Chapter 10 - Energy Balance.docx

Chapter 10: energy Balance Our bodies need energy to stay alive, produce heat and perform body movements. We eat, in part, to provide the energy to meet these needs. When the energy we consume matches the energy we use, we are in energy balance. Many Canadians are at a positive energy balance, meaning they consume more energy than they expend. This excess energy is mostly stored within our fat cells. If energy storage is consistently favoured, our total body fat and weight increase. While we need to store some energy on the body, storing too much can promote diseases that negatively aﬀect health and quality of life. Obesity, type 2 diabetes, cardiovascular disease and some cancers are associated with the overconsumption of energy. On the opposite side of the spectrum, consuming too little energy can negatively compro- mise our energy levels as well as our ability to sustain important biological processes. That is why the concept of energy balance is critical: we must consume enough energy to meet needs, but not so much and not so little that it increases health risk. By the end of this chapter, you will be able to: Outline how energy is stored and retrieved. List the complications associated with having too much or too little stored energy. Explain how appetite is regulated, including the key molecules involved. Describe methods for assessing body size and list their strengths and limitations. Outline the complex causes of obesity. Provide strategies for achieving and maintaining a healthy energy balance. Summarize eating disorders, including their characteristics, risk factors and health outcomes. Energy is the ability to do work. Our bodies must perform a lot of work each day in order to survive and thrive. The energy we obtain from the food we eat is our energy intake. We use this energy to fuel basal metabolism, physical activity and food processing. This is collectively referred to as our energy expenditure. We achieve energy balance when our energy intake equals our energy expenditure. Carbohydrates, lipids and proteins are our three energy-yielding nutrients. Recall from Chapter 3 that energy is found in the bonds that hold these molecules together. Cellular respiration breaks these bonds, releasing energy that can be captured in the bonds of ATP, the body’s energy currency (Figure 10.1a). While not a nutrient, alcohol also provides energy and contributes to our net energy intake. In Canada, energy is measured in kilocalories. Recall that carbohydrates and proteins provide 4 kcal/g, whereas lipids provide 9 kcal/g and alcohol provides 7 kcal/g. However, the total number of calories consumed each day, not the source of the calories, determines our net energy intake. Figure 10.1: Energy intake vs. energy expenditure. We burn energy for three purposes: basal metabolic rate, physical activity and thermogenesis (Figure 10.1b). Basal metabolic rate (BMR) is the amount of energy the body needs to perform its most basic, life-sustaining functions over a period of time. This energy helps us breath, pump blood and send nerve messages, among countless other critical functions. BMR accounts for 60–75% of the energy we burn. When we say someone has a fast metabolism, we typically mean that they burn a lot of calories to sustain their body, even before physical activity is factored in. This decreases the chance that they will store excess energy on the body. On the other hand, some people are said to have a slow metabolism, meaning that they expend fewer calories on foundational life-sustaining processes. These individuals might have a harder time achieving and maintaining energy balance and may need to consume fewer calories or burn more to achieve energy balance. BMR is mainly determined by factors out of our control (Figure 10.2). Organ size also plays a large role in deter- mining BMR (Müller et al., 2011); the larger the organs, the higher the BMR. The most significant determinant of BMR within our control is lean body mass. While unmodifiable factors such as organ size and height aﬀect lean body mass, muscle mass can also have an impact. Therefore, the best way to maintain or slightly increase BMR is to build lean body mass through resistance exercises. Figure 10.2: Factors that inﬂuence BMR. Diet-induced thermogenesis, also known as specific dynamic action or the thermic eﬀect of food, also contrib- utes to energy expenditure. It is the energy that is used and dissipated as heat following food intake. While food brings energy into the body, we also need energy to process it. Diet-induced thermogenesis accounts for about 10% of energy expenditure. More energy is required to process protein compared to the other nutrients, while less is used to process lipids. Accordingly, diets high in protein promote a higher thermic eﬀect, while those high in fat promote a lower thermic eﬀect (Westerterp, 2004). Even so, diet-induced thermogenesis accounts for no more than 15% of our total energy expendi- ture. The element of energy expenditure that is most under our control is physical activity. Physical activity is the body’s voluntary movement that leads to the expenditure of calories. Exercise is one form of physical activity that is structured, planned and done to promote fitness. We also get physical activity from the various other movements we do in our day, such as walking to work, gardening and cleaning. The more active we are, the more energy we expend. Energy balance is achieved when the number of calories taken in from carbohydrates, lipids, protein and alcohol matches the energy we expend through BMR, diet-induced thermogenesis and physical activity. Of these, the factors most in our control are the food energy taken in and the energy burned through physical activity. One day of an energy excess or deficit will not make much diﬀerence to our energy stores. However, a consistent energy excess or energy defi- cit will lead to a gain or loss of energy, respectively. Since most of the body’s energy is stored as fat, and fat has weight, a consistent energy excess will lead to fat and weight gain, whereas a consistent energy deficit will lead to loss of fat and weight. While some energy is stored as carbohydrate in the form of glycogen, most is stored as fat within adipocytes, or fat cells (Figure 10.3). Adipocytes are obvious under a microscope due to their empty-looking appearance. The part that looks empty is a vacuole and is where energy is stored. Adipocyte vacuoles contain triglycerides, fatty acids and fat-sol- uble vitamins. When lipids are stored in these vacuoles, adipocytes become larger. This increases body fat and weight (Figure 10.4). We are born with a certain number of adipocytes with a reserve of fat-storing potential. When adipocytes reach their maximum size, they can divide, increasing the total number of adipocytes. We can accordingly continue to add more and more energy to our bodies beyond our current capacity. Figure 10.3: Adipocytes within adipose tissue. Figure 10.4: An energy surplus favours energy storage and weight gain. An energy deﬁcit is reached when we consume less energy than our bodies need to perform its various func- tions. If the diet is inadequate to meet current energy requirements, it turns to its energy reserves (Figure 10.5). Glyco- gen will be turned into glucose and body proteins will be used for their amino acids, both of which can be metabolized to form ATP. However, most energy retrieval comes from our adipocytes. Here, fatty acids and triglycerides are released and enter the blood. At the cells, these can then be metabolised to form ATP. If we are consistently at an energy deficit, our adipocytes become smaller and smaller, leading to a loss of body fat and weight. Note that body proteins are also used for energy when we are at an energy deficit. Therefore, maintaining lean mass through physical activity is recommended while at an energy deficit. Figure 10.5: An energy deﬁcit favours energy retrieval and weight loss. Weight is typically gained when lean mass or fat mass increase. Lean mass can be increased by increasing muscle and bone mass through resistance exercises. Fat mass is gained when we are at an energy surplus over a longer period of time (Figure 10.3). While some weight is also gained with glycogen storage, this accounts for about 1–2 kg of weight at most (Acheson et al., 1988). Some individuals may also notice a shift in weight of a half or full kilogram in as little as a day or two. This is rarely due to major changes in lean or fat mass. Minor daily weight ﬂuctuations are typically due