Nutrition for Obesity and Eating Disorders

Nutrition for Obesity and Eating Disorders

Obesity is a chronic condition that typically develops over an individual’s lifetime. At its most basic level, obesity is a problem of excessive calorie intake. A far less common weight issue is disordered eating manifested as anorexia nervosa or bulimia. Historically, the study of obesity and eating disorders has been separate: The former has been rooted in medicine, and the latter has been the focus of psychiatry and psychology. Yet, there are commonalities between them, such as questions of appetite regulation, concerns with body image, and similar etiologic risk factors.

This chapter focuses on obesity—its causes, complications, and treatment approaches, including nutrition therapy, behavior change, physical activity, pharmacology, and surgery. Eating disorders and their nutrition therapy are described.


Obesity can be defined as an excessive amount of fat that increases the risk of illness and premature death (Fock & Khoo, 2013). The National Institutes of Health definitions of overweight and obesity are based on population studies that assess the relationship between obesity and rates of mortality and morbidity that are related to weight (Table 15.1).

Obesity is a major health issue and a global public health challenge. In the United States, in 2011 to 2014, the prevalence of obesity among adults was just over 36% (Fig. 15.1) (Ogden, Carroll, Fryar, & Fiegal, 2015). Trends in overweight, obesity, and extreme obesity are depicted in Figure 15.2 (Fryar, Carroll, & Ogden, 2014). The dramatic increase in extreme obesity is particularly noteworthy. Obesity prevalence has increased in both men and women, in all age groups, and in all racial and ethnic groups.

Overweight a body mass index (BMI) of 25 or greater.

Obesity a BMI of 30 or greater.

Table 15.1 National Institutes of Health Definitions of Overweight and Obesity

Body Mass Index

Risk of Developing Health Problems




Normal weight








Class I



Class II


Very high

Class III (extreme obesity)


Extremely high

* Because evidence suggests health risks begin at lower BMIs in Asians, China uses a cutoff of 28 for obesity, Japan uses 25, and the World Health Organization recommends a cutoff for Asians of >27.5.

U.S. Department of Health & Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute. (n.d.). Classification of overweight and obesity by BMI, waist circumference, and associated disease risks. Available at Accessed on 6/9/16.

Figure 15.1Prevalence of obesity in the United States, 2011-2014. (Source: Ogden, C., Carroll, M., Fryar, C., and Fiegal, K. [2015]. Prevalence of obesity among adults and youth: United States, 2011-2014. NCHS Data Brief No. 219. Available at Accessed on 1/17/17.)

Complications of Obesity

Obesity significantly increases mortality. On average, class I obesity lowers life expectancy by 2 to 4 years. Much less information is available for BMI >35, but in those with a BMI of 40 to 50, life expectancy seems to be reduced by 8 to 10 years, comparable to the effects of smoking (Prospective Studies Collaboration, 2009). Studies suggest that overweight and obesity were likely responsible for approximately 18% of deaths in black and white adult Americans from 1986 to 2006 (Masters et al., 2013). Beginning at a BMI of 30, as BMI increases, so does the risk of allcause mortality (Jensen et al., 2014).

Figure 15.2Trends in adult overweight, obesity, and extreme obesity among men and women aged 20 to 74 years. (Source: Fryar, Carroll, & Ogden, 2014.)

Complications of obesity have far-reaching negative effects on health—either directly because of obesity or indirectly, such as a sedentary lifestyle or poor-quality eating pattern (Fock & Khoo, 2013). Obesity increases the risk of morbidity from hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea, respiratory problems, and some cancers (Jensen et al., 2014). Other complications include gastroesophageal reflux disease, nonalcoholic fatty liver disease (NAFLD), and polycystic ovary syndrome. Obesity increases the risk of complications during and after surgery and the risk of complications during pregnancy, labor, and delivery. The biomedical, psychosocial, and economic consequences of obesity have significant impact on the health and well-being of the U.S. population (Jensen et al., 2014).

