Lucinda K. Lysen, RDN, RN, BSN, Dorene Robinson, RDN, CDN and Rebecca Rudel, MPH, RDN, CNSC
abdominal fat
activity thermogenesis (AT)
adipocyte
adiposity rebound
android fat distribution
bariatric surgery
body mass index (BMI)
brown adipose tissue (BAT)
carbohydrate-insulin theory of obesity
commercial weight loss centers
comorbidities
essential fat
fat mass
fat-free mass (FFM)
gastric banding
gastric bypass
ghrelin
gynoid fat distribution
Health at Every Size; HAES
hormone-sensitive lipase (HSL)
hyperphagia
hyperplasia
hypertrophy
hypophagia
incretin
insulin
intermittent fasting (IF)
intragastric balloon (IGB)
ketogenic diet
ketones
ketosis
laparoscopic sleeve gastrectomy (LSG)
lean body mass (LBM)
leptin
lipogenesis
lipoprotein lipase (LPL)
meal replacements
medically supervised weight loss programs
metabolic syndrome (MetS)
morbid obesity
night-eating syndrome (NES)
nonalcoholic fatty liver disease (NAFLD)
nonexercise activity thermogenesis (NEAT)
nutritional genomics
obesity
obesogen
overweight
resting metabolic rate (RMR)
self-help programs
sensory-specific satiety
set point theory
storage fat
semivolatile organic compounds (SVOCs)
telehealth
underweight
vagus nerve
very-low-calorie diets (VLCDs)
visceral adipose tissue (VAT)
white adipose tissue (WAT)
yo-yo effect
Body weight is the sum of bone, muscle, organs, body fluids, and adipose tissue. Some or all of these components are subject to normal change as a reflection of growth, reproductive status, variation in physical activity, and the effects of aging. Consistent body weight is orchestrated by neural, hormonal, and chemical mechanisms, as well as individual genetic polymorphisms that balance energy intake and expenditure within fairly precise limits. Abnormalities of these complex mechanisms can result in weight fluctuations.
On one end of the weight spectrum is underweight. Although the inability to gain weight can be a primary problem, low body weight is usually secondary to a disease state, an eating disorder, or a psychiatric disorder. In elders or in children, unintentional weight loss can be especially detrimental and should be addressed early to prevent malnutrition or other undesirable consequences including poor growth, depressed immune function, hormone imbalance, delayed healing, and loss of bone density. Most crucial is the in utero development of the fetus. Babies deprived of nutrition before birth and who have low birth weight may be primed for accelerated growth after birth when exposed to a nutrient-rich environment (that can sometimes start with excessive intake of infant formula). Furthermore, inadequate passage of nutrients across the placenta and low birth weight eventually can lead to an increased risk of developing obesity and diabetes (Apovian, 2011; Jornayvaz, 2016).
On the other end of the spectrum, and more common, are the conditions of overweight and obesity.
The growing amount of attention over the last four decades to the field of weight management and obesity has largely been brought about by the historical findings of a handful of researchers. In the forefront—beginning in the 1970s—was George L. Blackburn, MD, PhD, who, along with Bruce Bistrian, MD, PhD, at Harvard Medical School, and a number of other highly respected colleagues, provided the foundation for what eventually became the field of nutritional medicine. Publications highlighting the inadequate nutrition management of hospitalized patients put this topic and nutritional medicine on the “world map.” Despite the fact that Dr. Blackburn and his group found that many of the hospitalized patients were shockingly malnourished (Blackburn et al, 1977), they also discovered that the patients were often not underweight but instead, were overweight or even obese. This led to Dr. Blackburn’s development of nutritional liquid and solid diets, supplementing patients with protein to encourage loss of body fat while saving muscle and improving nutritional status. The protein-sparing modified fast, which spared protein and protected organs, became the basis of the very-low-carbohydrate diet for weight loss in obese patients (Blackburn et al., 1973). With obesity reaching epidemic proportions over the years, scientific research expanded, diet and weight loss programs grew dramatically, and the specialties of weight management and obesity quickly grew into a billion-dollar industry. Over time, Dr. Blackburn’s ongoing landmark studies and cutting-edge findings in weight management and obesity brought him recognition around the world, earning him the title “Father of Obesity” (Table 21.1). The growing population of obese individuals and the preponderance of evidence that it is associated with chronic disease has motivated intense research on the subject and resulted in obesity as a specialty in nutritional medicine. Obesity meets the criteria to be classified as a “disease,” which has made it reimbursable by insurance companies for medical treatment, and in many cases, for nutritional management by registered dietitian nutritionists (RDNs). In this chapter we will review the myriad of associations with obesity, including behavioral, psychological, medical, environmental, and social.
Table 21.1
From Ainsley B, Lucinda K. Lysen LK: George L. Blackburn, MD, PhD, Father of nutritional and obesity medicine (1936 to 2017
Body weight often is described in terms of its composition, and different models have been advanced to estimate body fat. Assessment of body composition is discussed in detail in Chapter 5. Traditionally, a two-compartment model divides the body into fat mass—the fat from all body sources including the brain, skeleton, intramuscular fat, and adipose tissue—and fat-free mass (FFM), which includes water, protein, and mineral components (Fig. 21.1). The proportions of FFM are relatively constant from person to person.
Although FFM often is used interchangeably with the term lean body mass (LBM), it is not exactly the same. Lean body mass (LBM) includes water, bones, organs, and skeletal muscle. LBM is higher in men than in women and represents the largest component of resting metabolic rate (RMR). Minimizing the loss of LBM is desirable during the weight loss process. Water, which makes up 60% to 65% of body weight, is the most variable component of LBM, and the state of hydration can induce fluctuations of several pounds.
Total body fat is the combination of “essential” and “storage” fats, usually expressed as a percentage of total body weight that is associated with optimum health. Muscle and even skeletal mass adjust to some extent to support the burden of excess adipose tissue.
Essential fat, necessary for normal physiologic functioning, is stored in small amounts in the bone marrow, heart, lungs, liver, spleen, kidneys, muscles, and the nervous system. In men, approximately 3% of body fat is essential. In women, essential fat is higher (12%) because it includes body fat in the breasts, pelvic regions, and thighs that supports the reproductive process.
Storage fat is the energy reserve, primarily as triglycerides (TGs), in adipose tissue. This fat accumulates under the skin and around the internal organs to protect them from trauma. Most storage fat is “expendable.” The fat stores in adipocytes are capable of extensive variation. This allows for the changing requirements of growth, reproduction, aging, environmental and physiologic circumstances, the availability of food, and the demands of physical activity. Total body fat (essential fat plus storage fat) as a percentage of body weight associated with the average individual is between 18% and 24% for men and 25% and 31% for women. On the other extreme, “elite fit” men are as low as 2% to 5% body fat and women 10% to 13%.
Adipose tissue exerts a profound influence on whole-body homeostasis. Adipose tissue is located primarily under the skin, in the mesenteries and omentum, and behind the peritoneum. This is often referred to as visceral adipose tissue (VAT). Although it is primarily fat, adipose tissue also contains small amounts of protein and water. White adipose tissue (WAT) stores energy as a repository for TGs, cushions abdominal organs, and insulates the body to preserve heat. Carotene gives WAT a slight yellow color. Small amounts of brown adipose tissue (BAT) can be found in a substantial proportion of adults as well as in infants. Unlike WAT, BAT is made of small droplets and many more iron-containing mitochondria, which makes it brown. In adults, BAT is activated via cold exposure helping to regulate body temperature; however, BAT is not activated in thermoneutral conditions. A general activation of BAT continues to interest drug manufacturers as a potential obesity therapy, but at present, BAT plays only a minor part in human energy metabolism (Tam et al, 2012).
The mature fat cell (adipocyte) consists of a large central lipid droplet surrounded by a thin rim of cytoplasm, which contains the nucleus and the mitochondria. These cells can store fat equal to 80% to 95% of their volume. Gains in weight and adipose tissue occur by increasing the number of cells, adding the size of cells as lipid, or a combination of the two.
Hyperplasia (increased number of cells) occurs as a normal growth process during infancy and adolescence. Cell number increases in lean and obese children into adolescence, but the number increases faster in obese children. In teens and adults, increases in fat cell size are more common, but hyperplasia also can occur after the fat content of existing cells has reached capacity.
During normal growth, the greatest percentage of body fat (~25%) is set by 6 months of age. In lean children, fat cell size then decreases; this decrease does not occur in obese children. At the age of 6 years in lean children, adiposity rebound occurs, especially in girls, with an increase in body fat. An early adiposity rebound occurring before 5½ years old is predictive of a higher level of adiposity at 16 years of age and in adulthood; a period of later rebound is correlated with healthy adult weight (Hughes et al, 2014).
With hypertrophy (increased cell size), fat depots can expand as much as 1000 times at any age, as long as space is available. In a classic study, Björntorp and Sjöström (1971) demonstrated, using weight loss as a result of trauma, illness, or starvation, that fat cell size decreases but cell numbers remain the same.
Most stored fat comes directly from dietary TGs. The fatty acid composition of adipose tissue mirrors the fatty acid composition of the diet. Even excess dietary carbohydrates and protein are converted to fatty acids in the liver by the comparatively inefficient process of lipogenesis. Under conditions of relative energy balance, little dietary carbohydrate is converted to fat for storage. In conditions of positive energy balance, carbohydrate oxidation increases while TGs are preferentially stored, and de novo lipogenesis from carbohydrate occurs when more carbohydrate is present than can be either oxidized or stored as (liver or muscle) glycogen (Song et al, 2018).
Semivolatile organic compounds (SVOCs) accumulate in adipose tissues from exposure to toxins, chemicals, and pesticides. When adipose tissue is mobilized during weight loss, SVOCs are released (see Clinical Insight: What’s in That Fat When You Lose It?). The effect of SVOCs on the developing fetal brain is not yet known (see Chapter 14), which adds to the health concern about obese pregnant women who lose weight.
Dietary TG is transported to the liver by chylomicrons. Endogenous TGs synthesized in the liver from free fatty acids (FFA) travel as part of very-low-density lipoprotein (VLDL) particles. The enzyme lipoprotein lipase (LPL) moves lipids from the blood into the adipose cell by hydrolyzing TGs into FFA and glycerol. Glycerol proceeds to the liver; fatty acids enter the adipocyte and are re esterified into TGs. When needed by other cells, TGs are hydrolyzed once again to fatty acids and glycerol by hormone-sensitive lipase (HSL) within the adipose cell; they then are released into the circulation.
Hormones affect LPL activity in different adipose tissue regions. Estrogen stimulates LPL activity in the gluteofemoral adipocytes, and thus promote fat storage in this area for childbearing and lactation. In the presence of sex steroid hormones, a normal distribution of body fat exists. With a decrease in sex steroid hormones—as occurs with menopause or gonadectomy—central obesity tends to develop.
Body weight is the product of genetic effects (DNA), epigenetic effects (heritable traits that do not involve changes in DNA), and the environment (Kaplan, 2018). Body weight regulation is usually described in terms of a homeostatic biological feedback system acting on energy intake and energy expenditure to maintain or “defend” a stable body weight. Similarly, set point theory originally arose to explain the intractable tendency to regain weight after weight loss. Body weight regulation is asymmetric in that there is little defense against weight gain while conversely both hunger and adaptations in various components of energy expenditure can make weight loss harder.