to changes in the body’s water content. The more cells an individual has, the greater room for water volume in the extra- cellular space (Lichtenbelt & Fogelholm, 1999). Accordingly, larger individuals may be more likely to see shifts in water weight from day to day. Weight loss typically occurs when we lose lean mass or fat mass. Lean mass can decrease if our muscle or bone mass decrease, for instance if resistance exercises are discontinued. This is not recommended, however, as having enough lean body mass supports the structure and function of our bodies, while promoting health. Even if resistance activities are continued, we may still lose lean body mass when we are at a caloric deficit, as some body proteins will be broken down for energy. Lean body mass also decreases over time as our organs become smaller. This is partly why energy needs decrease with age. As with weight gain, minor decreases in weight from day to day are often due to water losses. Many fad diets appear to show results by promoting these water losses, which are typically gained back quickly. The major determinant of weight loss is the loss of energy stored as fat. This occurs at an energy deficit. Inter- estingly, most of this weight is lost in the air we breathe out. In addition to ATP, recall that the metabolism of fuels leads to the production of water and carbon dioxide. For every 10 kg of metabolized body fat, 1.6 kg are lost as water and 8.4 kg are lost as carbon dioxide, which is expelled from the lungs (Figure 10.6) (Meerman & Brown, 2014). In a survey of doctors, dieticians and personal trainers, less than 5% knew that this is how fat is lost. Most thought that weight is lost through energy or heat (Meerman & Brown, 2014). Figure 10.6: Weight is lost from the body as water and carbon dioxide. We used to think that adipocytes are inactive, having no physiological role beyond energy storage. This view drastically changed in the 1990s with the discovery of the hormone leptin (Box 10.1). Leptin is secreted by adipocytes and communicates with the brain and other organs. It promotes fullness and energy expenditure and helps promote healthy energy balance. Since the discovery of leptin, hundreds of adipokines – messengers released from our fat cells – have been identified (Figure 10.7). Each communicates with one or more tissues and helps maintain homeostasis. Figure 10.7: Adipocytes communicate with the body by releasing adipokines. Below a certain level of fat mass, adipokines produce a health-promoting eﬀect on the body. Specifically, they tend to decrease the total amount of inﬂammation. However, above this threshold, adipokine secretion shifts towards a net negative eﬀect on the body, increasing inﬂammation and the risk of disease. Body fat is not inherently bad for us. In fact, it has many important physiological roles beyond energy storage. However, having too much of it can promote both physiological and structural consequences. Accordingly, the goal is not to eliminate fat from the body, but to achieve a healthy energy balance where health is promoted, and disease risk and physical limitations are minimized. Box 10.1: Leptin and the ob mouse. In 1950, researchers identified an obese mouse within a litter of otherwise lean mice. The obese mouse ate voraciously, was three times the size of its litter mates and had moderate diabetes. Genetic analysis found that this mouse had a spontaneous mutation in a region they called the ob gene – ob for obese. They did not know what this gene did, but it was later hypothesized that it coded for some sort of fullness factor in both mice and humans. This fullness factor was named leptin for the Greek word leptos, which means thin. It wasn’t until 1994 that a researcher named Jeﬀrey Friedman found that leptin is secreted by our adi- pocytes. This was a major discovery because until then it was believed that our fat cells didn’t interact with the body. In their paper, the authors concluded, “The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot,” (Zhang et al., 1994). In- deed, it was later concluded that leptin acts on the appetite regulation centre in the brain to decrease the desire to eat. Humans who are born with a non-functional ob gene product – leptin – become obese quickly in their lives. Luckily, they can quickly reverse the condition with the administration of external leptin. Obesity due to leptin deficiency is fortunately so rare that its prevalence is unknown. While this leptin gene mutation is rare, many people with obesity experience leptin resistance. Leptin resistance is similar to insulin resis- tance in type 2 diabetes – enough of the hormone is secreted, but the body does not properly respond to it. This means that individuals with obesity sometimes lack the proper feedback system from their fat cells that decreases appetite and increase energy expenditure. Leptin resistance is accordingly sometimes explained as the body is obese but the brain is starved, meaning that the brain does not realize the body is full and keeps promoting food intake. There is no cure for leptin resistance, but it may be improved by reducing fat mass. Currently, the mechanisms of leptin resistance are still being studied and are not fully understood (Gruzdeva et al., 2019). Obesity is the state of having an excessive amount of fat stored in the body. Obesity is not a choice in the same way that lung cancer is not a choice. These are outcomes associated with lifestyle factors that lead to a disease state. In 2015, the Canadian Medical Association recognized obesity as a chronic medical disease (Canadian Medical Associa- tion, 2015). This was a landmark declaration, as until then obesity had been considered a risk factor for disease and not a disease itself. A chronic disease is one that takes decades to become established, has a long duration and requires a long-term, systematic approach to management (World Health Organization, 2005). Diseases aﬀect the body’s structure and function and are associated with certain signs and symptoms. Obesity meets the definition of disease because it often takes years to develop and, once established, it compromises our anatomy and physiology and is often difficult to manage. Obesity can aﬀect the physical, mental and social wellbeing of an individual. Its physical aﬀects are sometimes categorized into two categories: sick fat disease and fat mass disease (Figure 10.8). Figure 10.8: Sick fat disease vs. fat mass disease. Sick fat disease (Figure 10.8a) refers to the negative physiological eﬀects excess body fat can have once it passes a certain threshold. Past this point, fat cells interact with the body in a way that promotes chronic low-grade inﬂamma- tion. This inﬂammation promotes several negative health eﬀects. Fat mass disease (Figure 10.8b) refers to the biomechanical and structural challenges that excess weight places on the body. In addition to the negative eﬀects these can have on quality of life, they can also compromise obesity inter- ventions. For example, added joint stress can make exercise painful for an individual with obesity. Some people with obesity may have an increased risk for certain mental health eﬀects, such as depression, low self-esteem and negative self talk. Furthermore, obesity is a common cause of discrimination in both adults and children. Individuals with obesity are more likely to face bias, poor treatment and less employment, education and healthcare opportunities (Puhl & Brownell, 2001). One of the key determinants of body size is genetics. Indeed, identical twins (same genes) have a much stronger correlation in body mass index (BMI) compared to fraternal twins (similar, but diﬀerent genes) (Mark Allyn L., 2008). Further, when one identical twin is overfed, they gain an amount of weight similar to their twin, but diﬀerent to others (Box 10.2). Another example of how genetics aﬀects both the size and shape of our bodies can be found by looking at members of the same family. There is a good chance that our body size and shape resemble our mother or father’s when they were the same age. It is rare that a single genetic mutation promotes weight diﬀerences. The genetic causes of obesity are typically polygenic, that is, caused by a combination of small eﬀects in several diﬀerent genes. A technique called genome-wide association studies has examined the genetic makeup of millions of individuals around the world and found approxi- mately 100 sites in the human genome that promote an increased risk for obesity (Locke et al., 2015). Most of these mutations are found around genes that are involved