Where excess body fat is stored also influences the risk of comorbidities. Central obesity, as part of the metabolic syndrome, increases the risk of coronary heart disease and type 2 diabetes (see Chapter 19). Central obesity also increases the risk of stroke, sleep apnea, hypertension, dyslipidemia, insulin resistance, inflammation, and some types of cancer (Tchernof & Després, 2013). This risk is usually confirmed at any degree of total body fatness. Evidence shows that as waist circumference increases, so do risk of obesity comorbidities (Jensen et al., 2014).

Central Obesity waist circumference exceeding 35 in in women or 40 in in men.

Metabolic Syndrome a cluster of interrelated symptoms, including obesity, insulin resistance, hypertension, and dyslipidemia, which together increase the risk of cardiovascular disease and diabetes.

Causes of Obesity

The cause of obesity seems obvious: Obesity occurs when calorie intake exceeds calorie expenditure (i.e., people eat more calories than they expend over time). Although we know how obesity occurs, why it occurs is not fully understood despite intensive study. A recent literature review found that there is no consensus among previously published reviews regarding the primary cause of obesity; however, combined “physical activity and diet” was the most popular cause identified in adult studies (Ross, Flynn, & Pate, 2015). It is likely that obesity occurs from a dynamic interaction of variables, such as metabolic, genetic, environmental, cultural, behavioral, and socioeconomic factors.

Body Fat Metabolism

The body converts an excess of calories from any source to fat (triglycerides) and stores it in fat cells in adipose tissue. The number of fat cells a person has increases most rapidly during the growth periods of late childhood and early puberty. Thereafter, the number of fat cells increases only in response to an excess calorie intake; an excess of calories leads to triglyceride accumulation in fat cells, which, as they expand, stimulate the formation of more fat cells. Obesity is caused by an increase in the number and/or size of fat cells.

When calorie intake exceeds need and adipose tissue cells and subcutaneous fat cells are saturated and unable to further expand, excess fat accumulates in organs such as the heart, liver, and kidney. Fat stored in these organs promotes insulin resistance and increased cardiometabolic risk (Tchernof & Després, 2013). Excess fat may also accumulate in the pancreas, impairing insulin secretion and increasing the risk of type 2 diabetes.

When calorie intake is less than calorie expenditure, stored triglycerides are metabolized for energy and the size of fat cells decreases, but their number does not. When excess calories are later available, these fat cells readily expand in size. In part, this explains why people with extra fat cells tend to regain lost weight more quickly than people with an average number of fat cells. Preventing an excess accumulation of fat cells during childhood and adolescence may have a critical role in preventing obesity later in life.

Lipoprotein Lipase

Lipoprotein lipase (LPL) is an enzyme found in adipose tissue and muscle. It functions to remove triglycerides from the blood to store them in adipose and muscle tissue. In women, LPL is abundant in the fat cells of the breasts, hips, and thighs; in men, LPL is abundant in the fat cells of the abdomen. These different enzyme levels account for the difference in where women and men tend to gain excess weight.

Obese people have higher levels of LPL in their adipose tissue than do lean people. The result is an increased propensity to store fat, even when the excess calorie intake is relatively small.
Adipose LPL activity increases after weight loss to promote fat deposition—the body’s attempt to maintain weight or composition through its own internal controls despite variations in calorie intake and energy expenditure. This phenomenon is known as the set-point theory.

Resetting Set-Point Theory

It appears that the body is more efficient in protecting against weight loss when calories are restricted than it is at preventing weight gain when calorie intake is excessive (Farias, Cuevas, & Rodriguez, 2011). Findings by Briggs et al. (2013) suggest that obesity caused by an excessive calorie intake changes the body’s set point to a higher weight, making it difficult for obese people to lose weight. Researchers speculate that when subjected to a low-calorie intake, the body interprets the negative energy balance as a threat to the set point and secretes ghrelin to stimulate appetite and defend this higher body weight. These physiologic mechanisms appear to have been designed to enable our primitive ancestors to survive through long intervals without food (Demaria, 2013).