Observational studies do not provide consistent evidence for a biological control of body weight (Müller et al, 2018). While the complete picture of body weight regulation is not clear, much of what is known falls into the realm of appetite regulation. Adaptation to energy restriction (a drop in RMR beyond what is expected from changes in body weight and composition) is well-known, but highly variable and not fully understood.
Because the precision of appetite control is undermined in the prevailing obesogenic environment that includes psychosocial, behavioral, and environmental factors that affect eating behavior (and therefore energy intake), new models of body weight regulation that also address these missing factors have been called for (Belfort-DeAguiar and Seo, 2018; Hall et al, 2014).
Satiety is associated with the postprandial state when excess food is being stored. Hunger is associated with the postabsorptive state when those stores are being mobilized. Physical triggers for hunger are much stronger than those for satiety, which external cues for eating can override.
When either overfeeding or underfeeding occurs in children, they exhibit spontaneous hypophagia (undereating) or hyperphagia (overeating), accordingly, Adults, however, are less consistent in naturally compensating for overeating, which can result in body weights slowly creeping up over time. Unexplained weight loss in adults is often a symptom of other factors, including stress or underlying disease. See Focus On: Signals from a Host of Hormones and Table 21.2 for further information and detail on the neurochemicals and hormones involved in appetite and satiety.
Table 21.2
Gut Hormones | Characteristics and Function |
---|---|
Incretins | Gastrointestinal (GI) peptides increase the amount of insulin released from the beta cells of the pancreas after eating, even before blood glucose levels become elevated. They also slow the rate of absorption by reducing gastric emptying and may directly reduce food intake. Incretins also inhibit glucagon release from the alpha cells of the pancreas. (See GLP-1 and GIP.) |
CCK | Released by the intestinal tract when fats and proteins reach the small intestine, receptors for CCK have been found in the GI tract and the brain. CCK causes the gallbladder to contract and stimulates the pancreas to release enzymes. At the brain level, CCK inhibits food intake. |
Bombesin | Released by enteric neurons; reduces food intake and enhances the release of CCK. |
Enterostatin | A portion of pancreatic lipase is involved specifically with satiety after the consumption of fat. |
Adiponectin | An adipocytokine secreted by the adipose tissue modulates glucose regulation and fatty acid catabolism. Levels of this hormone are inversely correlated with BMI. The hormone plays a role in metabolic disorders such as type 2 diabetes, obesity, and atherosclerosis. Levels drop after gastric bypass surgery for up to 6 months. |
Glucagon | Increased secretion of glucagon is caused by hypoglycemia, increased levels of norepinephrine and epinephrine, increased plasma amino acids and cholecystokinin. Decreased secretion of glucagon occurs when insulin or somatostatin is released. |
Apolipoprotein A-IV | Synthesized and secreted by the intestine during lymphatic secretion of chylomicrons. After entering the circulation, a small portion of apolipoprotein A-IV enters the CNS and suppresses food consumption. |
Fatty acids | Free fatty acids, triglycerides, and glycerol are factors that also affect the uptake of glucose by peripheral tissues. |
GLP-1 and GIP | Released by intestinal mucosa in the presence of meals rich in glucose and fat; stimulate insulin synthesis and release; GLP-1 decreases glucagon secretion, delays gastric emptying time, and may promote satiety; examples of incretin hormones. |
Insulin | Acts in the CNS and the peripheral nervous system to regulate food intake and is involved in the synthesis and storage of fat. It is possible that obese persons with insulin resistance or deficiency have a defective glucose disposal system and a depressed level of thermogenesis. The greater the insulin resistance, the lower the thermic effect of food. Fasting insulin levels increase proportionately with the degree of obesity; however, many obese persons have insulin resistance because of a lack of response by insulin receptors, impaired glucose tolerance, and associated hyperlipidemia. These sequelae can usually be corrected with weight loss. |
Leptin | An adipocytokine secreted by the adipose tissue, correlated with the percent of body fat. Primary signal from energy stores; in obesity loses the ability to inhibit energy intake or to increase energy expenditure. Compared with men, women have significantly higher concentrations of serum leptin. |
Resistin | An adipocytokine expressed primarily in adipocytes; antagonizes insulin action. |
Ghrelin | Produced primarily by the stomach; acts on the hypothalamus to stimulate hunger and feeding. Ghrelin levels are highest in lean individuals and lowest in the obese. Increased levels are seen in people who are dieting, and suppressed levels are noted after gastric bypass, possibly counteracted by adiponectin. |
PYY3-36 | Secreted by endocrine cells lining the small bowel and colon in response to food; a “middle man” in appetite management. PYY seems to work opposite from ghrelin; it induces satiety. |
IL-6 and TNF-α | Both are gut hormones. Cytokines secreted by adipose tissue, and participate in metabolic events. Impair insulin signals in muscle and liver. Levels are proportional to body fat mass (Thomas and Schauer, 2010). |
Oxyntomodulin | Secreted from the L-cells in the small intestine in response to a meal. Exerts its biological effects through activation of GLP-1 and glicentin-related pancreatic peptide (GRPP) (Bray and Bouchard, 2014). |
GLP-2 | Produced in the L-cells in the small intestine and in neurons of CNS. Is an intestinal growth factor. Inhibits gastric emptying and acid secretion while stimulating intestinal blood flow. Decreases gastric acid secretion and gastric emptying and increases mucosal growth (Bray and Bouchard, 2014). |
FGF-21 | Expressed in the liver and secreted mainly during fasting and after feeding a ketogenic diet. Can decrease body weight without affecting food intake. Increases insulin sensitivity, decreases gluconeogenesis, and increases glucose uptake in adipocytes (Bray and Bouchard, 2014). |
Other Hormones | Characteristics and Function |
---|---|
Thyroid hormones | Modulate the tissue responsiveness to the catecholamines secreted by the SNS. A decrease in triiodothyronine lowers the response to SNS activity and diminishes adaptive thermogenesis. Women should be tested for hypothyroidism, particularly after menopause. Weight regain after weight loss may be a function of a hypometabolic state; energy restriction produces a transient hypothyroid hypometabolic state. |
Visfatin | An adipocytokine protein secreted by visceral adipose tissue that has an insulin-like effect; plasma levels increase with increasing adiposity and insulin resistance. |
Adrenomedullin | A new regulatory peptide secreted by adipocytes as a result of inflammatory processes. |
BMI, Body mass index; CCK, cholecystokinin; CNS, central nervous system; CRF, corticotropin-releasing factor; GIP, glucose-dependent insulinotropic peptide; GLP-1, glucagon-like peptide 1; IL-6, interleukin-6; PYY3-36, peptide YY3-36; SNS, sympathetic nervous system; TNF-α, tumor necrosis.
(From Thomas S, Schauer P: Bariatric surgery and the gut hormone response, Nutr Clin Pract 25:175, 2010; Bray GA, Bouchard C: Handbook of obesity, ed 3, Boca Raton, FL, 2014, CRC Press).
The RMR (see Chapter 2) explains 60% to 70% of total energy expenditure (TEE). RMR declines with age. When the body is deprived of adequate energy from starvation or voluntary energy restriction, RMR drops, therefore conserving energy. The more severe the energy restriction, the greater the potential reduction in RMR; up to 15% with very-low-calorie diets (VLCDs). This suppression of RMR is beyond what is attributable to weight loss (which consists of both LBM and fat mass) and is a form of adaptation to energy scarcity. Most, but not all, reviews of the subject find RMR normalizes post weight loss with maintenance level energy intakes (Ostendorf et al, 2018). Ongoing suppression of RMR may result from extreme approaches to weight loss.
Activity thermogenesis (AT) is the energy expended in voluntary activity, the most variable component of energy expenditure. Under normal circumstances physical activity accounts for 15% to 30% of TEE. Nonexercise activity thermogenesis (NEAT) is the energy expended for all activity that is not sleeping, eating, or sports like exercise. It includes going to work, typing, doing yard work, toe-tapping, even fidgeting (see Chapter 2). NEAT varies as much as 2000 kcal/day between individuals, and it has been theorized to have untapped potential value in weight management. Proponents of NEAT suggest standing and ambulating for 2.5 hours per day, and reengineering work, school, and home environments to support a more active lifestyle (Garland et al, 2011). However, passive compensation, by reducing other forms of physical activity, may prove to balance off increases in NEAT (O’Neal et al, 2017) and there is presently no evidence showing that strategies promoting NEAT are effective for weight loss or obesity treatment (Chung et al, 2018).
Overweight and obesity occur as a result of an imbalance between total energy intake (food and beverages consumed) and TEE. Despite this seemingly straightforward model, the factors which act to dysregulate energy balance are complex. Lifestyle, environmental, and genetic factors have a multifaceted interaction with psychological, cultural, and physiological influences. Over the years, many hypotheses have evolved; however, no single theory can completely explain all manifestations of obesity or apply consistently to all persons.
The United States leads the world as far as the total number of persons with obesity. When looked at as a percentage of the population, however, the United States ranks 19th after the Oceania Islands, the Middle East, and South America. According to the World Health Organization (WHO), worldwide obesity has nearly tripled since 1975 (WHO, 2018).
In the United States the estimates of overweight and obesity among adults and children are based on measured weights and heights from the National Health and Nutrition Examination Survey (NHANES), conducted by the National Center for Health Statistics, Centers for Disease Control and Prevention (CDC) (Figs. 21.2 and 21.3). The 2015 to 2016 NHANES findings were that the prevalence of obesity was 39.8% in adults and 18.5% in youth. The prevalence of obesity remains higher among African American and Hispanic populations. The prevalence of obesity by state (based on the ongoing Behavioral Risk Factor Surveillance Study and published by the CDC) can be seen in Fig. 21.4.
With the exception of rare monogenic types of obesity (as in Prader-Willi syndrome and Bardet-Biedl syndrome), more and more research shows that the development of obesity involves a complex interaction with numerous genetic variants and environmental factors related to energy intake and expenditure (Goodarzi, 2018). Hormonal and neural factors involved in weight regulation include short-term and long-term “signals” that determine satiety and feeding activity. Small defects in their expression or interaction may contribute significantly to weight gain. Nutritional genomics is the study of the interactions between dietary components and the instructions in a cell or genome, and the resulting changes in metabolites that affect gene expression (Camp and Trujillo, 2014; see Chapter 6).
The number and size of fat cells, regional distribution of body fat, and RMR also are influenced by genes. Studies of twins confirm that genes determine 50% to 70% of the predisposition to obesity. Although numerous genes are involved, several have received much attention—the Ob gene, the adiponectin (ADIPOQ) gene, the “fat mass and obesity associated” gene or FTO gene, and the beta3-adrenoreceptor gene. The Ob gene produces leptin (Ferguson et al, 2010). The beta3-adrenoreceptor gene, located primarily in the adipose tissue, is thought to regulate RMR and fat oxidation in humans.
Nutritional and/or lifestyle choices can either activate or inhibit these obesity-triggering genes. Thus, the formula for successful long-term weight management could necessitate the behavioral application of individual genetics. Genetic research is currently drawing significant attention from private interests invested in capitalizing on genetic-based “individualized medicine and nutrition” (Loos, 2018). Despite hundreds of “obesity genes” having been identified, however, we are only at the point of being able to apply genetic information to a few individual treatments. One such treatment is congenital leptin deficiency, which can be treated with daily injections of recombinant human leptin (Choquet, 2011). Well-known obesity researcher Claude Bouchard, PhD, recently explained that regardless of the growing body of genetic research, “it is hard to see how we can [yet] anchor a prevention or treatment strategy on our genes,” and that, “despite all the noise surrounding this [obesity gene] issue, it still comes down to changing your behavior. It’s diet and exercise” (Endocrine Today, 2018) (see Clinical Insight: Randomized Controlled Trial Matching Diet to Genetic Predisposition Fails to Improve Weight Loss).