in appetite regulation. While the full implications of these findings are unclear, these results suggest that genetics is a contributing factor in why certain individuals consume excess calories and are at an increased risk for obesity. The Foresight map illustrates the various factors that promote obesity (Figure 10.9). Notice that these are divid- ed into seven main areas or nodes. One of the map’s main messages is that obesity is complex and is caused by many in- terrelated factors. The higher rates of obesity in Indigenous population in Canada highlight the complexity of the disease (Box 10.3) Figure 10.9: The Foresight map illustrates that the causes of obesity are complex and interrelated. Box 10.3: An Indigenous lens: Obesity. A 2019 review estimated that, based on self-reported data, the rates of obesity in First Nations people who live oﬀ reserve is 26%, while the rates in the Métis and Inuit samples they assessed were 22% and 26% respectively. These rates are significantly higher than the 16% rate of obesity evidenced in non-Indigenous people (Gionet & Roshanafshar, 2013). Before we explore potential reasons for this disparity, there are two important caveats to this data: first, our ability to collect robust data within certain Indigenous populations is limited, so these numbers may not be fully representative. Also, since these rates are based on BMI data collect- ed from self-reported height and weight, the true rates of obesity are likely much higher. Since obesity is a complex, multifactorial disease, there is likely several reasons why this obesity disparity occurs in Indigenous people. One potential reason is the higher rates of food insecurity. Food insecurity is the state where some or all members of a household have compromised access to food in sufficient quantity or quality. Indeed, 22% of First nations, 15% of Métis and 27% of Inuit individuals surveyed lived in households that were food insecure (Gionet & Roshanafshar, 2013). Individuals who are food insecure may be at a higher risk for obesity because they have less access to fresh fruits and vegetables and may rely more heavily on more aﬀordable highly processed foods (Drewnowski & Darmon, 2005) – ones that are also more available in remote areas where Indigenous people are more likely to live. It is further proposed that the scarcity of food promotes a physiological response which may increase fat deposition (Dhurandhar, 2016). It has also been proposed that the legacy of residential schools, which began in the 1880s and only officially ended in 1996, has contribut- ed to the higher prevalence of obesity in Indigenous people. Residential schools present a dark side of Canada. As former Prime Minister Stephen Harper stated in Canada’s official apology to Indigenous people: Two primary objectives of the residential school system were to remove and isolate children from the inﬂuence of their homes, families, traditions and cultures, and to assimilate them into the dominant culture. These objectives were based on the assump- tion that Aboriginal cultures and spiritual beliefs were inferior and unequal. Indeed, some sought, as it was infamously said, “to kill the Indian in the child.” Today, we recognize that this policy of assimi- lation was wrong, has caused great harm, and has no place in our country. In response to this statement, Phil Fontaine, the national chief of the Assembly of First Nations said in his official statement: Our peoples, our history, and our present being are the es- sence of Canada. The attempts to erase our identities hurt us deeply, but it also hurt all Canadians and impoverished the character of this nation. We must not falter in our duty now. Emboldened by this spectacle of history, it is possible to end our racial nightmare together. The memories of residential schools sometimes cut like merciless knives at our souls. This day will help us to put that pain behind us. Indeed, the legacy of residential schools is one of physical and emotional pain that time has not been able to erase. For instance, children in residential schools often faced a life of chronic hunger. As one survivor, Andrew Paul noted, “We cried to have something good to eat before we sleep. A lot of the times the food we had was rancid, full of maggots, stink. Sometimes we would sneak away from school to go visit our aunts or un- cles, just to have a piece of bannock.”(Truth and Reconciliation Commission of Canada, 2015). A potential outcome of severe undernutrition is height stunting, which may prioritize towards gains in fat mass over lean mass (Mosby & Galloway, 2017). Furthermore, this undernutrition could also predispose to obesity due to the stress-induced promotion of fat deposition, its negative immune eﬀects, and the potential for epigenetic programming for obesity (Mosby & Galloway, 2017). While residential schools cannot completely explain the significant disparity in obesity rates amongst Indigenous peo- ple, it highlights how compromised childhood nutrition can contribute to an increased risk for the disease. Further, by learning from our oppressive history, we can gain insight into the trauma we can inﬂict when we discount the cultures, individuality and spirituality of other people, as we did with those who first occupied this land. Our appetite plays a key role in determining how much food we consume. Appetite is the drive to consume food. It can be inﬂuenced by hunger, the physiological drive to consume. However, it is possible to have an appetite with- out being hungry – as anyone who has eaten past the point of fullness can attest to. Conversely, satiety is the sense of fullness that promotes the cessation of eating and keeps us feeling full after a meal. Our appetite and satiety centres are found beside each other in the brain’s hypothalamus. We will collectively refer to them as our appetite centre, because overall they inﬂuence our drive to consume food. Our appetite centre is constantly receiving messages from the body. For instance, our digestive tract, microbi- ome and fat cells tell our brain about our energy and nutrient status (Figure 10.10). These feedback cues are meant to keep our bodies in energy balance. However, other signals to the appetite centre can override them. The brain’s limbic system, which is associated with emotions, reward and learning, as well as its prefrontal cortex, associated with our thoughts, also communicate with our appetite centre. Depending on what we see, think and feel, these signals can su- persede other internal messages that aﬀect appetite. For instance, we might not be hungry, but our thoughts might tell our appetite centre that it is 6 pm and we should eat dinner. Alternatively, our thoughts may tell our appetite centre that we shouldn’t eat, even though our appetite centre is activated and wants us to consume food. Figure 10.10: Our appetite centre receives various cues that inﬂuence appetite. Recall that individuals with obesity are more likely to have genetic changes around their appetite-associated genes. This may aﬀect the ability of these genes to properly interpret the signals the body sends, promoting higher food consumption. Thus, advice like just eat less is not helpful for many who deal with excessive energy intake because it does not consider the complexity of appetite regulation. Our appetite centre also receives messages from our external environment that aﬀect our food intake (Figure 10.10). Our thoughts interpret what we see, connect the image with memory and emotion, and then a message about it may be sent to our appetite centre. For instance, we may feel extremely full, but if we see chocolate bars or chips, we might remember how much we like them and the emotions we associate with them. We might then want to consume them despite how uncomfortably full we might feel. The abundance of food and food cues in our environment promote a constant stream of signals to provoke high energy consumption. Large portion sizes, brightly coloured food packaging, constant advertising and cheap food are just some of the messages that our brains need to interpret. These signals compete with our internal appetite signals and often override them. Also, many foods in our food environment are energy dense and nutrient poor, favouring an energy surplus. Collectively, the high energy availability and low demand for physical exertion in our surroundings is referred to as our obesogenic environment. Our psychology can also have a significant eﬀect on our energy status. Stress, mental health status and the way we think about ourselves and our bodies