Carbs Flashcards

1
Q

What are carbs made of ?

A

All carbohydrates are made up of monosaccharides, or single sugaAr

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1
Q

What are carbs

A

Carbohydrates are organic molecules whose primary role is to provide energy. There are three main types of carbohydrates: 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-, do0uble0- or m0ul􏰀ple-unit chains. A carbohydrate’s structure affects how
quickly it is digested and absorbed, as well as its im

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2
Q

What are intrinsic and extrinsic sugars ?

A

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 tas􏰀ng and absorbed quickly from foods.

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3
Q

Monosacharides

A

There are many monosaccharides. However, three main ones exist in the foods we eat
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 o􏰁en 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.

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4
Q

Fructose

A

Fructose is o􏰁en 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.

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5
Q

Galactose

A

Galactose is o􏰁en called milk sugar because it is found in milk. It is similar in sweetness to glucose.

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6
Q

Disacharides

A

The three dietary monosaccharides just described are used to make up the three most common disaccharides in the diet: sucrose, maltose and lactose Disaccharides are sugars with two monosaccharide units.

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7
Q

Sucrose

A

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 Sucrose is made up of a glucose molecule bound to a molecule of fructose. The enzyme sucrase breaks down sucrose into its respec􏰀ve two sugars, which can then be absorbed at the villi of the small intes􏰀ne.

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8
Q

Briwn sugar vs white sugar

A

Both brown and white sugar originate from the same types of plants – sugarcane or beets. Brown sugar is typically white sugar that is mixed with molasses, giving it its darker colour. While there are nutri􏰀onal differences between white and brown sugar, they are minimal and the net difference between the two is small. For instance, half a cup of brown sugar contains 375 kcal, while the same quan􏰀ty of white sugar contains 387 kcal (United States Department of Agriculture, 2019a, 2019c). Brown sugar has slightly more calcium, sodium and potassium, but the differences are minimal when you consider that they are both very low in these nutrients as compared to the RDA. Accordingly, from a nutri􏰀onal perspec􏰀ve, there is no clear advantage to consuming brown sugar over white. However, tastes and culinary uses differ and the choice of which sugar to use may depend on the situa􏰀on and the personal preference.

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9
Q

Maltose

A

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-tas􏰀ng glucose-glucose disaccharide maltose is formed. Once in the small intes􏰀ne, the enzyme maltase breaks down maltose into glucose molecules, which can then be absorbed.

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10
Q

Lactose

A

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 o􏰁en used to refer to lactose. Some people lack the enzyme lactase that helps separate these two monosaccharides. This condi􏰀on, known as lactose intolerance, will be discussed in more detail later.

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11
Q

Extrinsic sugar

A

In addi􏰀on 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.

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12
Q

Canadas health policy about sugars

A

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 Ea􏰀ng Strategy mandates that sugars must be grouped together in ingredients lists.

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13
Q

Oligosacharides

A

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 intes􏰀ne, bacteria in the large intes􏰀ne can ferment them. Accordingly, both are prebio􏰀cs because bacteria use them for food and growth.

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14
Q

Polysacharides

A

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.

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15
Q

Startch

A

Starch is composed of long chains of glucose
molecules in either a straight-chain (amylose) or
branched-chain (amylopec􏰀n) forma􏰀on (Figure 5.4).
Amylopec􏰀n is the most common carbohydrate in the
human diet. Most foods that contain starch have a
greater degree of amylopec􏰀n than amylose. During
diges􏰀on, starch is first broken down into oligosac-
charides, then into disaccharides and eventually into
the monosaccharide glucose, which is then absorbed.
Accordingly, ea􏰀ng foods high in only starch increases
blood sugar rapidly.
We get starch from ea􏰀ng 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.

