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16.1.4: Obesity

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    According to the World Health Organization (2017b), 1.9 billion of the world’s people are overweight and 650 million of these are obese. In the United States, 70% of Americans are overweight, and 40% of these meet the criteria for obesity. For the first time in human history, most of the world’s population lives in countries where overweight and obesity kill more people than hunger does (see Figure 16.3). Improvements in public health and food production have allowed a greater number of people to live past childhood and to have enough food to eat. This does not include everyone. Many people still struggle with poverty, hunger, and disease, even in the wealthiest of nations, including the United States. On a global scale, however, many people not only have enough food to survive but also to gain weight—and, notably, enough extra weight to cause significant health problems. Several aspects of life in modern, industrialized societies contribute to the obesity crisis.

    image2-1-2.pngFigure \(\PageIndex{1}\): Obesity rates by country, 2017.

    Causes of Obesity

    Although studies show differences in daily energy expenditure between modern foraging and farming populations in comparison with industrialized peoples, the major contributor to obesity in Western populations is energy intake (Pontzer et al. 2012). Many people not only eat too much but too much of the wrong things. Biological anthropologist Leslie Lieberman (2006) argues that contemporary humans continue to rely on cues from foraging strategies in our evolutionary past that are now counterproductive in the obesogenic environments in which we now live.

    Examine your own eating habits in the context of how humans once hunted and gathered. We relied on visual cues to find food, often traveling long distances to obtain it, then transporting it back to our home base. There we may have had to process it, by hand, to render it edible. Think of how much less energy it takes to find food now. If we have the financial resources, we can acquire big energy payoffs by simply sitting at home and using an app on our mobile phone to place an order for delivery. And, voila! High-calorie (if not highly nutritious) food arrives at our door within minutes. Should we venture out for food, search time is reduced by signage and advertising directing us toward high-density “patches” where food is available 24 hours a day. These include vending machines, gas stations, and fast-food outlets. Travel time is minimal and little human energy is used in the process (Lieberman 2006).

    Foods are also prepackaged and prepared in ways that allow us to eat large quantities quickly. Think French fries or chicken nuggets, which we can easily eat with our hands while doing other things, like driving or watching television, rendering eating mindless and allowing us to take in food faster than our endocrine systems can let us know we are getting full. Modern “patches” offer low-fiber, calorie-dense resources, which allows us to eat larger quantities, a problem already encouraged by our larger portion sizes (Lieberman 2006). Processed foods are also engineered to appeal to hominin preferences for sweet tastes and fatty, creamy textures (Moss 2013). Remember from earlier chapters that natural selection favored depth perception, color vision, grasping hands, and coordinated eye-hand movements as general primate traits. Advertising and packaging now use our color vision against us, attracting us to products with little nutritional value and playing to our evolutionary predisposition toward variety. Remember those 50 different nutrients we require? That variety is now presented to us in the form of 55 different flavors of Oreo cookies (Cerón 2017), which we take out of the package and dip in milk using our hand-eye coordination and depth perception.

    Even if we are ostensibly eating the same things our ancestors did, these foods may not be all that much alike. Take potatoes, for example. One medium-sized, plain, baked potato is a healthy food, especially if we eat the skin too. It contains 110 calories, 0 grams of fat, 26 grams of carbohydrates, and 3 grams of protein, plus 30% of the U.S. Recommended Daily Allowance (RDA) of vitamin C, 10% of vitamin B6, 15% of potassium, and no sodium (http://www.potatogoodness.com). In contrast, a medium order of McDonald’s fries, which takes the potato and adds salt and fat, contains 340 calories, 16 grams of fat, 44 grams of carbohydrates, 4 grams of protein, and 230 mg of sodium (http://www.mcdonalds.com). Potato chips take food processing to a whole new level, removing even more nutrition and adding a host of additional ingredients, including oils, preservatives, and artificial flavorings and colors (Moss 2013). Let us use Ruffles Loaded Bacon and Cheddar Potato Skins Potato Chips, one of the top new flavors of 2018, as an example (St. Pierre 2018). The number of ingredients increases from one to 11 to 35 as we move from the potato to the potato chip, moving further from nature with each step (Figure 16.4). It should be noted that the nutritional information for the potato chips is based on a serving size of 11 chips, an amount likely smaller than many people eat. Our bodies also do not react to fries and chips the same way they do to potatoes. Added fat and calories translate into overweight and obesity. Sodium contributes to hypertension. And, artificial flavorings and colorings, including the Yellow 5 and Yellow 6 in the chips, have been linked to cancer, as well as allergies and hyperactivity in children (CSPI 2010). Many sweet, fatty, salty foods like fries and chips are cheap and easily available, which is why many people choose to eat them (Moss 2013). The price of a medium-sized order of McDonald’s fries as of this writing is US$1.79, and the potato chips are $2.98 for an 8.5-ounce bag. A single potato prewrapped for microwaving is available in many supermarkets for US$1.99 but requires travel to a market and access to a microwave and eating utensils, making it less convenient.