can aﬀect both how much we eat and how much we exercise. Our psychology aﬀects each one of us diﬀerently. For instance, some individuals experiencing depression may binge eat, while others lose their desire to eat. Similarly, some people respond to stress by overeating and stopping their exercise habits, while others might eat less and exercise more while stressed. Recall that our emotional brain communicates with our appetite centre. Sometimes, the desire to eat comes from a desire to feel a diﬀerent emotion, not because our bodies need nutrients or energy. Accordingly, practicing self- care strategies that promote positive emotional health can help improve this signalling system as well as our mental wellbeing. Figure 10.11: Our busy lifestyles can negatively aﬀect our weight-related choices. The psychology of our social surroundings can af- fect food preferences, body size acceptance and physical activity practices. Also, exposure to diﬀerent media, such as commercials and social media, can aﬀect our beliefs around food, physical activity and our bodies. Another major eﬀect of our social psychology is the rush, rush, rush culture we live in – one that gives many a perceived lack of time (Figure 10.11). Our busy lifestyles prioritize other activities over cooking, grocery shopping and exer- cise. Most of us have enough time to eat healthfully and move our bodies, but these may rank lower on our list compared to the many things we feel pressured to do. The amount of physical activity we participate in is the main controllable factor that aﬀects energy expenditure. Many things can aﬀect our activity levels. Our childhood experiences, our physical capacities and our perceptions of physical activity can increase or decrease our desire to be active. Furthermore, how much we move our bodies at work and in our leisure time all contribute to our total energy expenditure. Figure 10.12: The physical activity environment aﬀects our activity levels. Both the natural and built environment can aﬀect how much physical activity we engage in (Figure 10.12). In Canada, some areas have access to water, mountains and more favourable weather conditions compared to others. These can aﬀect whether we engage in physical activity and what activities we are able to perform. For instance, in January, we are more likely to see someone running outdoors in Vancouver, while in Winnipeg, most runners would be seen on an indoor treadmill. Our built environment can also aﬀect activity levels. This includes whether there are opportunities for being active that are free, safe and built into the existing infrastructure. Local, territorial, provincial and federal governments can inﬂuence the physical activity environment by improving transit opportunities, bike routes and hiking trails. Further, governments can support urban planning that favours walkable communities. We do not all handle energy the same way. Specifically, we each have diﬀerent BMRs, hormonal activity, genetics and various other biological factors that aﬀect our energy balance. This partly explains the diﬀerences in fat and weight status between people who eat and move similarly (Box 10.2). Furthermore, changes to our microbiome and appe- tite-related hormones can both inﬂuence how much we eat. We are learning more and more about how the microbes in our bodies, particularly in the digestive tract, aﬀect weight. For instance, it has been found that individuals with obesity are more likely to have a higher proportion of a phy- lum of bacteria called Firmicutes (Castaner et al., 2018; Chakraborti, 2015). Firmicutes are better at harvesting energy from otherwise indigestible carbohydrates and metabolizing them into short-chain fatty acids, which contribute to our energy intake. There is also mounting evidence of a gut-brain axis – a communication system between the organisms in our digestive tract and the brain. We are still researching all the various ways this can aﬀect health, including the abil- ity of these organisms to aﬀect appetite. To promote a healthy gut biome, a diet high in whole foods, including lots of fibre-rich plants is recommended. Being active and lowering stress levels can also improve the health of the microbiome. Leptin: The Satiety Hormone As we learned earlier, leptin is secreted by our fat cells to alert the brain of their energy status (Figure 10.13). When our adipocytes get larger due to more fat storage, leptin acts on the appetite centre, promoting satiety and energy expenditure. This leads to a caloric deficit, which can help shrink these fat cells to their former size. Conversely, when adipocytes are smaller, less leptin is released. This is evidenced by an increase in appetite and a decrease in energy expenditure. Accordingly, leptin is partly responsible for the establishment of a set weight in some people, one that doesn’t ﬂuctuate significantly. However, individuals with obesity are more likely to be resistant to the appetite-decreas- ing eﬀects of leptin. Ghrelin: The Hunger Hormone Ghrelin is secreted by the stomach and has many targets around the body, including the hypothalamus. Ghrelin levels have been shown to spike before meals, promoting appetite (Cummings et al., 2001). While there is still much to learn about this hormone, over-secretion of ghrelin is implicated in the development and maintenance of obesity. In- deed, levels of ghrelin often rise following weight loss, which may promote weight regain (Cummings et al., 2002). Sleep restriction is also associated with elevated ghrelin (Broussard et al., 2016), therefore getting a good night’s sleep may help promote a caloric deficit. GLP-1 Glucagon-like peptide 1 (GLP-1) is secreted by intestinal cells in response to food intake. It signals to the brain that the intestines have food in them, promoting satiety. Individuals with obesity may have impaired GLP-1 signalling, which can decrease satiety and promote higher energy consumption. Liraglutide, an obesity management medication, increases GLP-1 levels in the body, thus lowering appetite. It will be discussed later in the chapter. Figure 10.13: Hormones send appetite and satiety signals to the brain. Body composition is the proportion of fat mass versus lean mass in the body. A body that is higher in lean mass and lower in fat mass is associated with health. Weight gives an indication of body composition, but doesn’t fully capture it. Weight can vary significantly with height, for instance. That is why BMI, which considers both weight and height, is often used instead of weight alone. Even still, measures of weight and BMI have a significant limitation: they tell us very little about body composition. Spe- cifically, they cannot distinguish between fat mass and lean body mass. Accordingly, percent body fat is considered the gold standard for indicating how much fat a person has on their body. It expresses a person’s fat mass as a percentage of their entire body mass. Higher body fat percentages are associated with the increased side eﬀects associated with obe- sity. While percent body fat is more indicative of health risk than weight or BMI, the means of determining it are either expensive, require specialized equipment or are prone to human error. The amount of fat a person has on their body aﬀects health, as does where this fat is primarily located. There are two main areas where fat is stored. Subcutaneous fat is located just below the skin, while visceral fat is located within the abdominal cavity, where many internal organs are found (Figure 10.14). Visceral fat is associated with higher risk of disease compared to subcutaneous fat (Elﬀers et al., 2017; Goran & Gower, 1999). Some means of measuring body com- position can diﬀerentiate between visceral and subcutaneous fat, but most cannot. Figure 10.14: Visceral vs. subcutaneous fat. Dual X-ray absorptiometry (DEXA) is a low-dose x-ray that scans the body in two planes. An image of the body is produced that illustrates body composition. It is a valuable tool because in addition to body fat, it indicates bone density and muscle mass at various locations. It can also discern between visceral and subcutaneous fat. DEXA is a non-invasive procedure as well as quick and easy for the technician and subject to perform. However, the DEXA machine is extremely costly and paying for a scan out of pocket can cost over 100 dollars. Nonetheless, DEXA and air displacement are consid- ered the gold standards for measuring body composition. Body fat percentage can be estimated from body density (Figure 10.15). The body’s density is determined by di- viding its mass