The view that inactivity is a major factor in the development of overweight and obesity is debated. It is true that lack of regular physical activity is a fact for Americans of all ages. Only 21% of adults meet the recommended levels of weekly physical activity (150 min/week of moderate-intensity aerobic activity and two sessions of muscle strengthening) for general health. Meanwhile, 250 to 300 minutes of moderate-intensity aerobic activity per week is recommended for weight loss and weight loss maintenance (Chin et al, 2016). However, researchers pushing back on the physical activity emphasis point out that “you can’t outrun a bad diet,” and argue that avoiding sugary drinks, fast food, and overeating in general will save far more calories than people will expend hitting weekly physical activity targets (Fulton, 2016; Malhotra et al, 2015).
Although weight gain can be due to disease, clinicians also should consider the possibility that the patient’s medication may be contributing. Diabetes medications, thyroid hormone replacement, psychotropics, antidepressants, steroids, and antihypertensive medications can be problematic. The use of such medications must be considered carefully, and alternatives with less deleterious effects selected when possible (Appendix 13).
Lack of adequate sleep alters the endocrine regulation of hunger and appetite. Hormones that affect appetite are activated and may promote excessive energy intake. Recurrent sleep deprivation can modify the amount, composition, and distribution of food intake and may be contributing to the obesity epidemic. It is estimated that more than 50 million Americans suffer from sleep deprivation. Others may have shift work or exposure to bright light at night, increasing the disruption of circadian rhythms and enhancing the prevalence of obesity (Garaulet et al, 2010).
There is also a relationship between inadequate sleep, disrupted circadian rhythm, genes, and the development of metabolic syndrome (MetS). Stress is another factor. The adrenal hormone cortisol is released when an individual is under stress. Cortisol stimulates insulin release to maintain blood glucose levels in the “fight-or-flight” response; increased appetite eventually follows. Chronic stress with constantly elevated cortisol levels can also lead to appetite changes.
Cortisol levels are typically high in the early morning and low around midnight. Individuals with night-eating syndrome (NES) may have a delayed circadian rhythm of meal intake due to genetically programmed neuroendocrine factors, including altered cortisol levels (Stunkard and Lu, 2010).
Food and its taste elements evoke pleasure responses. The endless variety and reasonable cost of food (especially highly processed food) in the United States contributes to higher calorie intake; people eat more when offered a variety of choices than when a single food is available. Normally, as foods are consumed, they become less desirable; this phenomenon is known as sensory-specific satiety. The opposite situation is the “all-you-can-eat buffet,” in which the diner reaches satiety for one food but has many choices remaining for the next course. From an evolutionary perspective, sensory-specific satiety promoted the intake of a varied and nutritionally balanced diet; the modern food environment, however, provides too many (energy-dense, low-nutrient) choices.
Leptin is a hormone made by fat cells that decreases appetite. Ghrelin is a hormone that increases appetite in response to the time elapsed since the last meal. Levels of leptin, the appetite suppressor, are lower in individuals with a lower body weight and higher in the obese because they correlate to one’s total adipose tissue. However, for reasons yet to be elucidated, people with obesity are seemingly resistant to the appetite-suppressing effects of leptin and are sometimes referred to as leptin resistant.
Passive overeating is partly the result of excessive portion sizes that are now accepted as normal. The portions and calories that restaurants and fast-food outlets commonly serve in one meal can often exceed a person’s energy needs for the entire day.
Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that can interfere with any aspect of hormone action. Most EDCs are persistent organic pollutants (POPs), which are manufactured chemicals in the environment (water, food, and food packaging) that are becoming increasingly implicated in body weight dysregulation. The original “obesogen hypothesis” (Grün and Blumberg, 2006) pertained to fetal EDC exposure leading to obesity in later life. Most EDCs are lipophilic and stored in adipose tissue. Some EDCs have 3- to 8-year half-lives in the human body. Higher exposure levels may be associated with insulin resistance, expansion of fat storage, alterations in satiety and appetite regulation, greater reductions in RMR with weight loss, and a lesser increase in RMR with weight gain (Liu et al, 2018). Examples of suspected obesogens are BPA and phthalates (in food containers and packaging), organochlorine and organophosphate (banned pesticides), and perfluoroalkyl substances (industrial marine applications) (Nappi et al, 2016; see Clinical Insight: What’s in That Fat When You Lose It?)
In the last two decades, at least 10 adipogenic pathogens have been identified, including viruses, scrapie agents (spongiform encephalopathies from sheep or goats), bacteria, and gut microflora. Whether “infectobesity” is a relevant contributor to the obesity epidemic remains to be determined. A human adenovirus, adenovirus-36 (Ad-36), is capable of inducing adiposity in experimentally infected animals by increasing the replication, differentiation, lipid accumulation, and insulin sensitivity in fat cells and reducing leptin secretion and expression. A growing number of studies have found higher levels of Ad-36 antibodies in subjects with obesity (Ponterio and Gnessi, 2015). To date, three meta-analyses have shown an association between Ad-36 infection and obesity in both adults and children (Tambo and Pace, 2016).
Researchers studying the microbiome have proposed that the gut may have a bigger role in energy balance than previously thought. A number of theories attempt to explain how this complicated process might work (Krajmalnik-Brown et al, 2012). Essentially, indigestible complex polysaccharides promote and maintain a healthy microbiome. A highly processed-food diet (essentially devoid of indigestible polysaccharides) begins and reinforces a downward spiral of inflammation, increased tendency to store fat, as well as appetite and satiety dysregulation.
Overweight and obesity are defined as abnormal or excessive fat accumulation that may impair health (WHO, 2018). Body mass index (BMI) is calculated by the formula: weight (in kilograms)/height (in meters)2. It is possible to be overweight based on BMI but not be “overfat” or obese. It is also possible to have a healthy BMI but still have excessive body fat. In fact, normal weight obesity (NWO) allows patients at greater risk for cardiovascular disease (CVD) and coronary artery disease (CAD) to go unnoticed by their physicians (Ashraf and Baweja, 2013). These situations occur because BMI is only a proxy for adiposity rather than a direct measurement. However, because BMI is derived from readily available measurements of height and weight, it is the most convenient clinical approach to estimate body fat. The National Institutes of Health (NIH) guidelines classify individuals with a BMI of ≥25 as overweight and those with a BMI of ≥30 as obese (Table 21.3). Based on percent body fat content, obesity is ≥25% in men and ≥30% in woman. See Chapter 5 for a detailed discussion of body fat assessment.
Table 21.3
Classification of Overweight and Obesity by BMI, Waist Circumference, and Associated Disease Riska | ||||
---|---|---|---|---|
Disease Riska Relative to Normal Weight and Waist Circumference | ||||
BMI (kg/m2) | Obesity Class | Men ≤102 cm (≤40 in) Women ≤88 cm (≤35 in) | >102 cm (>40 in) >88 cm (>35 in) | |
Underweight | <18.5 | — | — | |
Normalb | 18.5–24.9 | — | — | |
Overweight | 25.0–29.9 | Increased | High | |
Obesity | 30.0–34.9 | I | High | Very High |
35.0–39.9 | II | Very High | Very High | |
Extreme Obesity | ≥40 | III | Extremely High | Extremely High |
aDisease risk for type 2 diabetes, hypertension, and CVD.
bIncreased waist circumference can also be a marker for increased risk even in persons of normal weight.
(From National Institutes of Health, National Heart, Lung, and Blood Institute: Clinical Guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: evidence report, NIH Publication No. 98-4083, 1998.)
Because BMI is a crude proxy for body fat, and also fails to account for body fat distribution, morbidity and mortality studies using BMI consistently produce “J” shaped curves, which at first seem to suggest that lower BMIs are as unhealthy as the higher BMIs (class II obesity or above). When waist-to-hip ratio (WHR) or weight-to-height ratio (WHtR) are substituted for BMI, however, both demonstrate positive (linear) relationships with mortality (Carmienke et al, 2013). Similarly, a body shape index (ABSI), which incorporates waist circumference (WC) with height and weight into one formula, has also been shown to be a better mortality predictor than BMI alone (Krakauer and Krakauer, 2014).
When WC and percentage of fat are both high, they are significant predictors of heart failure and other risks associated with obesity. WC is a strong correlate of insulin sensitivity index in older adults (Huth et al, 2016). A WHR of more than 0.8 for women and 1 for men is associated with high risk for cardiovascular events. Similarly, WC ≥40 inches in men and ≥35 inches in women signifies increased risk, equivalent to a BMI of 25 to 34.
In most people, obesity can be viewed as metabolically unhealthy. Chronic diseases such as heart disease, type 2 diabetes, hypertension, stroke, gallbladder disease, infertility, sleep apnea, hormonal cancers, and osteoarthritis tend to worsen as the degree of obesity increases (Fig. 21.5; see Table 21.3).
There is a subset of obese persons who present as metabolically healthy. This subgroup, the metabolically healthy obese (MHO), has appropriate insulin sensitivity and absence of diabetes, dyslipidemia, and hypertension (Boonchaya-anant and Apovian, 2014). There is currently no universal definition of MHO. However, the idea that MHO might be benign and not require treatment is debatable. In long-term follow-up, MHO adults were at increased risk for all-cause mortality and CVD (Kramer et al, 2013). Researchers are urging that treatment of MHO is not to be ignored until metabolic symptoms occur (Atkinson and Macdonald, 2018).
Obesity is now recognized as a chronic and systemic inflammatory disease, whereas it was once believed that excess adipose stores were inert. Adipose tissue is involved in the secretion of a wide range of active substances (tumor necrosis factor, interleukin-6, C-reactive protein [CRP], etc.), most, but not all, (adiponectin) are involved in inflammatory actions. The overall result underlies development of hyperlipidemia, MetS, diabetes mellitus, muscle protein loss, CVD, stroke, and some cancers (Bueno et al, 2014; Grimble, 2010; Rocha and Folco, 2011).
Irrespective of the growing body of data on the systemic inflammatory systems initiated by obesity, the precise trigger is yet to be determined. One theory is that nutrient overload in adipocytes induces intracellular stress, which results in activation of inflammatory cascades (Ellulu et al, 2017). As discussed earlier, other factors implicated in the development of inflammation include microbiome-derived endotoxins, environmental chemicals, viruses, saturated fats, and chronic overeating. A dietary change to an antiinflammatory diet and regular physical activity can reduce obesity-related inflammation. (For discussion of inflammation, see Chapter 7.)
Nonalcoholic fatty liver disease (NAFLD) is associated with overweight and obesity and may progress to end-stage liver disease (see Chapter 29). Obesity is also a risk factor for various cancers, infertility, poor wound healing, and poor antibody response to hepatitis B vaccine. Thus, the costs of obesity are staggering. The CDC estimates the direct cost of care for obesity at $147 billion (CDC, 2018). The Internal Revenue Service issued a rule in 2002 qualifying obesity as a disease, allowing taxpayers to claim weight loss expenses as a medical deduction if undertaken to treat an existing disease.
The US government recognizes the immense effect of obesity on the health and financial well-being of its citizens. Healthy People 2030 objectives also identify the implications of overweight and obesity (see Chapter 8). The objectives include targets to increase the proportion of adults who are at a healthy weight and to reduce the proportion of adults, children, and adolescents who are obese. Overweight adolescents often become obese adults; obese individuals are at increased risk for comorbidities of type 2 diabetes, hypertension, stroke, certain cancers, infertility, and other conditions.