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16
Q

Fibre

A

Dietary fibre is a collec􏰀ve 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 intes􏰀ne predominantly undigested. Here, bacte- ria can ferment certain fibres into short-chain fa􏰂y acids. These short-chain fa􏰂y 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 poten􏰀ally a source of short chain fa􏰂y acids. Whether fibre can or cannot be fermented into short chain fa􏰂y acids primarily depends on whether it is soluble or insoluble fibre

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17
Q

Soluble fibre

A

Soluble fibre dissolves in water to form a gela􏰀nous solu􏰀on, 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 intes􏰀ne can ferment soluble fibre to produce short-chain fa􏰂y acids (Figure 5.6). Each gram of soluble fibre provides around 2–3 kcal of energy. Soluble fibre consump􏰀on may improve cardiovascular health. Indeed, consump􏰀on 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

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18
Q

Insoluble fibre

A

Insoluble fibre does not dissolve readily in water and is best known for its ability to facilitate the passage of food material through the diges􏰀ve track. This contributes to the health of the diges􏰀ve 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 intes􏰀ne and passes through the diges􏰀ve tract mostly unchanged.

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19
Q

Glycogen

A

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 theore􏰀cal poten􏰀al to store hundreds of kilograms. Thus, fat is our main long-term energy storage loca􏰀on.

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20
Q

Refuned and unrefined carbs

A

Foods that are high in carbohydrates, such as grains, are sold either refined or unrefined. Unrefined sources of carbohydrates are those consumed in their en􏰀re form; the main edible parts of the plant have not been changed or removed (Figure 5.8). These are o􏰁en 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.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 s􏰀ll contains more fibre than a more refined grain.

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21
Q

Endosperm bran and germ

A

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 ge􏰃ng 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.

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22
Q

digestion of carbs

A

The stages of carbohydrate diges􏰀on are outlined in Figure 5.9. Only a small percentage (5–10%) of carbohydrate diges􏰀on occurs in the mouth. Salivary amylase begins the diges􏰀on of starch by breaking down amylose and amylopec- 􏰀n 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- ges􏰀ng enzymes, so no ac􏰀ve diges􏰀on occurs here. However, the amylase that was secreted by the mouth con􏰀nues to act on the starch. Since amylase is sensi􏰀ve to high acidity, it is inac􏰀vated in the stomach, where there are no carbohydrate-di- ges􏰀ng enzymes to take up its role. There is therefore no chemical diges􏰀on of carbohydrate in the stomach.
Most carbohydrate diges􏰀on occurs in the small intes􏰀ne. 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 pancrea􏰀c juice into the small intes􏰀ne. Pancrea􏰀c juice contains pancrea􏰀c amylase, which further digests
starch into shorter and shorter saccharide chains.
The microvilli provide another source of carbohydrate-diges􏰀ng enzymes. Recall that these very 􏰀ny finger-like
projec􏰀ons on the membranes of intes􏰀nal cells are collec􏰀vely referred to as the brush border. The brush border con- tains an essen􏰀al set of carbohydrate-diges􏰀ng enzymes that are released by intes􏰀nal cells to finish off the diges􏰀ng job that the amylases started. Lactase, maltase and sucrase, which respec􏰀vely 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- tes􏰀ne, so once carbohydrates have been digested into monosaccharides they can then be absorbed immediately (Figure 5.10). Some individuals have a compromised secre􏰀on of lactase, leading to a condi􏰀on known as lactose intolerance

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23
Q

Glucose fructose absorbtion

A

Glucose, fructose and galactose are absorbed across the walls of small intes􏰀ne 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 circula􏰀on. This leads to an increase in blood glucose.

24
Q

Lactose intolerant

A

Individuals who are lactose intolerant may experience symptoms such as cramps, bloa􏰀ng, 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 secre􏰀on 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 intes􏰀ne, where bacteria can ferment them. This process leads to the produc􏰀on 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 condi􏰀on (Barr, 2013). There is no cure for lactose intolerance, but symptoms can be limited by minimizing the consump􏰀on of lactose-containing milk products. There are several lactose-free dairy prod- ucts including lactose-free milk and ice cream. Bu􏰂er, yogurt and cheese o􏰁en have lower levels of lactose and may be tolerated well by those who have milder symptoms. Another op􏰀on is to take lactase tablets. There are various op􏰀ons on the market, with varying degrees of lactose diges􏰀on. Too much stomach acid could inac􏰀vate the enzymes found in these tablets, so they tend to work more effec􏰀vely in some people compared to others (O’Connell & Walsh, 2006).

25
Q

Glycemic response

A

The glycemic response is the spike in blood glucose that follows a meal once glucose enters the general circula- 􏰀on (Figure 5.11). Diets that produce a lower glycemic response are associated with improved insulin sensi􏰀vity, 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.