by its volume. On earth, our mass is represented by our weight. However, the body’s volume is trickier to determine. We are irregular objects so we cannot use volume equations like those for a sphere or cylinder. Volume can instead be determined by how much we displace a known volume of air or water. For instance, if someone submerges themselves in a large tank with 100 L of water and the total volume rises to 160 L, the person’s volume is 60 L. We used to perform this water displacement technique to determine body fat percentage, but it is costly, time consuming and requires a person to submerge themselves under water. Figure 10.15: Calculating body density. A newer technique, commonly known as the Bod Pod, uses air displacement to measure body volume. A person places themselves in a small pod and the volume of air in the pod before they entered is compared with the volume af- ter they entered. This is advantageous, because it oﬀers a quick, non-invasive and accurate measure of body density and thus body fat percentage. A limitation of this technique is that the person must wear spandex or tight-fitting clothing, so no air is trapped between a person’s body and their clothing. It also requires the person to sit still and be in a confined space, which may make some people uncomfortable. Skin fold analysis involves the use of calipers (Figure 10.16) that pinch and measure folds of skin and the fat that lies underneath them. Using specific sites on the body, these mea- surements are then put into an equation that is used to predict body fat percentage. This technique is easy to perform and requires low-cost equipment. However, if measurements are not performed properly, inaccurate results are obtained. Another limitation is that some people may feel uncomfortable with a measurement test that involves pinching their fat. Some scales and handheld devices estimate body fat percentage through bioelectrical impedance (Figure 10.17). This technique measures the rate at which electrical current passes through the body and determines its voltage. Voltage is calculat- ed by multiplying current by resistance. Since body fat produces greater resistance to current, the measured voltage can estimate how much body fat a person has. Conversely, since a lot of the body’s water is stored in our muscle, a lower resistance will be evidenced if that person has more muscle. The strengths of this technique are that it is fast, non-invasive and inexpensive to use. However, the accuracy is quite variable and can ﬂuctuate signifi- cantly based on hydration levels. As much as a 5 kg decrease in fat-free mass is found in those who are dehydrated, leading to an overestimation of body fat percentage (Lukaski et al., 1986). Figure 10.16: Skinfold measurement. Figure 10.17: Bioelectrical impedance. BMI is calculated according to the equation found in Figure 10.18. The result is then compared to a standardized chart that places people into diﬀerent categories based on their BMI (Figure 10.19). Individuals with a higher BMI are more likely to have an increased risk of health issues. Conversely, an under- weight BMI may also be associated with health complications. This is especially true if someone is underweight because of a health complication. Figure 10.18: BMI equation. Figure 10.19: BMI vs. health risk. Since many countries have used BMI for decades, it is useful for comparing diﬀerent populations over time. It is also a popular tool because it is easy to calculate from either measured or self-reported data. However, BMI calculated from self-reported data is more likely to underestimate true BMI because people may not know their weight and height or they may lie about them (Public Health Agency of Canada, 2011). Despite its ease of use and popularity, there are many limitations to using BMI, making it a weak determinant of individual body composition compared to the other methods. A lean person could have a higher weight due to more muscle or bone mass, but that person might be incorrectly placed in the overweight or obese category. For instance, Ar- nold Schwarzenegger was obese (BMI = 30.1) when he won the Mr. Olympia muscle contest. His highly lean body, not his fat mass, placed him in a higher BMI category. Another limitation of BMI is that it does not diﬀerentiate between visceral and subcutaneous fat. BMI is still widely used for population-based studies due to its simplicity. It may be especially useful at the popu- lation level, where diﬀerences in body composition that could place people in the wrong category are less important, and the big picture is what matters. To help make BMI data more accurate, many newer studies of populations and individu- als often use waist circumference in addition to BMI. Waist circumference is measured a few centimeters above the hip bones with a measuring tape. A waist circumference of more than 88 cm for women or 102 cm for men is considered high risk, especially if that person has an obese BMI. Waist circumference can also indicate visceral obesity. However, as with BMI, it still lacks the ability to properly diﬀerentiate between fat and lean body mass. There is a range of weights for which health is promoted and disease risk is minimized. However, when a high or low weight starts negatively aﬀecting us, reaching a healthier size may be indicated. According to two of Canada’s most prominent obesity doctors, a person’s best weight is, “…whatever weight they achieve while living the healthiest lifestyle they can truly enjoy. There comes a point when a person cannot simply eat less or exercise more and still like their life (Sharma & Freedhoﬀ, 2010).” Our healthiest weight is therefore one that sup- ports physical, mental and social wellbeing, reduces risk of disease, and still allows us to enjoy our lives. There is there- fore no ideal weight and our individual situation and starting point must be considered when determining appropriate weight interventions, if any. We sometimes also want to change our weight to look a certain way. For this weight change to be healthy, we need to make sure that balanced nutrition is promoted and that physical, mental and social wellbeing are not compromised. For most people, losing fat and weight boils down to one key concept: maintaining a consistent caloric deficit. All diets work on that same principle (Table 10.1). They diﬀer, however, in how that caloric deficit is achieved. Paying for weight loss programs is not required for weight loss, but a caloric deficit is. Whether a strategy works to promote sustain- able weight loss depends on whether it can be maintained. If we attain a particular weight but cannot maintain it, the strategies adopted are probably incompatible with our lives. It is therefore imperative to think in terms of lifestyle chang- es instead of quick fixes. We must figure out what works for us, which may be similar to or diﬀerent from what works for others. Table 10.1: Select weight loss diets. A good place to look for eﬀective long-term strategies with respect to weight loss and maintenance is the National Weight Control Registry. This database collects information from individuals who have lost at least 30 pounds (13.6 kg) and kept it oﬀ for at least a year. It contains data from more than 10,000 people, 80% of which are women, mostly in their 40s. The average subject lost about 70 pounds and kept it oﬀ for 5.5 years (Wing, n.d.). Accordingly, it is wealth of information for what works for some people. Nearly every member of the registry reported that the weight loss improved their energy levels, mobility, mood, self-confidence and overall physical health (Klem et al., 1997). Table 10.2 shows some of the study’s other main findings. Table 10.2: Findings of the National Weight Control Registry. Central to achieving a caloric deficit is consuming less calories than we currently consume. A good place to start is to assess current intake levels, perhaps through a dietary analysis or through food journaling (Figure 10.20). Once our typical food intake is determined, we can set a goal to reduce energy consumption from this baseline. However, it is important to not set an unre- alistic goal that is unsustainable or that does not pro- mote health. Our bodies need a base level of calories to maintain our critical functions. A modest caloric deficit of 500–1000 kcal per day can lead to significant changes in fat mass over time (Jakicic et al., 2001). This amount is also more likely to be sustainable compared to more drastic caloric deficits. Figure 10.20: We can use a journal to track our food consumption. Journals