Regional patterns of fat deposit are controlled genetically and differ between and among men and women. Two major types of fat deposition are excess subcutaneous truncal-abdominal fat (the apple-shaped android fat distribution) and excess gluteofemoral fat in thighs and buttocks (the pear-shaped gynoid fat distribution). The android shape is more common among men. Gynoid fat deposition in women during child bearing years is utilized to support the demands of pregnancy and lactation. Women with the gynoid type of obesity do not develop the impairments of glucose metabolism in those with an android deposition (Wajchenberg, 2013). Postmenopausal women more closely follow the male pattern of abdominal fat stores, sometimes referred to as “belly fat.”
Abdominal fat is an indicator of fat surrounding internal organs or visceral fat. According to a major study done through the Brigham and Women’s Hospital in Boston over 7 years and including more than 3000 people (Framingham Study patients were used), those with higher amounts of abdominal fat, versus fat in other parts of the body, were found to have higher risks of cancer and heart disease (Britton et al, 2013). Many other reputable scientific studies have been performed, validating the findings repeatedly.
Visceral obesity, or excessive VAT under the peritoneum and in the intraabdominal cavity, is correlated highly with insulin resistance and diabetes. Metabolic syndrome (MetS) consists of three or more of the following abnormalities: WC ≥102 cm (40 in) in men and ≥88 cm (35 in) in women, serum TGs ≥150 mg/dL, high-density lipoprotein (HDL) level <40 mg/dL in men and <50 mg/dL in women, blood pressure 135/85 mm Hg or higher, or fasting glucose 100 mg/dL or higher. Increased visceral fat is a risk factor for CAD, dyslipidemia, hypertension, stroke, type 2 diabetes, and MetS (Wajchenberg, 2013). By the same token, VAT and low cardiorespiratory fitness (CRF) levels are associated with a deteriorated cardiometabolic risk profile. Achieving a low level of VAT and a high level of CRF is an important target for cardiometabolic health.
Obesity is a risk factor for infection and hospitalization for all respiratory viruses, including SARS-CoV-2, the virus that causes COVID-19. The poorer COVID-19 outcomes associated with obesity are likely multifactorial, but it is widely accepted that the low-grade inflammation of obesity is a major contributor. Obesity affects lung function through a number of mechanisms (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460880/). Obesity is a known risk factor for thrombotic disorders likely related to inflammation. See Chapter 37 for a discussion of how obesity affects the immune system.
Widespread bias and discrimination based on weight have been documented in education, employment, and health care. Like other forms of prejudice, this stems from a lack of understanding of the chronic, complex, and sometimes intractable nature of obesity and its medical consequences. The United States is the first (and only) country that currently classifies obesity as a disease; the disease classification was necessary in order for insurance to cover obesity treatment within the US health care system (Müller and Geisler, 2017). The vast majority of the United States does not consider obesity a protected class and therefore weight-based employment discrimination does not have a basis for a legal claim (Pomeranz and Puhl, 2013). Both adults and children with a larger body size experience adverse social, educational, and psychological consequences as a result of weight bias. They also face discrimination from health care providers, and this can affect their willingness to seek medical care. It is essential to break down the barriers caused by ignorance and indifference. Patient support groups help to correct the negative effect of this type of discrimination.
In 1998, the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) issued the Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: Evidence Report. It was the first federal clinical practice guidelines to deal with overweight and obesity issues developed using evidence-based medicine methodology. The guidelines provided the scientific evidence behind the recommendations for weight loss and weight loss maintenance, as well as practical strategies for implementing the recommendations. The 1998 clinical guidelines were partially updated in 2013, addressing five specific questions and published in three major medical journals (NHLBI, 2014). The five areas addressed in 2013 were as follows: (1) what are the expected health benefits of weight loss as a function of the amount and duration of weight loss, (2) are current WC and BMI cut points appropriate (defined obesity) for certain population subgroups, (3) which diets—among a handful of popular diets—are effective for weight loss, (4) what is the efficacy and effectiveness of comprehensive lifestyle approaches to weight loss and weight loss maintenance, and (5) what is the efficacy and safety of bariatric surgical procedures.
Before the NHLBI evidence report, clinicians focused almost entirely on weight loss via caloric restriction, exercise was not routinely recommended, and weight loss maintenance was generally overlooked. The strategies for weight loss (and weight loss maintenance) analyzed, reviewed, and outlined in the NHLBI report were dietary therapy (CR), physical activity, behavior therapy (self-monitoring, stress management, stimulus control, problem solving, contingency management, cognitive restructuring, and social support), combined therapy (dietary, physical activity, and behavioral therapies), pharmacotherapy, and surgery. Today, a chronic disease-prevention model incorporates these interdisciplinary therapies and lifestyle interventions from physicians, dietitians, exercise specialists, and behavior therapists.
The goal of obesity treatment is to achieve enough weight loss to significantly improve overall health. Achieving a moderate loss is beneficial. Obese persons who lose 5% to 10% of initial body weight are likely to improve their blood glucose, blood pressure, and cholesterol levels and reduce various markers of systemic inflammation. Since continual, gradual weight gain is the norm, choosing to maintain present body weight is also beneficial (but also requires vigilance and effort).
Despite the recognition that moderate weight loss is beneficial and may be more easily achievable, patients usually have self-defined goal weights that are considerably higher. Therefore, health professionals need to encourage their patients to target more realistic initial weight loss goals.
In general, weight loss after age 65 is not advised; actuarial tables show no benefit and possible harm due to loss of LBM. In fact, in the obese older adult, sarcopenia (loss of muscle mass) is the strongest predictor of disability and inability to perform daily activities. A BMI below 23 is considered below desirable in older adults (see Chapter 20).
Reduction of body weight involves the loss of both protein and fat. The relative proportions of each depend on initial body composition and, to some degree, the rate of weight reduction. Strength training can help minimize loss of lean tissue in some subjects. Steady weight loss over a longer period favors reduction of fat stores, limits the loss of vital protein tissues, and minimizes the decline in resting energy expenditure (REE) that can accompany severe energy restriction. Recommended calorie deficit guidelines result in a loss of approximately 0.5 to 1 lb/week for persons with a BMI of 27 to 35, and 1 to 2 lb/week for those with BMIs greater than 35. These energy deficits need to be individually calculated, and continually adjusted with weight loss in order to maintain the targeted calorie deficits and, therefore, weekly rates of weight loss (Byrne et al, 2012).
Even with the same caloric intake, rates of weight reduction vary. Men reduce weight faster than women of similar size because of their higher LBM and RMR. The heavier person expends more energy than one who is less obese and loses faster on a given calorie intake than a lighter person.
Many people who do not lose weight when following a prescribed energy restriction may be consuming more energy than they report and may also overestimate their physical activity levels. Underreporting of energy intake is the norm and is shown to increase with BMI. Underreporting of estimated intake has been extensively studied; it impacts the reliability of epidemiologic studies and creates the illusion of resistance to weight loss during energy restriction (Dhurandhar et al, 2015).
Behavior modification is the cornerstone of lifestyle intervention. It focuses on restructuring a person’s environment, dietary intake, and physical activity by using goal setting, stimulus control, cognitive restructuring, and relapse prevention. It also provides feedback on progress and places the responsibility for change and accomplishment on the patient.
Stimulus control involves identifying stimuli that may encourage incidental eating and identifying and limiting exposure to high-risk situations. Examples of stimulus control strategies include learning to shop carefully for healthy foods, shopping when not hungry, keeping high-calorie foods out of the house, limiting the times and places of eating, and consciously avoiding situations in which overeating occurs.
Problem solving is the process of defining a problem, generating possible solutions, evaluating and choosing the best solution, implementing the new behavior, evaluating outcomes, and reevaluating alternative solutions if needed.
Cognitive restructuring teaches patients to identify, challenge, and correct the negative thoughts that frequently undermine their efforts to lose weight and keep it off. A cognitive therapy program that underscores the inextricable connection between emotions and eating, and how to manage that connection successfully using positive long-term mental strategies, has been developed and found useful (Beck, 2011).
Self-monitoring with daily food and activity records is positively associated with greater weight loss. Adding the place and time of food intake, as well as accompanying thoughts and feelings, adds complexity (which reduces compliance) but may help identify the physical and emotional settings in which eating occurs. Physical activity can be tracked in minutes, miles, or calories expended. Self-monitoring can also provide insight into the occurrence of relapses and how they can be prevented.
A comprehensive program of lifestyle modification produced a loss of approximately 10% of initial weight in 16 to 26 weeks in a review of RCTs, including the Diabetes Prevention Program. Long-term continued patient therapist contact significantly improves weight loss maintenance (AND, 2016).
E-mail and phone consults appear to be useful methods for contact and support as part of structured behavioral weight loss and weight loss maintenance programs. Multiple strategies for behavior therapy often are needed. Self-monitoring with mobile device apps (see Box 4.5 in Chapter 4), pharmacotherapy, targeted educational interventions from the web, meal replacements, and telephone interventions have taken over the weight loss industry. Body monitoring—a new monitoring method to measure weight change—involves wearing a device that tracks body processes like temperature, movement, acceleration, heating fluctuations, and so on—and records calorie burn. Combined with a food log entered into the system, a person can adjust food intake based upon data provided by the system.
Telehealth programs, which provide interaction with health care professionals through visual and verbal communication via phone and computer screens, are exploding in health care, while saving tremendous costs and time. Telehealth is now being used as an effective vehicle with dietitians for one-on-one and group consults and for providing nutrition education programs.
Weight loss programs should combine a nutritionally balanced dietary regimen with exercise and lifestyle modification. Selecting the appropriate treatment strategy depends on the goals and health risks of the patient. When these approaches fail to bring about the desired reduction in body fat, sometimes medication may be added. For morbid obesity (BMI ≥ 40), surgical intervention may be necessary.
Treatment options include the following:
A balanced, restricted-energy eating plan is the most widely prescribed method of weight reduction. The diet should be nutritionally adequate and meet but not exceed energy needs for weight reduction. A caloric deficit of 500 to 1000 kcal daily usually meets this goal for subjects ≥30 BMI. The prescribed energy level varies with the individual’s body size and activities. For example, for a 500-calorie deficit, the initial daily energy prescription for a 35-year-old female with a BMI of 30 who is 65 inches tall would be approximately 1400 calories, or approximately 1700 calories for a female with a BMI of 40 if the same height and age. Regardless of the level of CR, healthful eating and regular physical activity should be daily goals. All means possible (coaching, motivational interviewing, cognitive restructuring, etc.) should be utilized by the health care team to support healthy lifestyle changes.
All reduced calorie diets (low-fat, low-carbohydrate, balanced) produce similar (long-term) weight loss, which means recommendations can be tailored to individual preferences (Hall, 2017; Johnston et al, 2014). In all cases subjects should be encouraged to consume predominantly whole-food options (fresh, unprocessed vegetables, fruits, beans [legumes], and whole grains, plus a variety of seafood, poultry, and lean meats).
The recommended dietary allowance (RDA) for protein is based on maintenance level energy requirements and is not applicable to the situation of energy restriction. Too little attention to protein intake during energy restriction results in undesirable effects on LBM and underlying REE. Protein prescription of 1.2 g/kg appears to be necessary to minimize the loss of LBM, prevent reduced REE, and preserve bone mineral density in situations of energy restriction (Drummen et al, 2018; Leidy et al, 2015; Westerterp-Plantenga et al, 2012). However, higher levels of protein also tend to blunt improvements in insulin resistance in individuals with insulin resistance.
