in the development of type 2 diabetes. Box 5.5: The Diabetes Prevention Program. The Diabetes Prevention Program was a four-year long randomised control trial that took place at 27 centres across the Unites States and involved more than 3000 people. The researchers wanted to see wheth- er lifestyle intervention was superior to medication use in the reduction of diabetes incidence, as compared to controls. They divided the study participants into three groups as follows: Lifestyle intervention group: Received intensive training about diet and exercise. Were encouraged to eat less fat and fewer calories Were encouraged to lose 7% of their body weight. Were instructed to exercise 150 min per week. Metformin group: Took the diabetes drug metformin twice a day. Were given basic advice about diet and exercise. Placebo Group: Took a placebo twice a day. Were given basic advice about diet and exercise. Both the lifestyle and metformin groups showed lower rates of diabetes at the 15-year follow-up point (DPP Research Group, 2015). In earlier follow-ups, the lifestyle intervention group had a much lower incidence of diabetes than the metformin group (Knowler et al., 2002). This study shows that both pharma- ceutical and non-pharmaceutical options exist for lowering diabetes incidence in at-risk populations. There is no cure for diabetes. There are, however, sev- eral strategies that can help manage it and decrease the risk of negative health effects. The management of type 1 diabetes involves frequent (2–4) insulin injections throughout the day. People with type 2 diabetes may also require daily insulin injections as insulin production often decreases over time (American Diabetes Association, n.d.). This can be delivered by a syringe or a pump (Figure 5.16). With this treatment, plus lifestyle management that includes a healthy diet and exercise, people with type 1 dia- betes can live a long and healthy life. However, they will need to administer insulin daily for their entire lives. We can thank Cana- dian Sir Frederick Banting for providing this life-saving medicine (Box 5.6). Figure 5.16: Insulin can be administered by a syringe or an insulin pump. Lifestyle strategies, specifically those aimed at weight management or loss are the main course of diabetes management, especially for type 2 diabetes. Reducing calories, eating foods with lower glycemic indexes/loads and in- creasing exercise can all promote a healthier weight and a lower disease burden. People with diabetes may also require medications, such as metformin. This can be a financial burden, especially if the person also must purchase insulin or medications for the associated complications of diabetes. Self-monitoring is important in diabetes to make sure glucose levels are in the desired range. A glucose monitor can be used to test blood glucose levels daily. Bariatric surgeries – those that shrink the size of the stomach – are also very effective at reducing both obesity and diabetes (Buchwald et al., 2009). Access to these surgeries is limited in Canada; many people wait years (Obesity Canada-Obésité Canada, 2019). Hypoglycemia, or low blood glucose, can lead to symptoms that include dizziness, extreme hunger, headache, irritability, tiredness and mental confusion. Diabetic hypoglycemia occurs in individuals with either type 1 or type 2 dia- betes who take too much insulin, which dramatically drops blood glucose. The two main types of chronic hypoglycemia that are not related to diabetes are rare. Reactive hypoglycemia is low blood glucose due to an excessively high release of insulin. It occurs 2–5 h after a meal. The later hypoglycemia is experienced may suggest an abnormal insulin response and an increased risk of diabetes (Altuntaş, 2019; Carreau et al., 2018). Non-reactive hypoglycemia, formerly called fasting hypoglycemia, is low blood sugar that may or may not be related to meals. It can occur in people who eat very little, such as in conditions like anorexia, but can also be caused by certain medications, pregnancy, alcohol abuse or liver, heart and kidney disorders. If hypoglycemia and its associated symptoms persist, a doctor can help to determine the cause and an appropriate management strategy. Sugars are not inherently bad or good. They are a source of energy that the body can use to fuel its many needs. Also, sugars are found in many foods that we know promote health – like fruits and vegetables. However, modern diets tend to be high in extrinsic, or added sugar – those that are added into foods during processing. Intrinsic sugars and extrinsic sugars are chemically identical, but the sources of these sugars are often very different, with potential nutritional consequences. For instance, the fructose that is found intrinsically within a pineapple is chemically identical to the fructose found in the white sugar that might be added to sweeten a pineapple