can also help us with our emotional wellbeing. Tracking our daily intake can help provide accountability and a realistic goal to strive for. Furthermore, feedback is a powerful behaviour-change tool. When we see a record of our meal and exercise history, it may motivate us to make appropriate changes. Indeed, food tracking may help promote modest weight loss (Burke et al., 2012). However, caution should be taken with respect to how food tracking aﬀects mental health and quality of life. Some individuals find it de- manding and guilt-promoting (Lupton, 2018). We need to make sure that our mental health is supported and that food tracking and other weight-managing techniques are not causing more harm than good. One of the reasons higher weights are so common in North America is the large portion sizes we have grown accustomed to. Portion sizes in restaurants and in homes have increased dramatically over time, leading to higher caloric intake. A systematic review of 72 studies found that people consistently eat more when they are given larger portions (Hollands et al., 2015). Specifically, when portion sizes double, energy intake increases by 35% on average (Zlatevska et al., 2014). While we cannot control the size of portions in restaurants, we can control how we respond to them. We can split an entrée with a friend, package part of our meal for later or simply not finish what’s on our plate if we are full. We can, however, make changes to the size of our portions at home by using smaller plates or putting less food on them. A small change can have a large impact. For example, a 10% decrease in portion sizes would lead to a 10% decrease in caloric consumption. For a person on a 2000-kcal diet, that amounts to 200 kcal less a day. Over a year that can amount to about 9 kg (20 pounds) of energy weight. Controlling our hunger may help us consume a more modest number of calories. We can decrease our hunger and appetite by eating in a way that promotes satiety. Protein-rich food and fibre-rich foods are well established to pro- mote satiety (Fiszman & Varela, 2013; Halton & Hu, 2004; Van Kleef et al., 2012). Also, volume-rich foods like vegetables and soups may decrease hunger by stretching the stomach (Powley & Phillips, 2004). In general, whole foods are more likely to promote satiety than processed and ultra-processed foods (Fardet, 2016; Hall et al., 2019). Eating slowly may also promote meal fullness. A meta-analysis of 22 studies found that those who eat slower consume less calories overall (Robinson et al., 2014). It takes the brain about 20 min to receive the message that we are full. When we eat more slow- ly, we give the brain enough time to receive this message so we don’t overeat. Willpower is our thinking brain’s ability to override other signals. For instance, we may really want to eat, but our thoughts could override this drive and stop us from eating. When it comes to moderating food intake, willpower can help, but it is not typically sufficient to sustainably change behaviour (Dulloo, 2012). For one, our willpower can be exhausted. When we use it too much, our willpower depletes and making healthy decisions may become more difficult (Vohs et al., 2008). Also, willpower may be used to severely restrict food intake. Unhealthy food restriction may lead to inadequate nutrient and energy consumption. It may also compromise our mental health. This is partly why skillpower is recommended in addition to willpower. Skillpower means making the healthy decision the obvious and easy one. Exam- ples of skillpower are shown in Figure 10.21. Figure 10.21: Examples of skillpower. The component of energy expenditure that is most under our control is physical activity, and being physically active is one of the best things we can do for our overall health. It reduces disease risk and improves nearly all aspects of wellbeing. It may also promote fat loss by increasing energy expenditure and BMR. This is typically more evident at high- er intensities, longer durations and with exercise consistency over time. Physical activity, especially resistance exercises, can also preserve lean body mass while at a caloric deficit. However, in general, physical activity may not be sufficient to provide sustainable and clinically significant weight loss. Indeed, a review of the evidence found that most long-term physical activity programs only promoted a weight loss of approximately 2 kg on average (Swift et al., 2014) and individuals varied substantially in how much weight they lost on these programs. Further, beyond a threshold, more physical activity does not correlate with increased energy expendi- ture or weight loss (Pontzer, 2015). The body may adapt to long-term increases in activity by either moving less in other areas, or by decreasing energy expenditure elsewhere. For clinically significant weight loss, the American College of Sports Medicine recommends upwards of 250 min per week of moderate intensity activity (Table 10.3) (Donnelly et al., 2009). Regardless of its aﬀect on energy balance, a practice of regular physical activity is critical for our physical, mental and social wellbeing. Table 10.3: American College of Sports Medicine physical activity recommendations (Donnelly et al., 2009). Recall that one of the factors that aﬀects appetite is our emotional health. Sometimes when we are hungry or don’t want to exercise, it is our emotional centres driving the decision. Accordingly, factors that promote psychological wellbeing can help promote a caloric deficit as well as a healthier relationship with food, activity and our bodies. The following concepts and strategies may accordingly help manage weight. Self-efficacy is our belief in our ability to achieve a certain task. If we do not believe we can eat less, move more or change body composition, that makes it more difficult to do. Setting small, achievable goals, celebrating ourselves when we make a healthy choice and giving ourselves affirming thoughts may help improve self-efficacy with respect to weight-related behaviours. Emotions are physical feelings experienced in the body that are linked to mental states. Joy, excitement, sad- ness, guilt and shame are all emotions. These are messages that convey our current experiences, which may lean more negative or positive depending on the individual. Our appetite centre is constantly receiving messages from our brain’s emotional centres. If we do not want to accept or experience these emotions, we might numb them with distractions such as social media, drugs or food. Indeed, escape theory suggests that individuals exhibit emotional eating to cope with the stressors in their lives (Heatherton & Baumeister, 1991). Finding positive coping mechanisms, such as talking to others, spending time in nature, journaling, crying or speaking to a counsellor, may help to deal with the emotional triggers that promote overeating. Mindfulness is the practice of being aware of and experiencing the present moment, including its thoughts, emotions and sensations with a judgement-free, curious approach (Brown & Ryan, 2003). It may help us promote a healthy weight by regulating our emotions and improving our relationship with food, activity and our bodies. Indeed, a systematic review of mindfulness-based training on obesity-related eating found that most studies showed a decrease in emotional eating, mindless eating and excess weight (Mantzios & Wilson, 2015). There are diﬀerent ways mindfulness can be practiced, including meditation, breathing exercises and attention to the present moment regardless of the sur- roundings. We can also eat mindfully. Mindful eating means being aware of what we are eating and thinking about each bite. It may also mean an awareness of the various sensations our bodies experience while eating. Fad diets are ones that are popular for a limited time. They often promise quick results, are endorsed by celebri- ties and inﬂuencers, and are not based on sound dietary recommendations. Any diet that promotes a caloric deficit will eventually lead to weight loss if sustained. However, many fad diets are nutrient poor, which can compromise health. The other problem with many of these diets, is that they are so extreme that they cannot be maintained long-term, leading to weight regain. Many people who use fad diets get stuck on a never-ending fad diet cycle (Figure 10.22). This pattern does not promote a positive relationship with food and often leads to yo-yo dieting. If a diet is extreme and/ or not compatible with our lifestyle, it is less likely to be successful. Figure 10.23 outlines