    Table 16.5.1: The potato in three modern forms.
     

    image8-1-1.jpg

    Baked Potato

    [baked, skin on, plain]

    image12-1-1.jpg

    French Fries

    [medium order]

    image6-4.jpg

    Potato Chips

    [1 oz. serving of 11 chips]

    Calories 110 340 160
    Calories from fat 0 144 90
    Fat 0 g 16 g 10 g
    Carbohydrates 26 g 44 g 15 g
    Protein 3 g 4 g 2 g
    Sodium 0 g 230 mg 170 mg
    Dietary fiber 2 g 4 g 1 g
    Sugars 1 g 0 g 1 g
    Cholesterol 0 g 0 g 0 g
    Ingredients Potato Potatoes, Vegetable Oil (Canola Oil, Soybean Oil, Hydrogenated Soybean Oil, Natural Beef Flavor [Wheat and Milk Derivatives]*, Citric Acid [Preservative]), Dextrose, Sodium Acid Pyrophosphate (Maintain Color), Salt. Potatoes, Vegetable Oil (Sunflower, Corn, and/or Canola oil), Bacon & Cheddar Loaded Potato Skins Seasoning (Maltodextrin [Made from Corn], Salt, Cheddar Cheese [Milk, Cheese Cultures, Salt, Enzymes], Sour Cream [Cultured Cream, Skim Milk], Whey, Dried Onion, Monosodium Glutamate, Natural Flavor [including Natural Smoke Flavor], Skim Milk, Corn Oil, Canola Oil, Sugar, Buttermilk, Yeast Extract, Romano Cheese [Part-Skim Cow’s Milk, Cheese Cultures, Salt Enzymes], Whey Protein Concentrate, Dextrose, Spice, Citric Acid, Lactic Acid, Artificial Color [Yellow 5 Lake, Yellow 5, Yellow 6, Yellow 6 Lake], Butter [Cream, Salt], Sodium Caseinate, Garlic Powder, Blue Cheese [Milk, Cheese Cultures, Salt, Enzymes], and Bacon Fat.

    Not only have we transformed the food supply and our eating in ways that are detrimental to our health, but these changes have been accompanied by reductions in physical activity. Sedentarism is built into contemporary lifestyles. Think of how much time you spent sitting down today. Some of it may have been in class or at work, some may have been driving a car or perhaps binge-watching your favorite show, playing a video game, or checking in on social media. An inactive lifestyle is almost dictated by the digital age (Lucock et al. 2014). Levels of physical activity in many countries are now so low that large portions of the population are completely sedentary, including 28% of Americans (Physical Activity Council 2018). For a species whose biology evolved in an environment where walking, lifting, and carrying were part of daily life, this is unhealthy and often leads to weight gain.

    Obesity varies by gender, age, geography, and, to some degree, ethnicity (Brown 1991). In general, women tend to gain weight easier than men, but fat distribution is different between them. Women tend to put on weight in the thighs and hips, while men gain weight around their abdomen. The latter is a much greater health risk (Akil and Ahmad 2011). Weight gain also varies across the lifespan, with infants and toddlers tending toward chubbiness then becoming slimmer until adolescence and the onset of puberty (Lucock et al. 2014). This pattern is the result of selective pressure to maintain energy for brain development in early life, then again later on for reproduction. There is also the “thrifty gene” hypothesis: the idea that natural selection favored genotypes that clung to every calorie available to protect against the constant threat of food shortages throughout our evolutionary history, and that this was a species-wide adaptation (Neel 1962).

    Figure \{\PageIndex{2}\} Participants of a walk against diabetes and for general fitness around Nauru airport.