Alcohol and foods high in sugar, especially beverages, should be limited to small amounts. Alcohol makes up 10% of the diet for many regular drinkers and contributes 7 kcal/g. Heavy drinkers who consume 50% or more of daily calories from alcohol may have a depressed appetite, whereas moderate users tend to gain weight with the added alcohol calories. Habitual use of alcohol may result in lipid storage, weight gain, or obesity.
There is no evidence that using nonnutritive sweeteners reduces food intake or enhances an individual’s weight loss. A recent meta-analysis of the available studies on nonnutritive sweeteners concluded that the literature does not clearly support the intended benefits of nonnutritive sweeteners for weight management, and observational data suggest that routine intake of nonnutritive sweeteners may be associated with increased BMI and cardiometabolic risk. Further research is needed to fully characterize the long-term risks and benefits of nonnutritive sweeteners (Azad et al, 2017).
Vitamin and mineral supplements that meet age-related requirements usually are recommended when there is a daily intake of less than 1200 kcal for women and 1800 kcal for men, or when it is difficult to choose foods that will meet all nutrient needs at the restricted-energy intake.
Millions of Americans turn to commercial weight loss centers (NutriSystem, Jenny Craig, etc.; Table 21.4) or self-help programs (diet book or Internet-based) in search of permanent weight loss each year. Commercial weight loss centers usually require the use of proprietary prepackaged meals. Prepackaged diets allow subjects to avoid food preparation and reduce the number of choices about food (and what to eat) throughout the day. Some provide classes on behavior modification and healthy eating.
Table 21.4
aThe Academy of Nutrition and Dietetics has a page on their website devoted to evaluating weight loss and fad diets: https://www.eatright.org/health/weight-loss/fad-diets.
Some brands of meal replacements are available OTC in drug stores, supermarkets, or via home delivery (e.g., Weight Watchers, Healthy Choice, SlimFast, HMR, etc.). The goal of using these foods is to provide structure and replace other higher calorie foods. Per serving, most meal replacements include 10 to 20 g of protein, various amounts of carbohydrate, 0 to 10 g of fat, up to 5 g of fiber, and 25% to 30% of RDAs for vitamins and minerals. Usually drinks or shakes are milk (casein or whey), pea protein, rice protein, or soy based; are high in calcium; and have 150 to 250 kcal per serving. They are frequently ready-to-use, portion controlled, or made with a purchased powder. People who have difficulty with self-selection or portion control may use meal replacements as part of a comprehensive weight management program. Substituting one or two daily meals or snacks with meal replacements is a successful weight loss and weight maintenance strategy (AND, 2016). Meal replacements are also utilized in medically supervised weight loss programs (see VLCDs).
The Internet has spawned a new generation of web-based weight loss options including Noom.com, NutriSystem.com, SparkPeople.com, Cronometer.com, MyFitnessPal.com, and WeightWatchers.com. A handful of randomized controlled clinical trials have attempted to address whether personalization improves outcomes from these programs. Recent research shows that they appear to have some benefit, however more research needs to be done to determine if they are useful as a stand alone treatment. (Ghelani et al, 2020). In the US, doi:10.3389/fendo.2020.00412 apart from Noom and Weight Watchers, there is not a strong base of evidence behind most of the major commercial and self-help weight loss programs. The Federal Trade Commission (FTC) requires program advertisements to voluntarily include the phrase “results not typical,” but has insufficient resources to further protect consumers from misleading advertising. More controlled trials are needed to assess the efficacy of commercial programs; therefore, it is important to evaluate all weight loss programs for sound nutritional and behavioral practices.
Diets providing ≤800 kcal are classified as very-low-calorie diets (VLCDs). Little evidence suggests that an intake of fewer than 800 calories daily is of any advantage. An example of a significant exception to this would be the hospitalized patient on a metabolic unit who is monitored carefully, is less than 65 years old, and has a condition such as congestive heart failure secondary to obesity. In such a case, immediate and rapid weight loss is considered life-saving.
VLCDs are hypocaloric but relatively rich in protein (0.8 to 1.5 g/kg/day). They are designed to include a full complement of vitamins, minerals, electrolytes, and essential fatty acids, but not calories, and they are usually given for a period of 12 to 16 weeks as part of a medically supervised comprehensive lifestyle-modification program requiring regular medical monitoring and attendance of weekly group classes. Their major advantage (with patient compliance) is rapid weight loss.
Physicians often refer patients that would benefit medically (Fig. 21.6) from rapid weight loss (e.g., severe obstructive sleep apnea, congestive heart failure, and severe obesity with multiple comorbidities) to VLCD programs. Because of potential side effects, prescription of these diets is reserved for persons with a BMI of ≥30 (or ≥27 with at least one comorbidity) for whom other diet programs have been unsuccessful.
An OTC VLCD that first became popular in the early 1970s resulted in several deaths related to its low-quality, incomplete protein profile. The high-quality protein formulations used in medically supervised programs provide efficacy and safety for those with morbid obesity. Adverse side effects to VLCDs include higher risk for gallstones, cold intolerance, fatigue, weakness, lightheadedness, constipation or diarrhea, hair loss, dry skin, menstrual changes, and gout; some of these may be related to triiodothyronine (thyroid) deficiency (see Chapter 31). Emerging data seem to indicate that as fat stores diminish, molecules are released that can affect further weight loss (see Clinical Insight: What’s in That Fat When You Lose It?).
The current literature indicates that even though there is significantly greater weight loss with VLCDs in the short term (up to 13% greater than low-calorie diets, or LCDs, with behavioral counseling), there are on average no significant differences in the long term (Gudzune et al, 2015). Weight loss maintenance requires ongoing vigilance and permanent lifestyle changes—that target a reduced weight net-energy-balance—regardless of the methods employed to lose weight (Hall et al, 2011).
Each year, new books (or websites) promising weight loss find their way to the consumer through the popular press and media. Some of the programs are sensible and appropriate, whereas others emphasize fast results with minimum effort. Some of the proposed diets would lead to nutritional deficiencies over an extended period; however, the potential health risks are seldom realized because the diets usually are abandoned after a few weeks. Diets that emphasize fast results or highly restrictive eating patterns and encourage unrealistic expectations set the participant up for failure, subsequent guilt, and feelings of helplessness about managing their weight.
Online diet programs have grown dramatically in the past decade. A programmed approach, for people on the run who carry their phones and computers, with a product line offered and accessibility to counselors and health professionals, has made the business of diets a multibillion-dollar industry. One-on-one and group online counseling, phone access to discuss weight loss progress and setbacks, and delivery of “to-your-door” foods and meals are some of the enticing aspects of joining these programs. Consumers continue to need proper guidance to separate the good, sound diet programs from the bad. Popular diets come and go; some are reviewed or described by various websites (see Table 21.4).
Traditionally, fasting has been considered primarily the act of willingly abstaining from food, drink, or both for a set period of time and has been used at different times of the year in religious observances for centuries. Applying intermittent fasting (IF) type regimens as an approach to weight loss has recently been popularized by various diet books, which claim there are metabolic advantages to IF leading to faster, or more, weight loss.
In the popular literature, IF encompasses a variety of approaches including (1) limiting eating to within an 8 to 12 hour timeframe during the day, (2) an alternating pattern of low calorie and usual calorie intake, (3) fasting 2 days (500 calories or less each day) per week and eating normally the other 5 days, and/or (4) using a fasting mimicking diet program for 5 days each month or every 3 to 4 months.
While there are multiple studies pertaining to IF in the scientific literature, most are studying biomarkers of CVD or longevity and have not looked at weight loss as an outcome. Additionally, many have no control or comparison groups. Reviews of studies that have compared IF with a constant-calorie-restriction group (Davis et al, 2016; Harris et al, 2018; Headland et al, 2016) find no differences in weight loss, body composition, or insulin sensitivity.
Some popular IF regimes have been criticized for promoting an unhealthy “anything goes” diet on nonfasting days, which seems to border on encouragement for binging and/or disordered eating. Diet quality, however, becomes more—not less—important during any ongoing period of energy restriction.
In summary, IF is no more effective than other approaches to calorie restriction and the effects of using IF for weight loss maintenance have yet to be studied.
When carbohydrate intake is less than 50 g/day, ketosis provides the brain and skeletal muscles with an alternate energy source in the form of ketones derived from lipolysis (the breakdown of fat). Ketones are believed to improve satiety (suppress appetite), at least initially.
Low-carbohydrate and ketogenic diets provide rapid initial weight loss from diuresis secondary to the carbohydrate restriction; early weight loss may be ≥60% water. This diuretic effect is a result of depleted liver and muscle glycogen which holds three to four times its weight in water.
In a classic energy–nitrogen balance method study comparing an 800-calorie ketogenic diet with an 800-calorie mixed diet, subjects did lose weight more rapidly at the beginning of the ketogenic diet period, however the extra weight loss was due solely to excess water losses. Both diets led to the same amount of body fat and protein (LBM) losses (Yang and Van Itallie, 1976). A recent, much shorter version of this type of study by the NIH also found no advantage to the ketogenic diet (Hall et al, 2015).
The impact of a ketogenic diet on the microbiome and overall nutrient intake are two areas of concern. A recent study on the effect of a ketogenic diet on the gut microbiota found a bacterial group supposed to be involved in the exacerbation of the inflammatory condition of the gut mucosa associated with the ketogenic diet pattern (Tagliabue et al, 2017). The recommended upper limit for dietary fat is 35% of calorie intake per the dietary reference intakes, which are intended to ensure adequate micronutrients and shield against preventable diseases (see Appendix 19 on the ketogenic diet).
High-protein (rather than high-fat) variants of low-carbohydrate diets include the Zone and South Beach Diets, which restrict carbohydrates to no more than 40% of total calories, with fat and protein each providing 30% of total calories. These diets are considered moderate choices within the low-carbohydrate category and include generous amounts of fiber and fresh fruits and vegetables, and they stress the kind of fat, with emphasis on monounsaturated and polyunsaturated fat and limitation of saturated fat. For more information about a ketogenic diet and the conditions for which it has been studied see Appendix 19.
Unanswered questions about the ketogenic diet include:
The carbohydrate-insulin theory of obesity is the foundation of low-carbohydrate and ketogenic diets. The basic theory is that carbohydrates stimulate insulin secretion causing increased fat storage, which increases appetite and suppresses metabolism, resulting in weight gain. Low-carbohydrate intake does decrease insulin secretion (Abbasi, 2018). The insulin theory, however, only describes postprandial energy metabolism while ignoring the rest of the 24-hour energy metabolism picture. Insulin levels don’t remain elevated, and overnight—in the fasting state—fat oxidation increases, reducing fat stores. A net gain in fat stores only occurs with positive energy balance. Recent carefully controlled metabolic laboratory studies appear to have invalidated the insulin theory of obesity (Hall et al, 2015; Hall and Guo, 2017). A recent systematic review of high quality RCTs comparing low-carbohydrate with isoenergetic (having the same total calories) balanced diets found essentially no difference in weight loss, measures of glycemic control, blood pressure, or blood lipid between the two diets (Naude et al, 2014).