Genetic factors are to blame for very rare, single-gene forms of obesity. For instance, massive obesity and excessive appetite are characteristics of Prader-Willi syndrome, a genetic disorder caused by a chromosomal abnormality. Among the other characteristics of this syndrome are mental retardation and reproductive problems.

Emerging research has begun to identify the genetic influence on “common” obesity, which is not controlled by a single gene but probably influenced by dozens if not hundreds of genes. Supporting the case for a genetic basis to weight status is the tendency of adopted children to have similar weights to their biological parents, not their adoptive parents (Silventoinen, Rokholm, Kaprio, & Sorensen, 2010). Similarly, studies on twins show that identical twins are twice as likely as fraternal twins to weigh the same (Wardle, Carnell, Haworth, & Plomin, 2008).

Study results suggest that genetics play a role in whether a person may be predisposed to obesity, not that genes predestine a person to obesity. Even when a genetic susceptibility exists, exposure to an obesogenic environment is necessary for obesity to develop (Herrera & Lindgren, 2010). Likewise, in people with a genetic predisposition to obesity, the severity of the disease is largely determined by lifestyle and environmental conditions (Loos & Rankinen, 2005). The rapid rise in obesity around the globe has occurred without changes in the gene pool, suggesting that the root cause is lifestyle and environment, not biology.

Obesogenic Environment an environment that produces and supports overweight and obesity.


The Ob gene is one of the main genes linked to the obesity phenotype in humans. It directs fat cells in adipose tissue to secrete the protein leptin, which acts in the hypothalamus and other areas of the brain to decrease appetite and increase energy expenditure. The circulating level of leptin varies with the proportion of fat mass (Nabi, Rafiq, & Qayoom, 2016). For instance, an increase in body fat leads to an increase in leptin, which leads to a decrease in appetite and an increase in metabolism and energy expenditure. Conversely, when body fat decreases, leptin levels decrease which stimulates appetite and lowers metabolism and energy expenditure.

Leptin deficiency is very rare in humans. It is characterized by rapid weight gain in the first few months of life leading to severe obesity (Farooqi & O’Rahilly, 2009). Appetite is intense, and satiety after eating is impaired. Leptin therapy that raises leptin levels from undetectable to detectable has profound effects on diminishing appetite and promoting weight and fat loss. Interestingly, leptin levels increase with increasing BMI, yet the high leptin levels in people who are obese seem ineffective in suppressing appetite or increasing energy expenditure, suggesting leptin resistance (Nabi et al., 2016). Studies with leptin demonstrate that appetite and eating behavior is in part determined by biology.

Ghrelin a protein produced by stomach cells that enhances appetite and decreases energy expenditure.


The hormone-like protein ghrelin, which is secreted mostly by the stomach cells, promotes weight gain by stimulating appetite and promoting efficient energy storage. Ghrelin levels fall after eating and whenever the body is in a positive calorie balance
(e.g., when the body is gaining weight). Ghrelin levels are usually high before eating and when there is a negative energy balance or low-calorie intake, which may explain why maintaining weight loss is so difficult. Researchers have found that eventually—perhaps a year after weight loss—ghrelin levels adjust to a new lower weight and revert toward before-weight loss levels (Iepsen, Lundgren, Holst, Madsbad, & Torekov, 2016), which may then help maintain weight loss.

Obesogenic Environment

The increasing prevalence of obesity has been associated with changing culture, lifestyles, and economics (Demaria, 2013). The current environment, which encourages energy intake and discourages energy expenditure, has been labeled obesogenic. It, along with behavior, is believed to account for the increased prevalence of overweight and obesity in the world today (Corsica & Hood, 2011). Factors that contribute to an obesogenic environment include the following:

  • An abundance of readily accessible, low-cost, palatable, high-calorie foods in large portions

  • Increasing consumption of snacks

  • A high intake of added sugars, including soft drinks

  • A great proportion of the food budget spent on food away from home

  • The increasing portion size of restaurant meals

  • A decrease in energy expenditure related to labor-saving devices, such as remote control devices and motorized walkways

  • An increase in sedentary leisure activities, such as watching television, playing video games, and sitting in front of a computer. Television watching may promote obesity by leaving less time for physical activity, lowering resting metabolic rate, and/or promoting greater meal frequency and food intake (Chaput, Klingenberg, Astrup, & Sjodin, 2011).