26
Q

Glycemic index

A

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 rela􏰀ve ranking of a food’s poten􏰀al 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.

27
Q

Glycemic load

A

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.

28
Q

Hypoglycaemia and hyperglycaemia

A

Our bodies strive for glucose homeostasis, which is when there is neither too much nor too li􏰂le glucose is in the blood. Low blood glucose levels result in a state known as hypoglycemia, in which an individual may experience 􏰀redness, 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 regula􏰀ng blood glucose level: insulin and glucagon. Both are secreted by the pancreas (Box 5.3).

29
Q

Endocrine and exocrine

A

The pancreas has two very important yet very different func􏰀ons. Dif- ferent cells and parts of the pancreas are involved in these two func􏰀ons. These are some􏰀mes referred to as the pancreas’ exocrine and endo- crine roles.
Exocrine means outside of the body and typically refers to secre􏰀ons that occur into the diges􏰀ve tract. The diges􏰀ve 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 pancrea􏰀c juice into the small intes􏰀ne. Pancrea􏰀c amylase, lipase and protease promote the diges􏰀on of carbohydrates, lipids and proteins, respec􏰀vely.
Endocrine refers to the secre􏰀on of substances into the bloodstream, specifically hormones. The secre􏰀on of the hormones insulin and gluca- gon into the blood to regulate blood glucose is the main endocrine role of the pancreas.

30
Q

Insulin

A

summarizes how insulin regulates blood glucose levels. When blood glucose levels spike a􏰁er a meal, insulin secre􏰀on 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. 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, respec􏰀vely.

31
Q

Glucagon and blood glucose

A

When blood glucose levels are too low, the pancreas releases glucagon into the blood. This can occur during 􏰀mes of fas􏰀ng. Glucagon increases blood glucose by promo􏰀ng three main processes:
1. Glycogenolysis: the conversion of glycogen to glucose.
2. Gluconeogenesis: the conversion of certain amino acids into glucose.
3. Lipolysis: the breakdown of stored lipids. Glycerol from triglycerides can then be used to make glucose.

32
Q

Carb functions

A

Energy ,protein sparing,fat burns in carb flames

33
Q

Energy

A

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 􏰀ssues. While some 􏰀ssues can use fat for energy as well, the brain and red blood cells preferen􏰀ally 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.

34
Q

Protein sparing

A

Since our bodies preferen􏰀ally 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 restric􏰀on. Ge􏰃ng enough carbohydrates in the diet spares this from happening and helps maintain protein in 􏰀ssues such as the muscles.

35
Q

Fat and carb flames

A

Carbohydrates are involved in the metabolism of lipids. Recall that the metabolism of the glycerol and fa􏰂y acids that make up a triglyceride molecule leads to the produc􏰀on 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.

36
Q

Diabetes

A

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 fluctua􏰀ons 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.

37
Q

Diabetes symptoms

A

Acute , thirst , tiredness, slow healing infection , urination frequent, weight loss chronic numbness cvd blindess kidney amputation

38
Q

Diabetes negative effect

A

In later stages, diabetes nega􏰀vely effects several important body structures and func􏰀ons and increases mor- tality rate (Figure 5.14b). In 2017, diabetes ranked seventh in the leading causes of death in Canada (Sta􏰀s􏰀cs 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 nega􏰀ve effects on the cardiovascular system, for instance by promo􏰀ng cardiomyopathy, a condi􏰀on 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- 􏰀ve effects. Individuals with lower socioeconomic status are at increased risk for the nega􏰀ve effects of diabetes. It also dispropor􏰀onally affects Indigenous individuals (Box 5.4).

39
Q

Type 1 diabetes

A

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 a􏰂acks the in- sulin-secre􏰀ng 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 en􏰀rely sure why our immune system a􏰂acks our own body. This is an ac􏰀ve area of research. Regardless of the cause, individuals with type 1 diabetes develop toxic levels of blood glucose.

40
Q

Type 2 diabetes

A

Type 2 diabetes accounts for the remainder of cases of diabetes. In type 2 diabetes, the pancreas s􏰀ll secretes insulin, but the cells lose their sensi􏰀vity 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 ini􏰀al 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 secre􏰀on by the pancreas may decrease, and an individual may also require insulin injec􏰀ons.
Figure 5.15: In type 2 diabetes, cells become resistant to insulin.