Very-low-fat (high-carbohydrate) diets contain less than 10% of calories from fat, such as the original Dr. Dean Ornish’s Program for Reversing Heart Disease and the Pritikin Program. Ten percent of energy from fat, however, is well below the current acceptable macronutrient distribution range (AMDR) for fat, which is 20% to 35% of total calorie intake (NAS IOM, 2005). Less than 20% fat may negatively impact essential fatty acid intake and fat-soluble nutrient absorption (Table 21.5). Less restrictive and more popular variations of these diets do allow fat as 20% of total energy intake. Weight loss on these diets is due solely to energy restriction. Because fat provides more than two times the energy per gram as protein or carbohydrate (9 kcal vs. 4 kcal), limiting fat is theoretically the most efficient way to decrease calories. The unforeseen consequence of severe fat restriction, however, is compensatory intake of sugar and/or processed carbohydrates which can trigger MetS.
Table 21.5
2005 | Previous Guidelines | |
---|---|---|
Protein | 10%–35% | 10%–35% |
Carbohydrate | 45%–65% | 50% or more |
Fat | 20%–35% | 30% or less |
AMDR, Acceptable macronutrient distribution ranges.
(From NAS IOM: Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients), The National Academies Press. 2005.)
Balanced-nutrient reduction diets are less common among so-called “popular” diets. The full document of the (2015 to 2020) Dietary Guidelines for Americans outlines the details of three eating plans in its appendices that qualify: the Healthy US-Style Eating Pattern, Healthy Mediterranean-Style Eating Pattern, and Healthy Vegetarian Eating Pattern.
Reduced-energy diets for weight management should be nutritionally sound, not harmful, and feasible to maintain over time. This requires sustainability in terms of ease of adherence, using readily available and affordable foods, and social and cultural acceptability (Naude et al, 2014). The U.S. Department of Agriculture (USDA) supported a scientific review of popular diets to assess their efficacy for weight loss and weight maintenance, as well as their effect on metabolic parameters, mental well-being, and reduction of chronic disease. A summary is shown in Table 21.6.
Table 21.6
(From Freedman MR, King J, Kennedy E: Popular diets: a scientific review. Obes Res 9(Suppl 1):1 S, 2001.)
Over-the-counter medications and herbal supplements for weight loss have been popular for many years. With some exceptions, the majority of these supplements have limited data with regard to their efficacy and safety, and many of the most effective supplements for weight loss (caffeine and ephedra) have significant cardiovascular and neurologic risks or have been banned by the FDA (e.g., ephedra). Dietitians should be aware of popular supplements in order to best serve clients and patients. According to the FDA, a high percentage of weight loss products are adulterated and contain illegal drugs and stimulants that are not listed on the label. See Table 21.7 for popular nutritional supplements used for weight loss. Reliable information on dietary supplements can be obtained from the NIH Office of Dietary Supplements website as well as consumer warnings on recalled and banned products from the FDA’s website (see Chapter 11).
Table 21.7
CLA, conjugated linoleic acid; FDA, Food and Drug Administration; OTC, over-the-counter.
(Adapted from Natural Medicines Database: Natural medicines in the clinical management of obesity, 2022. Available from http://naturaldatabase.therapeuticresearch.com:80/ce/ceCourse.aspx?s5ND&cs5&pc509%2D32&cec51&pm5; Scott GN: Is raspberry ketone effective for weight loss? Available from http://www.medscape.com/viewarticle/775741, 2012; Esteghamati A, Mazaheri T, Vahidi Rad M, Noshad S: Complementary and alternative medicine for the treatment obesity: a critical review. Int J Endocrinol Metab 13:e19678, 2015. Available from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386228/; Pittler MH, Ernst E: Guar gum for body weight reduction: meta-analysis of randomized trials. Am J Med 110:724, 2001; Perreault L: Obesity in adults: drug therapy. Up to Date Available from https://www.uptodate.com/contents/obesity-in-adults-drug-therapy, 2021.)
Physical activity is the most variable component of energy expenditure (see Chapter 2). Increases in energy expenditure through exercise and other forms of physical activity are important components of interventions for weight loss and its maintenance. By increasing LBM in proportion to fat, physical activity helps to balance the loss of LBM and reduction of RMR that inevitably accompany intentional weight reduction. Other positive side effects of increased activity include strengthening cardiovascular integrity, increasing sensitivity to insulin, and expending additional energy and therefore calories.
The CDC’s Physical Activity Guidelines for Americans suggest a minimum of 150 minutes of physical activity weekly, with two sessions of weight training, to achieve health benefits. However, recent studies have shown that adhering to physical activity guidelines without adhering to a calorie-restricted diet will lead to only minimal or modest weight loss; proper nutritional intake is crucial for weight loss. For weight maintenance or prevention of weight gain, 200 to 300 minutes of weekly physical activity may be more effective. The majority of participants in the National Weight Control Registry (NWCR) who have kept off at least 10% of their weight for at least a year report 1 h/day of physical activity (at least 420 min/week).
Overweight and obese adults should gradually increase to optimal levels of physical activity. Even if an overweight or obese adult is unable to achieve this level of activity, there is evidence that significant health benefits can be realized by participating in at least 30 minutes of daily activity of moderate intensity. Targeting these levels of physical activity can improve health-related outcomes and facilitate long-term weight control.
Aerobic exercise and resistance training should be recommended. Resistance training increases LBM, raising the RMR and one’s ability to use more of the energy intake, and increases bone mineral density, especially for women (see Chapter 24). Aerobic exercise is important for cardiovascular health through elevated RMR, calorie expenditure, energy deficit, and loss of fat. In addition to the physiologic benefits of exercise, other benefits include relief of boredom, increased sense of control, and improved sense of well-being. The whole family can get involved in pleasurable exercise activities (Fig. 21.7).
The recommendations for exercise from the American College of Sports Medicine differ for weight loss versus weight maintenance. Physical activity of fewer than 150 min/week has a minimal effect on weight loss, whereas physical activity of greater than 150 min/week usually results in modest weight loss (defined as 2 to 3 kg), and physical activity between 225 and 420 min/week is likely to result in the greatest weight loss (5 to 7.5 kg). However, this high volume of physical activity may not be practical for the general population. Research on maintaining weight indicates that moderate to vigorous physical activity of 150 to 250 min/week, at an energy equivalent of 1200 to 2000 kcal/week (about 12 to 20 miles/week of jogging or running) is sufficient to prevent weight gain (Swift et al, 2014). However, obese individuals who have successfully lost weight may require a substantial amount of physical activity to maintain weight loss.
Failure to meet the recommended levels of aerobic physical activity leads to nearly $117 billion in annual health care costs and 10% of all premature deaths, according to the Department of Health and Human Services 2018 physical fitness report in the Journal of the American Medical Association (Piercy et al, 2018).
Appropriate pharmacotherapy can augment diet, physical activity, and behavior therapy as treatment for patients with a BMI ≥30 or patients with ≥27 who also have significant risk factors or disease. These agents can decrease appetite, reduce absorption of fat, or increase energy expenditure. As with any drug treatment, physician monitoring for efficacy and safety is necessary. Pharmacotherapy is not a “magic pill”; dietitians should collaborate with other health professionals regarding the use of FDA–approved pharmacotherapy. Not all individuals respond, but for patients who do respond, weight loss of approximately 2 to 20 kg can be expected usually during the first 6 months of treatment. Medication without lifestyle modification is less effective.
As of June 2021, six long-term weight loss drugs were listed as approved by the FDA: orlistat (Xenical), liraglutide (Saxenda, Victoza), lorcaserin (Belviq), naltrexone-bupropion (Contrave), phentermine-topiramate (Qsymia), and semaglutide (Wegovy/Ozempic) See Table 21.8 for mechanisms of action and common side effects of prescription weight loss drugs.
Table 21.8
Weight Loss Drug | Approved For | How It Works | Common Side Effects |
---|---|---|---|
Inhibits gastrointestinal lipase, which reduces the amount of fat absorbed from food by ~1/3—up to 150–200 calories less per day. | |||
Adults | Acts on the serotonin receptors in the brain. This may help you eat less and feel full after eating smaller amounts of food. | Headaches, dizziness, feeling tired, nausea, dry mouth, cough, and constipation. Should not be taken with SSRIs and MAOI medications. | |
Adults | A mix of two drugs: phentermine (suppresses your appetite and curbs your desire to eat) and topiramate (used to treat seizures or migraine headaches). May make you feel full and make foods taste less appealing. | Tingling of hands and feet, dizziness, taste alterations (particularly with carbonated beverages), trouble sleeping, constipation, dry mouth, and increased heart rate Note: Sold only through certified pharmacies. May lead to birth defects. Do not take Qsymia if you are pregnant or planning a pregnancy. | |
Adults | Dry mouth, difficulty sleeping, dizziness, headache, feeling nervous, feeling restless, upset stomach, diarrhea, and constipation | ||
Adults | Decreases appetite Thyroid tumor | GI upset |
MAOI, Monoamine oxidase inhibitor; SSRIs, selective serotonin reuptake inhibitors.
aNote: Metformin, used for type 2 diabetes, is a prescription drug which has been used by physicians as an “off-label” treatment of obesity.
(Adapted from www.niddk.nih.gov, March 3, 2014; Padwal R, Li SK, Lau DC: Long-term pharmacotherapy for obesity and overweight. Cochrane Database Syst Rev (4):CD004094, 2003. Perrault L: Obesity in adults: drug therapy. In Post TW, editor: UpToDate, Waltham, MA, 2018.)
The choice of weight loss drug is determined by the physician in partnership with the patient. In general, medications can be categorized as central nervous system (CNS)-acting agents and non CNS acting agents. Some CNS-acting agents focus on the brain, increasing the availability of norepinephrine. Drug Enforcement Agency Schedule II anorexic agents, such as amphetamines, have a high potential for abuse and are not recommended for obesity treatment. Other CNS-acting agents act by increasing serotonin levels in the brain. Two such drugs, fenfluramine (commonly used in combination with phentermine, known as “fen-phen”) and dexfenfluramine, were removed from the market in 1997 after concerns were raised regarding the possible side effects of cardiac valvulopathy, regurgitation, and primary pulmonary hypertension. Common side effects of many CNS-acting agents are dry mouth, headache, insomnia, and constipation.
Vitamins and supplements may be helpful in addressing a patient’s nutrition concerns while trying to lose weight. OTC and natural weight loss products hold varying degrees of safety and efficacy. See Table 21.7 for additional information.
The nondiet approach (also known as Health at Every Size; HAES) is a weight-neutral approach that proposes that the body will attain its natural weight if the individual eats healthfully, becomes attuned to hunger and satiety cues, and incorporates physical activity. Advocates for this approach promote size acceptance, respect for the diversity of body shapes and sizes, and promotion of intuitive eating. The approach is described as focusing on achieving health rather than attaining a certain weight.
A fat-acceptance movement responding to weight bias and stigma, which persist both within and outside of the health care system, preceded the nondiet movement (see section on Weight Stigma and Social Justice). Advocates for this approach generally feel that CR is harmful (leading to eating disorders, body dissatisfaction, low self-esteem, and psychological harms). Nondiet advocates do not believe that obesity in and of itself is a risk factor for chronic disease, but rather one risk factor, including stress, weight stigma, negative self-talk, and negative interactions with healthcare providers that can sometimes lead to avoidance of seeking care (Ulian et al, 2018a,b). HAES/nondiet advocates believe that for many people, obesity is natural (genetically determined) and unrelated to energy balance, and they point to relapse data as proof that attempts to lose weight often do not work.