some factors that indicate if a weight loss plan is a fad diet. Figure 10.22: The never-ending fad dieting cycle. Figure 10.23: Fad diet red ﬂags. While lifestyle management that promotes a caloric deficit is indicated for most individuals who are overweight, above a certain level of adiposity, lifestyle management alone may not be enough to improve physical and mental health. Doctors might then be consulted for potential medical interventions. Currently, there are three approved drugs for the management of obesity. They are only available by prescrip- tion, have side eﬀects and can be expensive. Orlistat blocks the activity of the lipid-digesting enzyme lipase in the small intestine. Accordingly, lipids cannot be digested into free fatty acids and absorption is limited. This promotes weight loss as fewer total calories are absorbed from food. Since fat absorption is blocked, fat-soluble vitamins are not readily absorbed and deficiency is more likely. Further, unabsorbed fat can pass into the large intestine, promoting oily stools, fecal incontinence and gastrointestinal issues (O’Meara et al., 2004). Liraglutide (brand name = Saxenda) increases the activity of the signalling molecule GLP-1. Recall that the pres- ence of food in the small intestine leads to the release of GLP-1, which acts on the hypothalamus to promote satiety. Since people with obesity may have compromised appetite regulation, this drug can promote the satiety that reduces food intake. Liraglutide was originally marketed as a diabetes drug as it also has positive eﬀects on blood glucose regu- lation. Its main limitation is that it is expensive and not covered by most extended medical plans. Also, it can promote nausea and vomiting, although this can typically be mitigated by altering the dose (Mancini & de Melo, 2017). Naltrexone/Bupropion (brand name = Contrave) was approved for use in Canada as an anti-obesity drug in 2018. It is a combination of two drugs that have historically been used to treat certain drug dependencies as well as depres- sion. Together, these drugs reduce food cravings by altering the reward circuit in the brain that drives food-seeking behaviour. Like liraglutide, it is expensive and not covered by most extended medical plans. Nausea is the most common- ly reported side eﬀect, though some people also experience headache, constipation, dizziness, vomiting and dry mouth (Greenway et al., 2010). Bariatric surgeries promote weight loss by altering the stomach. One of the main ways they promote weight loss is due to a smaller stomach size that can receive less food. This promotes satiety and a decrease in energy intake. Figure 10.24 outlines the three most common types of bariatric surgeries. Of these, Roux-en-y and sleeve gastrectomy typi- cally produce the greatest amount of weight loss – typically between 50 and 70% of a person’s highest weight (Peterli et al., 2013), while gastric banding typically results in a 50% reduction (Cunneen, 2008). With these procedures, there is typically a large initial weight loss in the first year, with small increases in the following two years. In addition to the weight-related outcomes, bariatric surgery is also associated with improvement in type 2 diabetes, CVD and quality of life (Cunneen, 2008; Peterli et al., 2013). Figure 10.24: Types of bariatric surgery. Following surgery, food intake patterns change for the rest of the person’s life. Not only will they typically have to eat less, they often must limit certain foods and beverages such as bread and alcohol. Since gastric surgery changes the digestion process, micronutrient deficiencies are more common. Vitamin and mineral supplements are therefore typically required. On the other side of the spectrum, some people have a lower body weight and struggle to gain weight. This is often due to physiological reasons such as a higher BMR or genetic factors that promote a lower appetite. If a thin person is eating healthy, being active and has good physical and mental health, there is nothing inherently unhealthy about their size. However, for health or aesthetic reasons some people want to gain body mass. This can be done by increasing either lean mass or fat mass. If we want to increase lean mass, the best way to do so is with consistent resistance exercises that focus on build- ing muscle, which in turn also build bone mass. It is important to remember that how much muscle mass can be gained is limited by our genetic and physiological makeup. We all have diﬀerent body sizes and shapes and there is only so much muscle mass a person can gain. If a person wants to gain fat mass, they will need to consume more calories than they burn. If they are also exercising, this might mean that energy intake may have to increase dramatically. Tracking calories through journaling or with an app might be helpful for determining baseline food intake. It can then be increased. However, healthy nutritional recommendations are still important. Focusing on increasing nutrient- and calorie-dense whole foods will promote a gain in fat mass while still promoting health (Figure 10.25). Figure 10.25: Foods that are energy- and nutrient-dense. Eating disorders (EDs) are not about food. The relationship with food is often indicative of another underlying cause. Eating disorders are multifactorial and include genetic, psychological and environmental risk factors. For years, a strong genetic component of EDs has been know (Thornton et al., 2011). The newer technique of genome-wide associ- ation studies has further shown that there may be specific genes at play in increasing risk. For instance, eight mutations have been found that are more common in individuals with anorexia nervosa (Watson et al., 2019). Some of these muta- tions are similar to those found in people with other psychiatric disorders. Women, especially younger women, are far more likely to experience eating disorders than men (Galmiche et al., 2019). Socio-cultural factors, such as the pressure to be thin, are believed to contribute to this disparity (Le et al., 2017). Perfectionism, obsessive tendencies and sensitivity to reward and punishment are also more common in individuals with EDs (Le et al., 2017; Thornton et al., 2011). A history of physical and/or sexual abuse may also promote EDs. For example, children who were sexually abused are more than two times more likely to develop bulimia nervosa (Sanci et al., 2008). Certain risk factors for EDs are also evidenced in individuals with obesity and depression, including body dissatisfaction and frequent dieting (Goldschmidt et al., 2016). Anorexia nervosa, bulimia nervosa and binge eating disorders are the three eating disorders recognized by the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). In addition, there are other disor- dered eating patterns that don’t have a clinical diagnosis but are also problematic for psychological and physical reasons. These include night eating syndrome and orthorexia. People who have bulimia nervosa and binge eat- ing disorder both experience recurrent episodes of binge eating (Figure 10.26). Binge eating involves a loss of con- trol, where the conscious regulation of eating is severely compromised and a person cannot stop themselves from overconsuming. A binging episode is one that occurs in a specific amount of time (e.g., two hours), where a person eats an amount of food much larger than most people would eat during a similar period. This binging typically occurs in the absence of hunger, at a fast rate, while the person is alone, and with feelings of guilt and shame (American Psychiatric Association, 2013). Figure 10.26: Binge eating typically occurs alone, at a fast rate and in the absence of hunger. Bulimia nervosa aﬀects 1.9% of women and 0.6% of men (Galmiche et al., 2019). It is evidenced by episodes of binge eating followed by compensation. This compensation is typically vomiting but may also include fasting, excessive exercising, or using laxatives or diuretics. For it to be diagnosed as an eating disorder, this behaviour must occur at least once a week for three months (American Psychiatric Association, 2013). People who have other psychological disor- ders such as depression and who diet frequently are at higher risk for bulimia (Goldschmidt et al., 2016). Warning signs include a preoccupation with food, distorted perceptions of body weight and frequent dieting. Bulimia nervosa is often difficult to spot because body size tends to be average. In addition to the potential negative mental eﬀects, bulimia that includes vomiting has other potential