41
Q

Gestational diabetes

A

Gesta􏰀onal 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 gesta􏰀onal diabetes – a number that has risen over 􏰀me (Diabetes Canada, 2020). It is more common in older mothers, perhaps due to higher weights at 􏰀me of pregnancy. While glucose management typically improves a􏰁er childbirth, women who develop ges- ta􏰀onal 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 gesta􏰀onal diabetes, a moderate diet and ac􏰀vity pa􏰂ern that promotes a healthy weight is recom- mended. It is also important that mothers are screened for gesta􏰀onal diabetes during pregnancy, so it can be detected early and properly managed.

42
Q

Risk factor type 1 diabetes

A

The risk factors for type 1 diabetes are not fully established. Environmental factors, including early infec􏰀on 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 gene􏰀c factor at play. Gene􏰀c studies of people with type 1 diabetes have found more than 40 changes in their DNA compared to people without this condi􏰀on (Barre􏰂 et al., 2009). The implica􏰀ons of these findings and how they affect disease development are not fully clear.

43
Q

Risk factors type 2 diabetes

A

The risk factors for type 2 diabetes are more well established. Obesity, a lack of physical ac􏰀vity, family history and a previous case of gesta􏰀onal diabetes all increase risk. Again, there is also likely a gene􏰀c component. Gene􏰀c stud- ies have found more than 40 gene􏰀c muta􏰀ons 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.

44
Q

Prevention diabetes

A

The Diabetes Preven􏰀on 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 interven􏰀on was superior to medica􏰀on use in the reduc􏰀on of diabetes incidence, as compared to controls. They divided the study par􏰀cipants into three groups as follows:
Lifestyle interven􏰀on 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.
Me􏰄ormin group:
* Took the diabetes drug me􏰄ormin 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 me􏰄ormin groups showed lower rates of diabetes at the 15-year follow-up point (DPP Research Group, 2015). In earlier follow-ups, the lifestyle interven􏰀on group had a much lower incidence of diabetes than the me􏰄ormin group (Knowler et al., 2002). This study shows that both pharma- ceu􏰀cal and non-pharmaceu􏰀cal op􏰀ons exist for lowering diabetes incidence in at-risk popula􏰀ons.

45
Q

Diabetes management

A

There is no cure for diabetes. There are, however, sev- eral strategies that can help manage it and decrease the risk of nega􏰀ve health effects.
The management of type 1 diabetes involves frequent (2–4) insulin injec􏰀ons throughout the day. People with type
2 diabetes may also require daily insulin injec􏰀ons as insulin produc􏰀on o􏰁en decreases over 􏰀me (American Diabetes Associa􏰀on, 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 en􏰀re lives. We can thank Cana- dian Sir Frederick Ban􏰀ng for providing this life-saving medicine Lifestyle strategies, specifically those aimed at weight management or loss are the main course of diabetes management, especially for type 2 diabetes. Reducing calories, ea􏰀ng 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 medica􏰀ons, such as me􏰄ormin. This can be a financial burden, especially if the person also must purchase insulin or medica􏰀ons for the associated complica􏰀ons 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 effec􏰀ve 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).

46
Q

Fred and insulin

A

Sir Frederick Ban􏰀ng won the Nobel Prize for medicine in 1923 for the discovery of insulin. He used scien􏰀fic reasoning to determine that there was a substance in the pancreas that was able to reverse the effects of type 1 diabetes in dogs. He later isolated this substance, made it stronger and tested it on young people who were very sick from the disease. The results were astounding and are one of the greatest med- ical discoveries of our 􏰀me. The doses of insulin were able to improve the symptoms of the pa􏰀ents almost immediately, though they had to be repeatedly administered (Riedlinger et al., 2018; Tan & Merchant, 2017). He later sold the patent for $1 to the University of Toronto, sta􏰀ng that “Insulin does not belong to me, it belongs to the world.” Unfortunately, patents expire and now drug companies around the world sell their versions of insulin at extremely high mark-ups, making the management of this disease more difficult for individuals of lower socioeconomic status.
Viewers of the Canadian Broadcas􏰀ng Corpora􏰀on voted the discovery of insulin as the “Greatest Ca- nadian Inven􏰀on of All Time” (Wikipedia, n.d.). This is impressive, given the s􏰀ff compe􏰀􏰀on it faced against the Canadian inven􏰀ons of basketball, the map of the brain and the zipper.