An expert panel convened in 2008 to update the National Institutes of Health’s 1998 Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults—The Evidence Report (Jensen et al., 2014). Guided by critical questions, the panel evaluated new evidence related to key issues on overweight and obesity evaluation and treatment, particularly in people with diabetes and other risk factors for cardiovascular disease. The culmination of their work is the next generation evidence-based report entitled “2013 American Heart Association/American College of Cardiology/The Obesity Society Guidelines for the Management of Overweight and Obesity in Adults” (Jensen et al., 2014). The report includes a treatment management algorithm, identifies the best low-calorie diets, and summarizes the expected impact of comprehensive lifestyle and surgical interventions. The following sections include many of the expert panel’s recommendations.

Identifying Patients Who Need to Lose Weight

The first step in managing overweight and obesity is to identify who should lose weight based on BMI, cardiovascular risk factors, and the patient’s readiness for behavior change (Jensen et al., 2014).

  • Weight loss is indicated for anyone with a BMI ≥30 (obese) or with a BMI of 25 to 29.9 (overweight) who have one risk for cardiovascular disease, such as diabetes, prediabetes, hypertension, dyslipidemia, high waist circumference, or other obesity-related comorbidities. Patients who are not ready or able to lose weight should be advised to avoid additional weight gain and are treated for cardiovascular and obesity-related conditions.

  • People who are overweight but without any risk factors or who are of normal weight with a history of overweight or obesity should be advised to frequently monitor their weight and adjust their calorie intake if they start to gain weight. They should also be encouraged to engage in regular physical activity to help avoid weight gain.

  • People who are at normal weight (BMI 18.5-24.9) should be advised to not gain weight.

Evaluating Readiness to Lose Weight

Objectively identifying who may benefit from weight loss is not the only criterion to be considered before beginning treatment; assessing the patient’s level of readiness to make changes is crucial. Because patients at the two earliest stages of the transtheoretical stages of behavior change model are ambivalent about behavior change, patients in those stages are not likely to benefit from weight loss counseling (Fig. 15.3) (Wee, Davis, & Phillips, 2005). Even worse, counseling before readiness may preclude subsequent attempts at weight loss when the patient may be more likely to succeed.

To assess the patient’s stage of readiness, ask (Rhee, McEachern, & Jelalian, 2014)

  • If the patient intends to make changes to improve intake, physical activity level, and behavior, such as keeping a food diary, monitoring weight, and limiting sedentary time.

  • If the patient has made any changes to eat healthier, be more physically active, or improve specific behaviors in the last month.

  • How long the patient has been eating healthier, engaging in greater physical activity, and using behavior strategies.

Goals of Treatment

Ideally, treatment would “cure” overweight and obesity; that is, weight would gradually fall into the healthy BMI category and would be permanently maintained. In reality, this ideal is seldom achieved. The goal of losing large amounts of weight may be unrealistic and overwhelming and, from a health perspective, not necessary to achieve medically significant health benefits. A sustained weight loss of as little as 3% to 5% of body weight can cause clinically significant improvements in some cardiovascular risk factors, such as lower levels of triglycerides, blood glucose, hemoglobin A1c, and lowered risk of type 2 diabetes (Jensen et al., 2014). Greater weight loss leads to greater benefits, such as improved blood pressure and low-density lipoprotein (LDL) cholesterol
and reduced need for medications to control blood glucose, triglycerides, and cholesterol. A 5% to 10% weight loss within 6 months is recommended.

Figure 15.3Stages of change graphic.

Setting a modest weight loss goal and sustaining that weight loss are far more realistic than striving for thinness. Yet, for some people, even modest weight loss may be unattainable. A more appropriate weight management goal for clients who are not ready or unable to lose weight is to prevent additional weight gain. Although this may sound like a passive approach, it requires active intervention, not simply maintenance of the status quo.