smoothie. However, the intrinsic sugar in pineapple is packaged with other nutrients including water, fibre, potassium, calcium, vitamin C and vitamin A, as well as phytochemicals (United States Department of Agriculture, 2019b). Conversely, added white sugar is only sugar – it lacks the nutrient density of whole pineapple. Diets high in extrinsic sugars are associated with a higher Figure 5.17: Sugar-sweetened beverages are high in extrinsic sugar and low in nutrient density. risk of CVD, diabetes and obesity (Bray & Popkin, 2014; Yang et al., 2014). A lot of research has specifically explored the link between the consumption of sugar sweetened beverages (SSBs) and negative health outcomes (Figure 5.17). A meta-analysis of seven prospective epidemiological studies involving more than 300,000 people found that higher intakes of SSBs are associated with a higher risk of both heart attacks and strokes (Narain et al., 2016). A separate meta-analysis reviewed 11 different epidemi- ological studies and found that SSB consumption is also linked with a higher risk of obesity (Ruanpeng et al., 2017). Since most studies on the link between SSBs and health outcomes are epidemiological in nature, caution should be taken in not assuming causation: we cannot say for sure that SSBs cause cardiovascular events and obesity. However, most studies and reviews point to an association between these factors, suggesting that reducing consumption could improve health. Indeed, Canada’s Food Guide recommends replacing sugary drinks with water when possible (Health Canada, 2018). The easiest way to minimize all extrinsic sugars is to focus on consuming more whole foods, minimizing the amount of processed foods in the diet, and checking the ingredients list of prepackaged foods for added sugars. If the word sugar appears at or near the beginning of the ingredients list, one of the product’s main ingredients is extrinsic sugar (Figure 5.4). Non-nutritive sweeteners (NNSs) are also known as sugar substitutes or artificial sweeteners (Table 5.3). They have a negligible number of calories and nutrients yet have a sweet-tasting flavour. Artificial sweeteners bind to sweet-detecting receptors on the tongue, allowing the brain to sense sweetness, without the calories that come with sugary substances. Depending on the sweetener, they are 30–1300 times sweeter than sugar, therefore a much small- er amount is required for a sweetening effect. They are an area of much debate and their full effects on health are still unclear. Table 5.3: Non-nutritive sweeteners. Since NNSs provide negligible calories and can replace calorie-laden sugar-sweetened products, it stands to reason that their consumption would be associated with a lower weight. The evidence to support this claim is conflicting. For example, rats fed an artificially-sweetened liquid gained more body weight than those that consumed a liquid sweet- ened with regular sugar (Swithers et al., 2010). In humans, prospective epidemiological studies have found an increase in body mass index (BMI) with the consumption of NNSs (Sylvetsky & Rother, 2018). The potential reason for this increase is that sensing sweetness without the delivery of calories may compromise our appetite regulation pattern and promote more food consumption (Swithers, 2013). It may also be that those who already have or are at risk for higher body weight are more likely to consume NNSs (Sylvetsky & Rother, 2018). Confounding these results is that a meta-analysis of ran- domized control trials found small but statistically significant reductions in body weight when NNSs were substituted for regular-calorie options (Fernstrom, 2015; Miller & Perez, 2014). However, these intervention studies are typically short term and cannot fully capture the long-term effects of NNS consumption on body weight or factors such as diabetes and metabolic health. Indeed, epidemiological studies have found an increased risk of metabolic disturbance with NNS use (Swithers, 2013) and research in this area is ongoing (Box 5.7). Taken together, there is currently not enough evidence to support the inclusion or elimination of NNSs from the diet, since their benefits and disadvantages are not clear. A take-home message is to again focus on reducing the amount of processed foods in the diet, which are more likely to contain added sugars and artificial sweeteners. Box 5.7 Is aspartame safe? Aspartame is one of the most rigorously tested food additives on the market (Mitchell, 2006). It has been deemed safe by Health Canada, the Food and Drug administration of the United States and more than 100 international regulatory agencies (Butchko et al., 2002). While claims on the internet have suggested that aspartame causes cancer, large-scale systematic reviews have found no link between the two (Butchko et al., 2002; Kirkland & Gatehouse, 2015; Marinovich et al., 2013). It has also been claimed