compli- cations. Stomach acid that is vomited can lead to stomach rupture, tears in the esophagus and gastroesophageal reﬂux. One of the hallmarks of bulimia with vomiting is deterioration of the teeth due to stomach acid. More seriously, however, is the fact that vomiting can lead to electrolyte imbalances, which can negatively impact the heart and other tissues. Binge eating disorder is the most common eating disorder, aﬀecting approximately 2.8% of women and 1% of men (Galmiche et al., 2019). Like bulimia, binge eating disorder involves episodes of binge eating. Unlike bulimia, there is no post-binge compensation. Accordingly, it is more likely to promote obesity and its related complications. However, binge eating disorder can also occur in individuals who are not obese. Binge eating disorder is more likely to occur in individuals who diet (Dingemans et al., 2002). Body dissatisfaction and depressive symptoms increase risk, as does the inability to interpret hunger and satiety signals (Dingemans et al., 2002). Unlike the other eating disorders, binge eating disorder is more likely to occur past adolescence and occurs in all age groups. Figure 10.27: Individuals with anorexia may have an obsession with perfection and an Approximately 1.4% of women and 0.2% of men experi- ence anorexia nervosa during their lives (Galmiche et al., 2019). Anorexia involves a significant restriction in energy intake leading to a unhealthfully low body weight. Individuals with anorexia typ- ically have an intense fear of weight gain and spend a lot of eﬀort to avoid it (Figure 10.27) (Morris & Twaddle, 2007). They may feel disturbed by their body weight and shape and may struggle with self-worth and acceptance. There are diﬀerent manifestations of anorexia. Some individuals with anorexia may exercise excessively or consume laxatives. There is also a binging/purging subcategory of anorex- ia, which involves episodes of binge eating followed by vomiting or excessive exercise. This is similar to bulimia but is considered anorexia because body weight is at an unhealthfully low level. intense fear of weight gain. Anorexia is the psychiatric condition with the highest mortality rate (Hoek, 2006). Suicide is believed to account for 20% of anorexia-related deaths (Arcelus et al., 2011). However, most cases are due to the side of eﬀects of a severe nutritional deficiency or an excessively low body weight. Nutrient deficiencies are common in anorexia, as are fatigue, hair loss, insomnia, dizziness and fainting. Females with anorexia may also develop amenorrhea – a cessation in men- struation. In the purging type of anorexia, there is an increased risk of tooth decay, ulcers and electrolyte imbalances. Treatment is imperative for all forms of this disorder. Night eating syndrome is found in the DSM-5 under Other Specified Feeding or Eating Disorders. It does not have diagnostic criteria, though some were proposed at an international research meeting in 2008 (Allison et al., 2010). These criteria include an abnormal increase in food intake at night resulting in at least 25% of total calories being con- sumed after dinner. It could also include the person waking up in the middle of the night to eat. An individual with night eating syndrome is aware that these episodes are taking place and an increase in stress surrounding the episode or condition is common. Other features include a lack of appetite and food intake in the morning and/or insomnia at night. Some who experience the condition might exhibit a belief that they need to eat in order to go to sleep or return to sleep. Night eating syndrome increases the risk for obesity. Those who are not overweight or obese might purposely delay their food intake throughout the day to eat more at nighttime. Orthorexia nervosa is an obsession with eating healthy that has negative psychological implications. Individu- als with orthorexia may severely restrict food intake for the sake of promoting health, though it may have the opposite eﬀect. It does not have formal diagnostic criteria, so incidence is unknown. Even so, it is the subject of a lot of current research, as it is believed to be promoted by the increasing societal pressure towards healthy or clean eating (Costa et al., 2017). An individual who experiences orthorexia might compulsively check nutrient facts boxes and ingredients lists and be preoccupied with the health of a food’s constituents. They may limit food intake to a narrow number of foods or food groups and cut out others, including sugar, carbohydrates, dairy or animal products. While this may be done for health reasons, it is the obsession and negative mental health implications of these restrictions that may cause it to be a disor- dered eating pattern. Since individuals with orthorexia may consume a less varied diet, they may also be at higher risk for micronutrient deficiencies (Dunn & Bratman, 2016). They may also experience higher levels of stress and their obsessive behaviour may compromise their social, academic and work functions. Treatment of EDs typically begins with proper diagnosis by a healthcare professional. This presents a challenge, however, as symptoms often go unrecognized. Bulimia, binge eating disorder and anorexia each have screening tools that can be used for diagnosis. Once diagnosed, the main treatment strategies are psychological in nature (Sim et al., 2010). One of the most common psychological treatments is cognitive behavioural therapy (CBT). CBT is a type of talk therapy aimed at identifying thought patterns and behaviours that are unhelpful. The practitioner then guides the individual to replace these limiting beliefs and actions with helpful ones. Medication may also help certain individuals regulate their appetite and/or manage the other psychiatric conditions that might accompany an ED. Energy balance occurs when energy intake from food matches the energy used to keep us alive and perform our various activities. While minor ﬂuctuations in energy balance are normal, ones that promote a caloric surplus leading to obesity can have numerous physical and mental complications. There is a complex set of causes for the high rates of obesity seen in Canada and the developed world. Both physiological, psychological and environmental factors promote a caloric surplus. Learning to recognize and manage these factors can help promote energy balance and a reduced risk of disease. However, restrictive food behaviours, compulsive dieting and participating in fad diets may compromise both physical and mental wellbeing. These factors are also associated with higher risk of eating disorders. Eating disorders are psychological in nature and often require professional intervention. Energy balance is achieved when energy intake equals energy expenditure. Carbohydrates, lipids, proteins and alcohol contribute to our energy intake. BMR, physical activity and diet-induced thermogenesis form our energy expenditure. If a consistent energy surplus is achieved, energy storage and weight gain are favoured. Higher energy storage can lead to obesity and its related physical, mental and social eﬀects. Obesity is caused by a complex set of interrelated factors. Body composition is the relative contribution of fat and lean mass to our overall weight. DEXA and air displacement are the gold standards for assessing body composition. Our best weight is the weight achieved while practicing our healthiest lifestyle, one that also allows us to enjoy our lives. If a consistent energy deficit is achieved, energy retrieval and weight loss are favoured. Healthy, evidence-based practices to achieve a caloric deficit include tracking food intake, regulat- ing hunger levels, decreasing portion sizes, practicing mindfulness, and performing self-care. High levels of physical activity are required to promote clinically significant weight loss. Individuals with obesity may only respond modestly to lifestyle interventions and can also seek medical interventions such as pharmaceuticals and bariatric surgery. Eating disorders are multifactorial. They have genetic, psychological and environmental risk fac- tors. Achieve a healthy energy balance by moderating caloric intake and regularly participating in phys- ical activity. To lose fat mass, consume less calories than are expended. To gain fat mass, consume more calories than are expended. Individualize fat loss programs to support physical, mental and social wellbeing. Practice self-care, mindfulness and skillpower. Participate in regular physical activity to promote health. 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