Weight loss interventions include

  • Comprehensive lifestyle treatment, which serves as the foundation of weight management for all people. It includes nutrition therapy, physical activity, and behavioral strategies to facilitate adherence to a low-calorie diet and increased physical activity. Comprehensive lifestyle treatment alone will cause a substantial proportion of patients to lose enough weight to improve health (Jensen et al., 2014).

  • Medication may be considered as adjunct therapy for those who are not able to lose weight or maintain weight loss and have a BMI ≥30 or BMI ≥27 with comorbidity.

  • Bariatric surgery may be considered as an adjunct therapy when BMI ≥40 or BMI ≥35 with comorbidity.

Nutrition Therapy for Weight Loss

Weight loss requires a negative calorie balance, which is achieved by eating fewer calories, increasing physical activity, or both. Based on the assumption that 1 pound of fat mass is approximately equivalent to 3500 calories, a deficit of 500 cal/day theoretically leads to a 1 pound weight loss in 7 days. However, metabolic adaptations occur during weight loss (e.g., fewer calories expended during daily activities because body weight is lower) that require a further decrease in calorie intake to achieve a negative calorie balance and continued weight loss (Finkler, Heymsfield, & St-Onge, 2012). This is one factor that contributes to the decreasing rate of weight loss that occurs as the duration of a diet increases (Finkler et al., 2012).

A hypocaloric eating pattern may be achieved by any of the following methods (Jensen et al., 2014).

  • Choose a general target to create a calorie deficit, such as 1200 to 1500 cal/day for women and 1500 to 1800 cal/day for men. These levels are adjusted according to the individual’s body weight and physical activity levels.

  • Prescribe a calorie level that is 500 to 750 cal/day less than estimated need. Estimated need can be determined by indirect calorimeter if available. If it is not, the Mifflin-St. Jeor equation using actual body weight is used to estimate resting metabolic rate, which is then multiplied by an activity factor to estimate total calorie needs per day (Box 15.1). A hypocaloric plan is achieved by either subtracting 500 to 750 cal or 30% from the total estimated needs.

  • An ad lib approach that does not necessarily prescribe a specific calorie level but achieves a calorie deficit by restricting or eliminating particular food groups, such as a low-carbohydrate or low-fat eating plan

The “Best” Weight Loss Diet

The question of which diet is the “best” diet for weight loss has been debated for decades. Attention has focused on the relevance of the macronutrient composition of the diet—the proportion of carbohydrates, protein, and fat—in achieving and maintaining weight loss (Hooper et al., 2012; Johnston et al., 2014). Keep in mind that as the percentage of calories from one macronutrient changes, so do the proportion of calories provided by one or both other macronutrients. For instance, lowering the percentage of fat increases the percentage of carbohydrates. In reality, as long as the diet achieves the target number of calories, many different dietary approaches are effective (Raynor & Champagne, 2016).

Evidence of low to moderate quality from a meta-analysis of randomized controlled trials showed that both low-carbohydrate and low-fat diets are associated with an estimated 8-kg weight loss at 6-month follow-up compared to no diet (Johnston et al., 2014). At 12-month follow-up, approximately 1 to 2 kg of this loss was regained. Small statistical differences existed among several of the diets, but it was likely unimportant in people who want to lose weight. These results support the idea that most low-calorie diets lead to clinically important weight loss if the diet is followed (Johnston et al., 2014). The “best” diet is the one the patient will adhere to. Table 15.2 summaries the 15 evidence-based diets associated with weight loss if a reduction in calorie intake is achieved (Jensen et al., 2014). A comparison of various weight loss plans and sample menus appears in Table 15.3.

Low-Fat Approach

The low-fat diet craze began during the 1990s with the hope it would ensure weight loss and improve cardiometabolic risk factors such as serum cholesterol and triglycerides. Because fat has more than twice the calories as an equivalent amount of protein or carbohydrate, in theory lowering fat intake lowers total calorie intake. The percentage of calories from fat in a diet classified as low fat may be ≤20% to <30% of total calories. The Ornish diet, at ≤20% of calories from fat, is a low-fat diet approach.