that aspartame can promote negative neurological symptoms such as seizures, headaches and shifts in moods, but, again, there is a lack of scientific evidence to support these claims (Butchko et al., 2002; Magnuson et al., 2007). Individuals with a rare genetic disorder named phenylketonuria are unable to metabolize the ami- no acid phenylalanine, which is found in aspartame. While they may choose to not consume aspartame to reduce the potential for negative effects, evidence to support the negative effects of aspartame in these individuals is lacking (Butchko et al., 2002). Considering the current evidence, aspartame does not seem to pose an increased risk to health. The belief that carbohydrates are fattening is flawed and oversimplifies how weight is gained and lost. The single most important dietary factor that determines whether an individual will store energy on the body is the total number of calories they take in, regardless of the source of those calories, be it from carbohydrates, fats or protein (Carreiro et al., 2016). However, certain sources of carbohydrates, like liquid carbohydrates may promote less fullness, or satiety, when consumed (Pan & Hu, 2011). This may, in turn, lead to overconsumption. A strong argument against the sweeping generalization that carbohydrates promote weight gain is that fibre is well established to have a role in reducing energy intake and promoting a healthier weight. Epidemiological evidence has long supported a link between dietary fibre intake and reduced risk for obesity (Kromhout et al., 2001; Ludwig et al., 1999). A 2017 review of 12 randomized control trials involving various durations of dietary fibre supplementation also supports this assertion (Thompson et al., 2017). Individuals who were overweight or obese and increased their soluble fi- bre consumption saw an average reduction in BMI of 0.84 (a mean drop in body weight of 2.52 kg). These individuals also saw a reduction in blood sugar and insulin levels with fibre supplementation. While these results are promising for fibre’s effect on lowering obesity, the authors of this study recommended caution in interpreting the results as there were a lot of differences in the types of studies they reviewed. Strong and healthy teeth are essential to proper nutrition and overall health. When teeth are damaged or lost the types of foods we can eat, and therefore our nutrient intake, may be affect- ed. Dental caries, or cavities, are holes that develop in the teeth (Figure 5.18). They can promote pain and lead to more serious issues, even tooth loss, if left untreated. For decades, researchers have known the strong link between the consumption of sugar and the development of dental caries (Gustafsson et al., 1954). Sugars provide food for bacteria in the mouth to grow and thrive. In so doing, bacteria produce enamel-destroying acid, which eats away at the surface of the teeth (Selwitz et al., 2007). The risk of dental caries increases when more sugar and sugary foods that stick to the teeth are consumed. Figure 5.18: Sugar intake increases the risk of dental caries. The Canadian Dental Association recommends limiting added sugars in the diet (Canadian Dental Association, n.d.). Conversely, sugar alcohols such as xylitol may have the potential to reduce the cavity-causing bacteria in the mouth (Ly et al., 2006). They may accordingly be part of a strategy to minimize the production of cavities, together with reduced sugar consumption. Whether and how carbohydrates affect CVD risk depends on the types of carbohydrates that are found in the person’s diet. In general, diets that are high in added sugars and refined carbohydrates pose a greater cardiovascular risk. Conversely, foods that are high in fibre, such as fruits, vegetables and whole grains, are associated with a decreased risk of CVD. Refined carbohydrates and added sugars promote a higher glycemic response. A high-GI diet has been associated with an increase in cardiovascular risk factors such as high blood triglyceride levels, and lower levels of good cholester- ol, high-density lipoprotein (Livesey et al., 2008). Further, added sugars have been shown to increase the risk of CVD in large-scale epidemiolocal studies. For instance, a prospective epidemiological study of Americans found that individuals who consumed more than 25% of their daily calories from added sugar had a three-fold higher risk of dying from CVD than those who consumed less than 10% (Yang et al., 2014). In this study, those who consumed between 10 and 24.9% of calories from added sugar had a risk that was 40% higher than the lower group. Conversely, dietary fibre has a beneficial effect on cardiovascular risk. A 2019 meta-analysis and systematic re- view of both prospective epidemiological studies and randomized control studies found a 15–30% decrease in CVD-relat- ed deaths, heart disease, stroke and type 2 diabetes