47
Q

Hypoglycaemia

A

Hypoglycemia, or low blood glucose, can lead to symptoms that include dizziness, extreme hunger, headache, irritability, 􏰀redness and mental confusion. Diabe􏰀c hypoglycemia occurs in individuals with either type 1 or type 2 dia- betes who take too much insulin, which drama􏰀cally drops blood glucose. The two main types of chronic hypoglycemia that are not related to diabetes are rare. Reac􏰀ve hypoglycemia is low blood glucose due to an excessively high release of insulin. It occurs 2–5 h a􏰁er 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-reac􏰀ve hypoglycemia, formerly called fas􏰀ng hypoglycemia, is low blood sugar that may or may not be related to meals. It can occur in people who eat very li􏰂le, such as in condi􏰀ons like anorexia, but can also be caused by certain medica􏰀ons, 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.
143

48
Q

Sugar and health

A

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 iden􏰀cal, but the sources of these sugars are o􏰁en very different, with poten􏰀al nutri􏰀onal consequences. For instance, the fructose that is found intrinsically within a pineapple is chemically iden􏰀cal 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.
Figure 5.17: Sugar-sweetened beverages are high in extrinsic sugar and low in nutrient density.
Diets high in extrinsic sugars are associated with a higher risk of CVD, diabetes and obesity (Bray & Popkin, 2014; Yang
et al., 2014). A lot of research has specifically explored the link between the consump􏰀on of sugar sweetened beverages (SSBs) and nega􏰀ve health outcomes (Figure 5.17). A meta-analysis of seven prospec􏰀ve epidemiological studies involving more than 300,000 people found that higher intakes of SSBs are associated with a higher risk of both heart a􏰂acks and strokes (Narain et al., 2016). A separate meta-analysis reviewed 11 different epidemi- ological studies and found that SSB consump􏰀on 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, cau􏰀on should be taken in not assuming causa􏰀on: we cannot say for sure that SSBs cause cardiovascular events and obesity. However, most studies and reviews point to an associa􏰀on between these factors, sugges􏰀ng that reducing consump􏰀on 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

49
Q

Non nutritive sweeteners

A

Non-nutri􏰀ve sweeteners (NNSs) are also known as sugar subs􏰀tutes or ar􏰀ficial sweeteners (Table 5.3). They have a negligible number of calories and nutrients yet have a sweet-tas􏰀ng flavour. Ar􏰀ficial sweeteners bind to sweet-detec􏰀ng 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 􏰀mes 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 s􏰀ll unclear.

50
Q

Nns and weight control

A

Since NNSs provide negligible calories and can replace calorie-laden sugar-sweetened products, it stands to reason that their consump􏰀on would be associated with a lower weight. The evidence to support this claim is conflic􏰀ng. For example, rats fed an ar􏰀ficially-sweetened liquid gained more body weight than those that consumed a liquid sweet- ened with regular sugar (Swithers et al., 2010). In humans, prospec􏰀ve epidemiological studies have found an increase in body mass index (BMI) with the consump􏰀on of NNSs (Sylvetsky & Rother, 2018). The poten􏰀al reason for this increase
is that sensing sweetness without the delivery of calories may compromise our appe􏰀te regula􏰀on pa􏰂ern and promote more food consump􏰀on (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 sta􏰀s􏰀cally significant reduc􏰀ons in body weight when NNSs were subs􏰀tuted for regular-calorie op􏰀ons (Fernstrom, 2015; Miller & Perez, 2014). However, these interven􏰀on studies are typically short term and cannot fully capture the long-term effects of NNS consump􏰀on 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 elimina􏰀on 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 ar􏰀ficial sweeteners.