Table 15.2 Evidence-Based Dietary Approaches Associated with Weight Loss if Low-Calorie Intake Is Achieved

Dietary Approach


Diet from the European Association for the Study of Diabetes Guidelines

Food group approach without formal prescribed calorie restriction

Higher protein diet

Prescribed calorie restriction of 25% protein, 30% fat, and 45% carbohydrate

Higher protein Zone-type diet

Five meals a day, each composed of 30% protein, 30% fat, and 40% carbohydrate without prescribed calorie restriction

Lacto-ovo vegetarian-style diet

Prescribed calorie restriction

Low-calorie diet

Prescribed calorie restriction

Low-carbohydrate diet

Initial carbohydrate intake of <20 g/day without prescribed calorie restriction

Low-fat vegan-style

10%-25% of calories from fat without prescribed calorie restriction

Low-fat diet

20% of calories from fat without prescribed calorie restriction

Low-glycemic load diet

With or without prescribed calorie restriction

Lower-fat, high-dairy diet

≤30% fat, four servings of dairy per day, with or without increased fiber and/or low-glycemic index foods with prescribed calorie restriction

Macronutrient-targeted diets

Prescribed calorie restriction with 15%-25% protein, 20%-40% fat, and 35%, 45%, 55%, or 65% carbohydrates

Mediterranean-style diet

Prescribed calorie restriction

Moderate-protein diet

12% protein, 30% fat, 58% carbohydrates without prescribed calorie restriction

High-glycemic load or low-glycemic load meals

Prescribed calorie restriction

The American Heart Association-style Step 1 diet

Prescribed calorie restriction of 1500-1800 cal/day with <30% fat, <10% saturated fat

* In diets without a prescribed calorie restriction, calorie deficits result from restricting or eliminating specific foods or food groups.

Source: Jensen, M., Ryan, D., Apovian, C., Ard, J., Comuzzie, A. G., Donato, K. A., … Yanovski, S. Z. (2014). 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Obesity Society. Circulation, 129, S102-S138.

Although the amount of weight loss has not been shown to be greater with low fat (<30% total calories) versus a higher fat intake (>40% total calories), the cardiometabolic outcomes are different: With moderate weight loss, low-fat diets produce a greater decrease in LDL cholesterol but are not as effective at lowering serum triglycerides or raising high-density lipoprotein (HDL) cholesterol (Jensen et al., 2014). Because of this, a low-fat diet approach may not be best suited to people with metabolic syndrome or diabetes.

Low-Carbohydrate Approach

Low-carbohydrate diets have become a popular weight loss strategy in recent years. A low-carbohydrate diet is commonly defined as being limited to no more than 20 g of carbohydrate per day without a restriction on the total calorie intake. This level of carbohydrate intake results in ketone formation, which helps dampen hunger. Carbohydrate content is liberalized to 50 g/day after desired weight is achieved. An example of a low-carbohydrate diet is the Atkins Diet.

As stated earlier, over 12 months or longer, the amount of weight loss from a low-carbohydrate diet is not different than that achieved by a calorie-restricted, low-fat diet (Jensen et al., 2014). However, not all researchers agree. A study by Bazzano et al. (2014) found that at 12 months follow-up, participants on the low-carbohydrate diet had greater decreases in weight and fat mass. In addition, the low-carbohydrate diet resulted in a greater decrease in triglyceride levels and a greater increase in HDL level than those on the low-fat diet.

High-Protein Approach

High-protein diets provide 25% to 30% of calories from protein without defined proportions of carbohydrate and fat. For weight loss, high-protein diets must also restrict calories. Weight loss
resulting from high-protein diets (25% of calories) is the same as that from a typical protein diet (15% of calories) when the diets provide the same number of total calories (Jensen et al., 2014). High-protein weight loss diets do not result in better cardiometabolic outcomes than normal protein weight loss diets.