To date there have been 10 studies (described in 15 research papers) using a nondiet approach published between 1999 and 2016. Among these 10 studies were a total of 697 subjects who were almost exclusively white women ages 30 to 50. Two of six papers reported a significant improvement in total and LDL cholesterol (Bacon et al, 2002; Mensinger et al, 2016), and one paper reported a significant improvement in HDL (Carroll et al, 2007). Two of three papers reported a small change in systolic or diastolic blood pressure (Bacon et al, 2002; Carroll et al, 2007). Only one study (which provided supervised exercise) reported a clinically and statistically significant change in body mass, 3.6% loss of initial body weight (3.5 kg; Ulian et al, 2015). Only three trials have compared a nondiet approach with traditional weight loss interventions (Bacon et al, 2002; Mensinger et al, 2016; Steinhardt et al, 1999).
The nondiet studies do consistently show improvements in psychological variables (self-esteem, quality of life, and depression). When behavioral-type weight loss studies collect data on psychological variables (self-esteem, body image, health-related quality of life), they consistently report improvements as well (Blaine et al, 2007; Lasikiewicz et al, 2014). Furthermore, in contrast to the idea that intentional weight loss precipitates mood disturbance, reductions in depressive symptoms are consistent via any active treatment (lifestyle modification, exercise, nondiet, etc.; Fabricatore et al, 2011).
A 5% weight loss leads to clinically significant improvements in metabolic variables. On average, professional weight loss interventions induce a 9.5% weight loss from baseline and maintain 54% of the loss at 1 year (Ramage et al, 2014). Weight regain data from clinical weight loss interventions, however, are not randomizable (applicable) to the general population. The most recent available data (collected via NHANES) found that 36.6% of 14,306 US adults were maintaining at least a 5% weight loss (Kraschnewski et al, 2010).
While people with body image disturbances are at higher risk for the development of eating disorders, intentional weight loss programs, when administered by a trained and empathetic professional, do not appear to increase the incidence of eating disorders. In fact, some studies report increased body satisfaction and a healthier relationship with food in addition to weight loss (National Task Force on the Prevention and Treatment of Obesity, 2000; Palavras et al, 2017; Wadden and Sarwer, 2004).
Well-designed behavioral weight loss interventions are able to reduce weight, improve metabolic profiles, and improve psychological outcomes. Behavioral programs vary but typically address: (1) emotional eating triggers, (2) balanced nutrition, (3) social support, and (4) exercise, and sometimes also include cognitive restructuring via exploration of dysfunctional thoughts regarding weight, body shape, or dieting.
Pursuing weight loss, or not, is an individual choice. For individuals who choose not to focus on weight, a nondiet approach can lead to improved body image and psychological variables. This approach appeals to many people and warrants more research, especially on diverse populations of people. The effects on metabolic variables and the quality of dietary intake are unclear (Leblanc et al, 2012; Ulian et al, 2018b) and passive weight loss is not an expected an outcome.
Bariatric surgery is currently considered the only long-term effective treatment for extreme or class III obesity with a BMI ≥40, or a BMI ≥35 with comorbidities. According to the American Society for Metabolic and Bariatric Surgery (ASMBS), 228,000 bariatric surgeries were done in 2017 with an increase of 16% from 2015. Sleeve gastrectomy and Roux-en-Y gastric bypass (RYGB) are the two most common bariatric surgeries in the United States, with 58.1% and 18.7% performed, respectively. The laparoscopic adjustable gastric banding (LAGB) and biliopancreatic diversion with duodenal switch (BPD/DS) are still done, but prevalence is decreasing; with LAGB making up 3.4% of bariatric surgeries, and BPD/DS 0.6%, (American Society for Metabolic and Bariatric Surgery [ASMBS], 2016).
Before any extremely obese person is considered for surgery, failure of a comprehensive program that includes calorie reduction, exercise, lifestyle modification, psychological counseling, and family involvement must be demonstrated. Failure is defined as an inability of the patient to reduce body weight by one-third and body fat by one-half, and an inability to maintain any weight loss achieved. Such patients have intractable morbid obesity and should be considered for surgery.
If surgery is chosen, the patient is evaluated extensively with respect to physiologic and medical complications, psychological problems such as depression or poor self-esteem, and motivation. Behavioral counseling, especially in the postoperative period, can improve weight loss (Stewart and Avenell, 2016). Postoperative follow-up requires evaluation at regular intervals by the surgical team and a RDN. In addition, behavioral or psychological support is necessary. Studies indicate some positive physiologic changes in liver fibrosis, BMI, branched-chain amino acid production, and reversal of insulin-induced increases in brain glucose metabolism (Abdennour et al, 2014; Tuulari et al, 2013).
Weight loss surgery procedures reduce the amount of food that can be eaten at one time and produce early satiety (Fig. 21.8). The new stomach capacity may be as small as 30 mL or approximately 2 tablespoons. After surgery the patient’s diet progresses from clear liquid to full liquid to purée, soft, and finally to a regular diet as tolerated, with emphasis on protein and fluid intake (Table 21.9). The results of gastric surgery are more favorable than those from the intestinal bypass surgery practiced during the 1970s. On average, the reduction of excess body weight after gastric restriction surgery correlates to approximately 30% to 40% of initial body weight. In addition to the greater absolute weight loss observed, the gastric bypass tends to have sustainable results with significant resolution of hypertension, type 2 diabetes mellitus, osteoarthritis, back pain, dyslipidemia, cardiomyopathy, nonalcoholic steatohepatitis, and sleep apnea. However, late complications may be seen, such as vitamin deficiencies, electrolyte problems, or even intestinal failure. Patients should be nutritionally assessed regularly (see Appendices 11 and 12). Thirty-day major complication rates for all bariatric procedures have been found to be 1.15% anastomotic leak, 0.37% myocardial infarction, and 1.17% pulmonary embolism (Chang et al, 2018).
Table 21.9
Mayo Clinic: Gastric bypass diet: what to eat after the surgery (website). Available from https://www.mayoclinic.org/tests-procedures/gastric-bypass-surgery/in-depth/gastric-bypass-diet/art-20048472.)
The laparoscopic sleeve gastrectomy (LSG) initially was used for patients with a BMI >60 as a precursor to the BPD/DS, but it is now used as a stand-alone procedure and currently is the most popular bariatric surgery in the United States. The sleeve gastrectomy involves removing approximately 80% of the stomach, creating a long, thin gastric pouch by stapling or sewing the stomach longitudinally. The pyloric sphincter is left intact (Meek et al, 2016). Complications associated with the LSG can include gastric bleeding, stenosis, leak, and reflux. One of the most common complications from sleeve gastrectomy involves acid reflux, occurring in 20% to 30% of patients (Braghetto et al, 2012). Occasionally, RYGB is necessary to resolve reflux complications (Weiner et al, 2011; see Fig. 21.6).
Gastric bypass involves reducing the size of the stomach with the stapling procedure, but then connecting a small opening in the upper portion of the stomach to the small intestine by means of an intestinal loop. The original operation in the late 1960s evolved into the RYGB. Because use of the lower part of the stomach is omitted, the gastric bypass patient may have dumping syndrome as food empties quickly into the duodenum (see Chapter 27). The tachycardia, sweating, and abdominal pain are so uncomfortable that they motivate the patient to make the appropriate behavioral changes and refrain from overeating and choosing less healthful foods, such as sugar-sweetened beverages. Eventually the pouch expands to accommodate 4 to 5 oz at a time. Sometimes gastric bypass surgery can lead to bloating of the pouch, nausea, and vomiting. A postsurgical food record noting the tolerance for specific foods in particular amounts helps in devising a program to avoid these episodes.
Up to 16% of patients may experience postoperative complications (Beebe and Crowley, 2015). These include anastomotic leaks, strictures, perforation, gastric fistulas, bowel obstructions, wound infections, respiratory failure, and intractable nausea and vomiting.
LAGB, the band creating the reduced stomach pouch, can be adjusted so that the opening to the rest of the stomach can be made smaller or enlarged. The band, filled with saline, has a tube exiting from it to the surface of the belly just under the skin; this allows for the injection of additional fluid or reduction of fluid into the band. Rates of lap-band placement have been decreasing across the United States, with some bariatric centers and surgeons no longer performing the procedure. Many patients are drawn to the band as an option as it is reversible; however, many practitioners and researchers find the complications outweigh the benefits (Ibrahim et al, 2017).
Bariatric surgery places an individual at risk for malnutrition that requires lifelong follow-up and monitoring by the multidisciplinary team. Nutritional status should be frequently evaluated by an RDN. Monitoring should include an assessment of total-body fat loss and a full micronutrient assessment. Pre- and postsurgical micronutrient assessment should include thiamine, vitamin B12, folate, iron, vitamin D, calcium, other fat-soluble vitamins, zinc, and copper. In many cases, a liquid multivitamin mineral supplement is used. Recommended vitamin supplementation after bariatric surgery can be found in Table 21.10 (Parrott et al, 2017).
Table 21.10
BPD/DS, Biliopancreatic diversion with duodenal switch; LAGB, laparoscopic adjustable gastric banding; LSG, laparoscopic sleeve gastrectomy; RDA, recommended dietary allowance; RYGB, Roux-en-Y gastric bypass; WLS; weight loss surgery.
Bariatric surgery is increasing in popularity as a treatment of extreme obesity for the adolescent population. Similar preoperative requirements exist; however, the age and cognitive emotional maturity of the patient need to be taken into consideration given the lifelong nutritional, psychological, and physical ramifications.
Surgical management of weight continues to evolve. Select bariatric surgery centers across the United States have started utilizing the intragastric balloon (IGB). The IGB, which is made of silicone, is endoscopically placed in the stomach for 6 months. During the 6 months in which the balloon resides in the stomach, patients are expected to learn and develop healthy eating habits that persist after the balloon has been removed. Complications include abdominal pain, nausea, esophagitis, flatulence, and gastric ulcer. An IGB can increase weight loss by 14.25% (Saber et al, 2017). There is currently insufficient evidence regarding the IGB’s efficacy or safety. The Aspire Assist is a gastrostomy tube placed during gastroscopy. Patients can aspirate contents of a meal approximately 20 minutes after eating, thus decreasing caloric absorption.
Energy requirements for weight maintenance after weight reduction are lower than at the original weight because smaller bodies have smaller energy requirements. Most studies show that the RMR of reduced weight subjects versus stable-weight-controls (of the same height, weight, and gender) are not different (Clamp et al, 2018). A follow-up study of participants in The Biggest Loser television show (who lost significant amounts of weight) found that after weight regain, RMR remained suppressed (Fothergill et al, 2016). These results open questions about possible long-term effects of extreme energy restriction—especially coupled with extreme levels of physical activity—on eventual RMR. People who have lost weight will always have reduced-energy requirements due to reduced body mass, which necessitates permanent lifestyle changes to maintain the net energy balance supporting their reduced body weight (Hall et al, 2011).
The NWCR consists of more than 5000 individuals who have been successful in long-term weight loss maintenance. The purpose of establishing the NWCR is to identify the common characteristics of those who succeed in long-term weight loss maintenance. There is very little similarity in how these individuals lost weight, but there are some common behaviors they all have for keeping the weight off. Lifestyle modification and a sense of self-efficacy appear to be essential. To maintain weight loss, NWCR participants report the following:
A national weight loss registry is contributing to our understanding of those tactics that lead to long term success. Dietary restriction of fat, frequent self-weighing, and ongoing leisure time physical activity were factors associated with maintaining weight loss (Thomas et al, 2014). Support groups are valuable for obese persons who are maintaining a new lower weight; they help individuals facing similar problems. Two self-help support groups are Overeaters Anonymous (OA) and Take Off Pounds Sensibly (TOPS). These groups are inexpensive, continuous, include a “buddy system,” and encourage participation on a regular basis or as often as needed. Weight Watchers programs offer free lifelong maintenance classes for those who have reached and are maintaining their goal weights.