51
Q

Spartame

A

Aspartame is one of the most rigorously tested food addi􏰀ves on the market (Mitchell, 2006). It has been deemed safe by Health Canada, the Food and Drug administra􏰀on of the United States and more than 100 interna􏰀onal regulatory agencies (Butchko et al., 2002). While claims on the internet have suggested that aspartame causes cancer, large-scale systema􏰀c 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 nega􏰀ve neurological symptoms such as seizures, headaches and shi􏰁s in moods, but, again, there is a lack of scien􏰀fic evidence to support these claims (Butchko et al., 2002; Magnuson et al., 2007).
Individuals with a rare gene􏰀c 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 poten􏰀al for nega􏰀ve effects, evidence to support the nega􏰀ve 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.

52
Q

Carb and weight management

A

The belief that carbohydrates are fa􏰂ening 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 sa􏰀ety, when consumed (Pan & Hu, 2011). This may, in turn, lead to overconsump􏰀on.
A strong argument against the sweeping generaliza􏰀on that carbohydrates promote weight gain is that fibre is well established to have a role in reducing energy intake and promo􏰀ng 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 dura􏰀ons of dietary fibre supplementa􏰀on also supports this asser􏰀on (Thompson et al., 2017). Individuals who were overweight or obese and increased their soluble fi- bre consump􏰀on saw an average reduc􏰀on in BMI of 0.84 (a mean drop in body weight of 2.52 kg). These individuals also saw a reduc􏰀on in blood sugar and insulin levels with fibre supplementa􏰀on. While these results are promising for fibre’s effect on lowering obesity, the authors of this study recommended cau􏰀on in interpre􏰀ng the results as there were a lot of differences in the types of studies they reviewed.
146

53
Q

Carb and dental

A

Strong and healthy teeth are essen􏰀al to proper nutri􏰀on 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 cavi􏰀es, are holes that develop in the teeth (Figure 5.18). They can promote pain and lead to more serious issues, even tooth loss, if le􏰁 untreated. For decades, researchers have known the strong link between the consump􏰀on 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 s􏰀ck to the teeth are consumed.
Figure 5.18: Sugar intake increases the risk of dental caries.
The Canadian Dental Associa􏰀on recommends limi􏰀ng added sugars in the diet (Canadian Dental Associa􏰀on, n.d.). Conversely, sugar alcohols such as xylitol may have the poten􏰀al to reduce the cavity-causing bacteria in the mouth (Ly et al., 2006). They may accordingly be part of a strategy to minimize the produc􏰀on of cavi􏰀es, together with reduced sugar consump􏰀on.

54
Q

Carb and cvd

A

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 prospec􏰀ve 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.

55
Q

How fibrr decreases cvd

A

There are two poten􏰀al mechanisms by which fibre, par􏰀cularly soluble fibre, decrease CVD risk.
1. 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 absorp􏰀on in the diges􏰀ve tract.
2. Soluble fibre regulates blood sugar
Diabetes is one of the main risk factors for CVD. Blood glucose regula􏰀on 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 recommenda􏰀on 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.

56
Q

Fibre and colon cancer

A

Dietary fibre intake may reduce the risk of developing cancers of the large intes􏰀ne. 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 preven􏰀on of breast cancer, but more studies are s􏰀ll required. Fibre’s poten􏰀al to reduce colon cancer incidence may be due to its ability to dilute the con- centra􏰀ons of cancer-causing agents in the large intes􏰀ne, thus lowering their potency. Also, since fibre improves transit 􏰀me through the large intes􏰀ne, this poten􏰀ally reduces the nega􏰀ve 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 ac􏰀on, dietary fibre consump􏰀on is associated with reduced overall disease risk.

57
Q

FODMAPS and irritable bowel syndrome

A

Irritable bowel syndrome (IBS) is a chronic condi􏰀on that promotes symptoms such as abdominal pain, diarrhea, cons􏰀pa􏰀on, gas and bloa􏰀ng. 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 prac􏰀ces are s􏰀ll a topic of research and debate. Currently, IBS is believed to be associated with poor interac􏰀ons between the diges􏰀ve 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 intes􏰀ne and are fermented by bacteria in the large intes􏰀ne, producing gas. These carbo- hydrates may promote IBS symptoms. Accordingly, a diet low in fermentable oligosaccharides, disaccharide, monosac- charide and polyols (FODMAPs) is o􏰁en 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 restric􏰀ve, its sustainability, poten􏰀al for nutri􏰀onal 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 prac􏰀􏰀oner to determine the best management op􏰀on.