Table 15.3 A Comparison of Weight Loss Diet Plans and Sample Menus

Low Fat (20% of total calories)

Balanced (Moderate Fat/Moderate Protein)

Low Carbohydrate (20 g/day)

Approximate composition of sample plans and menus

Total calories
















Intake patterns

Total servings from each group per day





Nonstarchy vegetables








Milk or yogurt

3 fat-free

2 fat-free


Protein foods

12 oz lean protein

5 oz lean protein

16 oz medium fat protein





Sample menu


½ cup orange juice

¾ cup scrambled egg beaters

1 slice whole wheat toast

1 tsp butter

½ cup orange juice

1 oz shredded wheat

2 slices whole wheat toast

1 cup skim milk

2 tsp butter

½ cup orange juice

4 scrambled eggs cooked in 2 tsp butter

1 oz pork sausage


2/3 cup plain yogurt with ¾ cup blueberries


Salad greens topped with

2 cups (total) of raw vegetables (carrots, cucumber, onions, mushrooms, tomatoes, and peppers)

4 oz grilled chicken breast

Fat-free dressing

5 whole wheat baked crackers

1 ¼ cup diced watermelon

1 cup fat-free milk

2 slices whole wheat bread

2 oz deli turkey

1 tsp mayonnaise

1 cup salad made with greens, carrots, onions, and mushrooms

1 tbsp Italian dressing

6 oz grilled hamburger (without bun) topped with lettuce, ketchup, and mustard


1 small apple

20 peanuts (counts as 2 fats)


5 oz baked haddock

½ cup steamed broccoli

½ cup baked sweet potato

1 tbsp light lower fat margarine spread

½ cup fat-free, sugar-free pudding

3 oz baked haddock

1/3 cup brown rice

½ cup steamed broccoli

1 tsp butter

1 ¼ cup strawberries

5 oz fried haddock

½ cup steamed broccoli

1 tsp butter


3 cups no-fat-added popcorn

1 oz whole wheat crackers

Dietary Pattern Approach

Pattern-based approaches, such as the Mediterranean diet, Dietary Approaches to Stop Hypertension (DASH) diet, and vegan diet, generally lower calorie intake and result in at least a 3% decrease in body weight (Jensen et al., 2014). With these approaches, calorie intake is either reduced because a restricted calorie level is specified (e.g., a 1500-calorie Mediterranean or 1800-calorie DASH diet) or because specific foods and/or food groups are eliminated or restricted (e.g., vegan diet).

Dietary pattern approaches emphasize the overall diet by providing guidance on the types of food to consume rather than prescribing specific levels of macronutrients or calories. This approach may not produce greater weight loss than other approaches but tends to result in improved overall diet quality due to the emphasis on foods that are commonly underconsumed, such as fruits and vegetables.

Meal Replacement Approach

Consuming liquid meal replacements or prepackaged foods is one approach that may promote more weight loss than standard low-calorie diets and behavior counseling (Rock et al., 2016). Prepacked foods overcome several barriers to dietary adherence, including portion control, convenience, and reduced decision making. Commercial diet programs, such as Jenny Craig and Nutrisystem, feature one to two meals per day of vitamin- and mineral-fortified, low-calorie “meals,” which may be in the form of a shake, frozen entrée, or meal bar.

In overweight and obese women, the use of liquid and bar meal replacements is associated with greater weight loss at up to 6 months compared to a balanced low-calorie diet of conventional food (Jensen et al., 2014). Rock et al. (2016) found that incorporating portion-controlled prepackaged entrees in the context of intensive behavioral weight loss counseling promotes greater weight and fat loss than a standard self-selected diet with comparable meal satisfaction. Longterm studies are needed to determine how meal replacements impact weight loss maintenance.

Very-Low-Calorie Diet

Very-low-calorie diets (VLCDs) provide less than 800 cal/day, usually in the form of a liquid shake that is enriched with high biologic value protein and 100% of the Daily Value for micronutrients. Initial weight loss is quick and substantial, but VLCDs are associated with gallstones and sudden death and greater weight regain compared with weight loss achieved through a more moderate calorie restriction (Hemmingsson et al., 2012). A meta-analysis of randomized controlled trials shows anti-obesity drugs and meal replacements are the most effective strategies for maintaining weight loss maintenance after a VLCD (Johansson, Neovius, & Hemmingsson, 2014).