    More recent genetic research indicates there are multiple genetic variants that influence weight gain, and they are not spread evenly across or within human populations. Tuomo Rankinen and colleagues (2006) identified 127 genes associated with obesity, of which 22 were supported by research indicating that they contributed to positive energy balance and weight gain. Claude Bouchard (2007) went further, identifying five categories of obesity-promoting genotypes. These include genotypes that promote sedentarism, result in low metabolism, and lead to poor regulation of appetite and satiety and a propensity to overeat. An example of the impact such genotypes can have in an environment of plenty is found among the population of the Micronesian island of Nauru. Historically, the island was geographically isolated and the food supply was unpredictable. These conditions favored genotypes that promoted the ability to rapidly build up and store fat in times of food availability. In Nauruans, there are two genetic variations favoring weight gain and insulin resistance, and both are associated with obesity and Type 2 diabetes. One variant is also associated with higher diastolic blood pressure. One of these variants is also found in Pima Indians in the United States, where it is associated with a high and Type 2 diabetes, although it is not associated with the same outcomes in Japanese and British subjects (de Silva et al. 1999). The other variant was also analyzed in Finnish and South Indian populations, neither of whom experienced the same outcome as Nauruans. This suggests these alleles may act as modifying genes for Type 2 diabetes in some population groups (Baker et al. 1994). Unfortunately, Nauruans are one of those groups. Eventually, they became wealthy through phosphate mining on the island, gaining access to a calorie-rich Western diet of imported foods and developing a sedentary lifestyle. This resulted in rates of Type 2 diabetes as high as 30–40% of Nauruans over the age of 15, which became the leading cause of death (Lucock et al. 2014), something Nauruans are taking seriously (See Figure 16.5).

    Factors other than biology influence which populations carry and express a genetic predisposition toward obesity and which populations carry but do not express it. The Pima Indians, for example, were seriously impacted by U.S. government policies that affected water rights, forcing the population away from subsistence farming to dependence on government commodities and convenience food. This resulted in a significant loss of physical activity and sedentarism, as well as malnutrition and obesity. Those living on the reservation continue to experience hardship due to high rates of unemployment and poverty, as well as depression, sometimes made worse by alcoholism. In the absence of these pressures, the Pima were diabetes free for centuries prior, even though they relied on agriculture for subsistence, suggesting genetics alone is not responsible for high rates of obesity and diabetes in current populations (Smith-Morris 2004).

    Obesity also has an epigenetic component. You learned about epigenetics in Chapter 3. With regard to obesity, epigenetics is counterintuitive in that mothers who do not take in enough calories during pregnancy often give birth to babies who grow up to be fat. What takes place is that the fetus receives signals from the mother through the placenta and intrauterine environment about environmental conditions during pregnancy, in this case food insecurity. These signals encourage the turning on and off of genes related to metabolism, for example. This alters the phenotype of the fetus so that if the child is born into an environment where food is readily available, it will put on weight rapidly whenever possible, falling prey to obesity and related diseases later in life. What is worse is that if the child is a girl, her own eggs are formed in utero with the same genetic changes coded in, meaning she will pass along this same genetic predisposition to gain weight to her children. Hence, a biological propensity toward obesity can continue across generations (Worthman and Kuzara 2005). This same mechanism operates in populations born into poverty that are now growing into plenty. Epigenetic changes to genes that promote weight gain are argued to be partly responsible for the rapid rise in obesity and diabetes in recent years in developing countries gaining access to Western diets (Stearns et al. 2008).

    Obesity and overweight put a tremendous strain on several biological systems of the body, including the circulatory, endocrine, and skeletal systems, contributing to hypertension, heart disease, stroke, diabetes, and osteoarthritis (See Figure 16.6). Obesity also elevates the risk of cancers of the breast, endometrium, kidney, colon, esophagus, stomach, pancreas, and gallbladder (National Institutes of Health 2017; Vucenik and Stains 2012). Diabetes, one of the fastest growing health conditions around the globe (WHO 2016) and one tightly connected to obesity and overweight, is the focus of the following Special Topics feature.

    image4-7.pngFigure \{PageIndex{3}\} Medical Complications of Obesity.