among those with higher fibre consumption (Reynolds et al., 2019). In this study, the lowest risk was found in those whose daily fibre consumption was between 25 and 29 g. There are two potential mechanisms by which fibre, particularly soluble fibre, decrease CVD risk. Soluble fibre lowers LDL (“bad”) cholesterol Meta-analyses of randomized control trials have shown that soluble fibre decreases LDL and total cholesterol levels in the blood (Brown et al., 1999; Ho et al., 2017). It is hypothesized that soluble fibre helps to lower LDL and total cholesterol levels by decreasing cholesterol absorption in the digestive tract. Soluble fibre regulates blood sugar Diabetes is one of the main risk factors for CVD. Blood glucose regulation is important for decreasing the risk of as well as managing type 2 diabetes. Soluble fibre has been shown to decrease glucose spikes. It can slow the glycemic response by adding bulk to the diet, leading glucose to be absorbed more slowly. Indeed, randomized control trials have shown a lower glycemic response when more soluble fibre was included in the diet in individ- uals with type 2 diabetes (Abutair et al., 2016; Silva et al., 2013). Since diets that are higher in fibre and lower in added sugars are associated with a lower cardiovascular risk, a simplified dietary recommendation would be to consume more whole foods, especially plants. These foods have no add- ed sugars, spike glucose levels less and are far higher in fibre content. Dietary fibre intake may reduce the risk of developing cancers of the large intestine. Epidemiological studies have shown that individuals who consumed the most fibre had the lowest risk of developing cancers in different parts of the colon (Ma et al., 2018; McRae, 2018). There may also be a beneficial effect on the prevention of breast cancer, but more studies are still required. Fibre’s potential to reduce colon cancer incidence may be due to its ability to dilute the con- centrations of cancer-causing agents in the large intestine, thus lowering their potency. Also, since fibre improves transit time through the large intestine, this potentially reduces the negative impact carcinogens can have on our colon cells. Another possibility is that fibre might bind to cancerous compounds and promote their removal. Regardless of its mecha- nism of action, dietary fibre consumption is associated with reduced overall disease risk. Irritable bowel syndrome (IBS) is a chronic condition that promotes symptoms such as abdominal pain, diarrhea, constipation, gas and bloating. It can present both physical, mental and social challenges that affect a person’s daily life. While it has been known and studied for more than a century, its causes and best treatment practices are still a topic of research and debate. Currently, IBS is believed to be associated with poor interactions between the digestive tract and the brain, but its full mechanisms are unclear. Certain carbohydrates may play a role. Short-chain carbohydrates are not fully absorbed in the small intestine and are fermented by bacteria in the large intestine, producing gas. These carbo- hydrates may promote IBS symptoms. Accordingly, a diet low in fermentable oligosaccharides, disaccharide, monosac- charide and polyols (FODMAPs) is often recommended (Table 5.4). Several randomized control trials have found an improvement in IBS symptoms with a low-FODMAP diet (Altobelli et al., 2017; Bohn et al., 2015). However, since this diet is restrictive, its sustainability, potential for nutritional inadequacies, unfavourable changes to the gut microbiome and and psychological impacts, are worth considering (Hill et al., 2017). Accordingly, individuals with IBS should speak to their healthcare practitioner to determine the best management option. Table 5.4: High-FODMAP foods. Carbohydrates are single or multiple chains of sugar units. Sugars have one or two saccharides in their structure, while starches and fibre are long chains of the sugar glucose. Fibre has a different type of bond holding its structure together, one that human enzymes cannot break down. Therefore, fibre is not a source of carbohydrate to the body. For carbohydrates to be digested and absorbed, they need to be broken down into single-sugar units. The health effects of carbohydrates depend on the type and quantity that is consumed. Consuming carbohydrates from whole foods and plants is associated with positive health outcomes. Carbohydrates are made up of single- or multiple-unit chains of single sugars molecules called monosaccharides. Sugars include mono- and disaccharides. These are found naturally or artificially in food. Amylose and amylopectin are the two forms of starch and are made up of a long chain of glucose molecules. Fibre is also made up of long chains of glucose, but humans lack the enzymes to digest it. 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