VLCDs should be used only in limited circumstances in a medical care setting with the provision of medical supervision and high-intensity lifestyle intervention (Jensen et al., 2014). VLCDs are often used prior to bariatric surgery to reduce overall surgical risk in people with severe obesity (Faria, Faria, de Almeida Cardeal, & Ito, 2015). They have also been shown to be safe, well tolerated, and effective in reducing preoperative weight and operative time when used 2 weeks prior to elective laparoscopic cholecystectomy in obese patients (Burnand, Lahiri, Burr, Jansen van Rensburg, & Lewis, 2016).

Eating Strategies

As previously stated, any number of dietary approaches will result in weight loss as long as a calorie deficit is achieved. Eating strategies frequently used to implement dietary approaches are featured in the following sections.

Portion Control

The increasing size of portions observed in the United States over the last few decades is one factor that promotes higher calorie intake and likely contributes to the increase in obesity prevalence over this time period (Piernas & Popkin, 2011). Evidence from randomized controlled trials supports portion control as a weight loss approach (Raynor & Champagne, 2016). Providing clients with common household equivalents to estimate portion sizes is a useful tool. Proportioned 100-calorie packages and smaller dinner plates, serving utensils, and glassware may also help “right size” portions.

Eliminating Sugar-Sweetened Beverages

It has been proposed that “small changes” in intake that result in a daily decrease in calorie intake by 100 to 200 calories may be a useful strategy for promoting weight management (Hills, Byrne, Lindstrom, & Hill, 2013). If reducing or eliminating sugar-sweetened beverage (SSB) intake does not result in a compensatory increase in calories from other sources, this approach should promote weight loss. A randomized controlled trial found that replacing SSB with water or artificially sweetened beverages leads to a 2% to 2.5% weight loss over a 6-month period (Tate et al., 2012).

Eating Frequency

A common belief is that regular, frequent meals and snacks may help control hunger and thereby promote weight management. The few randomized controlled trials that have examined the impact of eating frequency on weight loss have not found that high eating frequency leads to greater weight loss (Kulovitz et al., 2014).


Another commonly held belief is that eating breakfast helps achieve and maintain healthy weight. Observational evidence suggests an association between breakfast and body weight and weight loss, but evidence to support this idea is lacking (Dhurandhar et al., 2014). Only three randomized controlled trials, all of short duration, examined the impact of eating breakfast on weight loss, and none found that breakfast promotes greater weight loss (Raynor & Champagne, 2016).

Physical Activity

It is clear that reducing calorie intake is more likely to result in clinically significant weight loss compared to increasing physical activity (Swift, Johannsen, Lavie, Earnest, & Church, 2014). However, the combination of a lower calorie diet with increasing physical activity produces greater weight loss over 12 months than interventions based on diet or physical activity alone (Johns, Hartmann-Boyce, Jebb, & Aveyard, 2014). Increasing activity during weight loss helps preserve or increase lean body mass, which favorably impacts metabolic rate. Other benefits of high levels of physical activity and cardiorespiratory fitness are lowered risks of cardiovascular disease, type 2 diabetes, and all-cause mortality (Swift et al., 2013). High cardiovascular fitness level is associated with greater survival in all BMI categories (McAuley, Kokkinos, Oliveira, Emerson, & Myers, 2010).

Research has consistently demonstrated that a high level of physical activity is crucial for maintaining weight loss (Donnelly et al., 2009). High calorie expenditure allows a higher calorie intake to be consumed while still achieving calorie balance.

Regardless of weight loss goals, increasing physical activity should be an integral part of any obesity treatment plan. Current physical activity guidelines recommend the following (Donnelly et al., 2009):

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Nov 8, 2018 | Posted by in NURSING | Comments Off on Nutrition for Obesity and Eating Disorders

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