    SPECIAL TOPIC: DIABETES

    image14-1-1.pngFigure \{PageIndex{4}\}: Glucose metabolism is the body’s evolved mechanism by which we turn food into energy for bodily functions. Carbohydrates are eaten and broken down into simple sugars (e.g., glucose). Glucose enters the bloodstream from the intestines, and the increase in glucose stimulates the pancreas to release insulin into the bloodstream. Insulin deposits glucose in the muscles and fat cells, where it is stored and used for energy.

    Diabetes Mellitus is an endocrine disorder characterized by excessively high blood glucose levels (Martini et al. 2013). According to a report released by the World Health Organization, the number of people living with diabetes is growing in all regions of the world. Rates of diabetes have nearly doubled in the past three decades, largely due to increases in obesity and sugary diets (WHO 2016). One in 11 people around the world, 435 million people, now have diabetes, including over 30 million Americans. In the United States, the disease is rising fastest among millennials (those ages 20-40) (BCBSA 2017), and one in every two adults with diabetes is undiagnosed (IDF 2018). Obesity and diabetes are linked: that is, obesity causes a diet-related disease (diabetes) because of humans’ evolved metabolic homeostasis mechanism, which is mismatched to contemporary energy environments (Lucock et al. 2014).

    image3-2-e1568591669817.pngFigure \{\PageIndex{5}\}: Glucose metabolism is the body’s evolved mechanism by which we turn food into energy for bodily functions. Carbohydrates are eaten and broken down into simple sugars (e.g., glucose). Glucose enters the bloodstream from the intestines, and the increase in glucose stimulates the pancreas to release insulin into the bloodstream. Insulin deposits glucose in the muscles and fat cells, where it is stored and used for energy.

    To function properly, cells need a steady fuel supply. Blood sugar is the primary fuel for most cells in the body, and the body produces the hormone insulin to help move energy into cells that need it. Insulin functions like a key, turning on insulin receptors located on the surface of the cell. The receptor then activates glucose transporters (GLUTs) that do the work of hauling glucose (blood sugar) out of your bloodstream and into your cells (McKee and McKee 2015; see Figure 16.7). Foods that most readily supply glucose to your bloodstream are carbohydrates, especially starchy foods like potatoes or sweet, sugary foods like candy and soda. The body can also convert other types of foods, including protein-rich foods (e.g., lean meats) and fatty foods (e.g., vegetable oils and butter), into blood sugar in the liver via gluconeogenesis. Insulin’s main job is to tell your cells when to take up glucose. The cell also has to listen to the signal and mobilize the glucose transporters. This not only allows your cells to get the energy they need, but it also keeps blood sugar from building up to dangerously high levels when you are at rest. Muscles can use glucose without insulin when you are exercising; it does not matter if you are insulin resistant or if you do not make enough insulin. When you exercise, your muscles get the glucose they need, and, in turn, your blood glucose level goes down. If you are insulin resistant, resistance goes down when you exercise and your cells use glucose more effectively (Leontis n.d.).

    This system is efficient, but there are limits. Keep in mind that, like the rest of our biology, it evolved during several million years when sugar was hard to come by and carbohydrates took the form of fresh foods with a low . Our ancestors were also active throughout the day, taking pressure off of the endocrine system. Now, sedentary lifestyles and processed-food diets cause many of us to take in more calories—and especially more carbohydrates—than our bodies can handle. The fact is, there is only so much blood sugar your cells can absorb. As soaring rates of diabetes show, many modern populations are taxing those limits. After years of being asked by insulin to take in more glucose than they can use, cells eventually stop responding (McKee and McKee 2015). This is called Type 2 diabetes or insulin resistance, which accounts for 90–95% of diabetes cases in the United States. People with Type 1 diabetes do not produce insulin (O’Keefe Osborn 2017; see Figure 16.8).

    image11-1-2.pngFigure \{\PageIndex{6}\} Type 1 and Type 2 Diabetes.

    Type 2 diabetes is a progressive metabolic condition that occurs over time when our evolved biological mechanism that turns food into energy is derailed by the obesogenic environments in which we live. This is compounded by a sedentary lifestyle. Think about how living in a college environment contributes to the development of diabetes. How much time do you spend sitting each day? How many sugary—and often cheap—carbohydrates are within easy reach? Making simple changes now can head off health complications later. Carrying an apple or orange in your backpack instead of a candy bar and walking or biking instead of driving can make a big difference.


    16.1.4: Obesity is shared under a CC BY-NC license and was authored, remixed, and/or curated by LibreTexts.