Interestingly, “repetitive” and “monotonous” diets can provide a strategy for reducing food intake. For some people, diets that are repetitious (without change from meal-to-meal) are a potential consideration for controlling intake, because people tend to overeat when they have many mealtime choices. This can be a particular problem in a society where one in three meals is eaten away from home. Restaurants, food trucks, and vending machines generally offer many options, most of them high in calories (see Focus On: Restaurant and Vending Machine Nutrition Labeling). Overall, common sense and individualized approach is needed.
A common experience for the person in a weight reduction program is arrival at a weight plateau, as weight loss slows and eventually seems to stop. Recent research explains that the plateau effect is mainly due to a lack of ongoing energy deficit. Subjects tend to maintain an energy deficit for only about 6 weeks, then gradually return to their baseline energy intake. This means a state of equilibrium has been reached at which the energy intake is equal to energy expenditure. To move out of this phase, reestablishing an energy deficit is required.
There are several factors that reduce RMR and TEE during energy restriction and weight loss, including: energy restriction—RMR can decrease at the onset of energy restriction by as much as 15% within 2 weeks, which varies with the magnitude of energy restriction; loss of metabolically active body tissue. Weight loss consists of both LBM and fat, and less of either (but especially LBM) reduces RMR; the cost of physical activity is also less because a body that weighs less requires less energy expenditure to move around; and the thermic effect of food is generally about 10% of energy intake, which is automatically less with energy restriction. These are not the major factors stalling weight loss, however; it is necessary to reestablish an energy deficit.
Repeated bouts of weight loss and regain, known as weight cycling or the yo-yo effect, occurs in men and women and is common in overweight and lean individuals. Research is mixed on whether weight cycling results in increased body fatness and weight with the end of each cycle. Undesirable psychological effects are less disputed.
About one-third of US children ages 2 to 19 are overweight or obese (State of Obesity, 2018). Childhood obesity increases the risk of obesity in adulthood. For the child who is obese after 6 years of age, the probability of obesity in adulthood is significantly greater if either the mother or the father is obese.
The BMI tables for determining childhood obesity are available for use by health care practitioners (see Appendix 8). High preschool BMI is consistently associated with adult obesity, central obesity, and early onset MetS (Lloyd et al, 2012).
Children or adolescents with a BMI in the 85th percentile or higher with complications of obesity, or with a BMI in the 95th percentile or higher with or without complications, should be carefully assessed for genetic, endocrinologic, and psychological conditions, and secondary complications such as hypertension, dyslipidemias, type 2 diabetes, sleep apnea, and orthopedic problems.
Assessment involves investigating all of the social and environmental factors, including family dynamics, that influence eating and activity habits as well as readiness for change. The primary goal of treatment is to achieve healthy eating and activity, not to achieve an ideal body weight (IBW). For children aged 2 to 5, the goal is prolonged weight maintenance or slowing of the rate of weight gain, which allows for a gradual decline in BMI as children grow in height. This is an appropriate goal in the absence of any secondary complication of obesity. However, if secondary complications are present, children in this age group may benefit from weight loss if their BMI is at the 95th percentile or higher. For children aged 6 and older, prolonged weight maintenance is appropriate if their BMI is between the 85th and 95th percentile and if they have no secondary complications. If a secondary complication is present, or if the BMI is at the 95th percentile or above, weight loss may be advised. Comprehensive, intensive behavioral interventions should be offered (Kaiser Permanente, 2012).
If the weight appropriate for the child’s or teen’s anticipated adult height has already been reached, maintenance at that weight should be the lifetime goal. The child who already exceeds an optimal adult weight can safely experience a slow weight loss of 10 to 12 lb per year until the optimal adult weight is reached. Balanced micronutrient intake for children includes 45% to 60% of kilocalories from carbohydrates, 25% to 40% from fat, and 10% to 35% from protein. New directions in childhood obesity research since the turn of the 21st century have uncovered 25(OH)D deficiency (defined as a level ≤57 nmol/L or 20 ng/mL). This has been manifested by a lack of sun exposure and the increase in use of sunscreen—blocking the skin’s absorption of ultraviolet light. Low vitamin D is predominant in obese children. The accompanying proinflammatory association with diabetes and atherogenic pathways has prompted recommendations to test kindergarten and first grade children. Children with low levels of vitamin D could have the systemic inflammatory mediators and reduced insulin sensitivity pathways inhibited by vitamin D supplementation (Reyman et al, 2014).
The child or adolescent who needs to reduce weight requires attention from family and health professionals. This attention should be directed to all the areas mentioned previously, with family modification of eating habits and increased physical activity. The program should be long term, over the entire growth period of the child and perhaps longer.
Inactivity often is coupled with sedentary hobbies, excessive TV watching, or prolonged sitting in front of a computer or game screen. Some theorize that physical inactivity appears to be the result of fatness rather than its cause (Metcalf et al, 2011); however, others have postulated that environmental factors such as a decrease in active commuting, high school physical education, and outdoor play are contributing factors as well (Bassett et al, 2015). Additional research is required; however, it is possible that factors other than inactivity may be more important in obesity development in children (see New Directions: Partnership for a Healthier America Addressing Childhood Obesity).
Almost eclipsed by the attention focused on obesity is the need for some people to gain weight. The term underweight is applicable to those who are 15% to 20% or more below accepted weight standards. Because underweight is often a symptom of disease, it should be assessed medically. A low BMI <18.5 in adults, BMI <5% for children, and <23 in older adults, is associated with greater mortality risk than that of individuals with optimal BMI. Undernutrition may lead to under functioning of the pituitary, thyroid, gonads, and adrenals. Other risk factors include loss of energy and susceptibility to injury and infection, as well as a distorted body image and other psychological problems (see Chapter 22).
Underweight or unintentional weight loss can be caused by (1) inadequate oral food and beverage intake, with insufficient quantities to match activity; (2) excessive physical activity, as in the case of compulsive athletic training; (3) inadequate capacity for absorption and metabolism of foods consumed; (4) a wasting disease that increases the metabolic rate and energy needs, as in cancer, AIDS, or hyperthyroidism; or (5) excess energy expenditure during psychological or emotional stress.
Assessing the cause and extent of underweight before starting a treatment program is important. A thorough history and pertinent medical tests usually determine whether underlying disorders or food insecurity are causing the underweight. From anthropometric data such as arm muscle and fat areas, it is possible to determine whether health-endangering underweight really exists (see Appendix 11). Assessment of body fatness is useful, especially in dealing with the patient who has an eating disorder. Biochemical measurements indicate whether malnutrition accompanies the underweight (see Chapter 5 and Appendix 11).
Any underlying cause of unintentional weight loss or low BMI must be the first priority. A wasting disease or malabsorption requires treatment. Nutrition support and dietary changes are effective, along with treatment of the underlying disorder (Table 21.11).
Table 21.11
Concern | Tips |
---|---|
Anxiety, stress, depression | Antidepressants can help; monitor choice to be sure they do not contribute to weight fluctuations. Ensure adequacy of physical activity as well as folate, B6, B12 and essential fatty acids (see Chapter 40). |
Cancer | Gastrointestinal (GI) cancers are especially detrimental. Some treatments and medications can cause loss of appetite, as can the cancer itself (see Chapter 35). |
Celiac disease | Ensure that all gluten-containing foods and ingredients are eliminated from the diet. |
Changes in activity level or dietary preparation methods | Avoid skipping meals; prepare foods with high energy density; add snacks between meals. |
Diabetes, new onset | See a physician; monitor medications and ensure adequate intake (see Chapter 29). |
Dysphagia or chewing difficulties | Alter food and liquid textures accordingly to improve chewing and swallowing capability (see Chapter 39). |
Hyperthyroidism | Too much thyroxine can cause weight loss (see Chapter 30). |
Inflammatory bowel disease | Small frequent protein and calorie-rich meals, low residue, may need enteral or parenteral nutrition (see Chapter 27). |
Intestinal ischemia | Needs medical intervention and potentially enteral or parenteral feedings (see Chapters 12, 26, and 27). |
Medications | Some medications can cause weight loss; check with physician; add protein and calorie-rich meals and snacks; manage GI side effects like nausea, constipation, and diarrhea. |
Nausea and vomiting | Infections, other illnesses, hormonal changes, and some medications cause nausea and vomiting; small, frequent meals; serve liquids between meals instead of with meals to reduce fullness (see Chapters 26 and 35). |
Pancreatitis and cystic fibrosis | Monitor for sufficiency of pancreatic enzyme replacement, easy to digest, small frequent meals and snacks, lower fat if steatorrhea is present (see Chapters 28 and 33). |
Food insecurity | Provide resources for food assistance programs |
If the cause of the underweight is inadequate oral food and beverage intake, activity should be limited, and psychological counseling initiated if necessary. If the cause is food insecurity, provide local resources for food assistance.
The FDA has approved orexigenic agents that include corticosteroids, cyproheptadine, loxiglumide (cholecystokinin antagonist), megestrol acetate, mirtazapine, dronabinol, oxoglutarate, anabolic agents (testosterone or Anadrol), Oxandrin (oxandrolone or oxandrolona), and growth hormone. Use of orexigenic agents for weight loss in seniors is saved for those whose conditions are refractory to usual treatments. One-third of older adults, especially women, exhibit weight loss in combination with depression. Mirtazapine is an effective antidepressant that is well tolerated and increases appetite. It is particularly effective in elderly patients with dementia-related weight loss (Fox et al, 2009). Dronabinol is used for chemotherapy-induced nausea and vomiting in cancer and AIDS patients; it has been shown to induce weight gain in patients with dementia. For older adults, moderate amounts of alcohol can also help to increase appetite.
A careful history may reveal inadequacies in dietary habits and nutritional intakes. Meals should be scheduled and eaten when relaxed instead of hastily planned or quickly eaten. The underweight person frequently must be encouraged to eat, even if not hungry. The secret is to individualize the program with readily available foods that the individual enjoys, with a plan for regular eating times throughout the day. In addition to meals, snacks are usually necessary to adequately increase the energy intake. High-calorie liquids taken with meals or between meals are often effective in those who have loss of appetite or early satiety. Everyday foods can be fortified to increase the calories and protein (see Focus On: Food First! in Chapter 20).
The energy distribution of the diet should be approximately 30% of the kilocalories from fat, with the majority from monounsaturated or polyunsaturated sources and at least 12% to 15% of the kilocalories from protein. In addition to an intake according to estimated energy requirements for the present weight, 500 to 1000 extra kcals per day should be planned. If 2400 kcal maintains the current weight, 2900 to 3400 kcal would be required for weight gain.
The intake should be increased gradually to avoid gastric discomfort, discouragement, electrolyte imbalances, and cardiac dysfunction. Step-up plans are outlined in Table 21.12. In underweight children, nonnutritional factors, insufficient caloric intake, excessive nutrient losses, and abnormal energy metabolism may contribute to growth failure and morbidity. Thus, adequate nutritional support should be an integral part of the management plan. Lipid-based nutrient supplements are fortified products that are often ready-to-use therapeutic foods or highly concentrated supplements that can be administered at “point of service” or emergency settings (Chaparro and Dewey, 2010).
Table 21.12
(From US Department of Agriculture Food Data Central. https://fdc.nal.usda.gov.)