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The Growing Problem of Obesity
Len Kravitz, Ph.D.

Introduction
Worldwide there are an estimated one billion obese (body mass index [BMI] equal to or greater than 30 kg/m2) persons, a phenomenon that has been increasing rapidly over the last two decades (Loos and Bouchard, 2003). In the United States, 65% of Americans are overweight (BMI equal to 25 –– 29.9 kg/m2) and of these, 31% are obese. Some contributing factors to this epidemic can be credited largely to the progression from a rural lifestyle into a highly technological urban existence, and the alluring ability of our environment to promote us to eat more and move less. Let’s face it; there weren’t many food courts to choose from a thousand years ago. Almost all countries are experiencing this spectacular increase in obesity. For instance, from 1989 to 1997 the prevalence of overweight individuals in China almost tripled in men and doubled in women (Hill et al., 2003). This review will focus on the physiological and biological mechanisms of obesity and review key areas such as energy balance, fat tissue role’s in energy metabolism, the effects of inflammation, appetite and appetite suppression, and body fat distribution. In addition, steps for the treatment of obesity will be presented as well as a brief summary examining future directions to consider for combating obesity.

Energy Balance Basics
Weight management is impacted fundamentally by energy balance: energy input via foods taken in versus energy expenditure via physical activity. Thus, for overweight and obesity to develop, the energy balance is disrupted when food intake over-matches the body’s energy output in physical activity. Our genome has evolved from times of neediness for food and shelter. Food was only periodically accessible and famine was constantly a threat to sustenance (Loos and Bouchard, 2003). In addition, major amounts of physical exertion were necessary to obtain food or to escape a harsh living environment. Thus, the human species has evolved with a remarkable ability to biologically function with great energy efficiency by storing large amounts of excess fat intake into fat tissue. Our present sedentary, food abundant circumstances may be a by-product of our success as a society, but it clearly creates an energy imbalance in our lifestyle, leading to obesity.

Fat Tissue Regulation of Energy Metabolism and Immune Responses
Fat tissue, for the most part, has typically been perceived to be an extra layer of cushioning with few metabolic responsibilities. For years fat was viewed and described like a balloon that inflates when one eats more food and expends less calories, and deflates when there is greater physical activity and less food consumption. More recent research reveals that fat tissue (composed of adipocyte cells that specialize in fat storage) functions like other endocrine organs (glands that secrets hormones) in the body, sending signals to the brain which affect several intricate physiological mechanisms of energy expenditure regulation, insulin sensitivity, and fat and carbohydrate metabolism. A few key hormones of interest for energy metabolism regulation are leptin and adiponectin, while a host of other hormones are involved in immune reactions of the body.

Leptin
Although leptin has been elegantly described by Jenna A. Bell-Wilson (The Lowdown on Leptin, IDEA Health and Fitness Source, 2003), this article will highlight some of its key physiological roles and complexities in energy balance. Leptin, which resides in all fat cells, communicates directly with the hypothalamus in the brain, providing information about how much energy is currently stored in the body’s fat cells. Leptin functions in what is referred to in biology as a negative feedback loop. For example, when fat cells decrease in size, leptin decreases, sending a message to the hypothalamus to direct the body to eat more. Contrariwise, when fat cells increase in size, leptin increases and the message sent to the hypothalamus is to instruct the body to eat less. However, it appears that the primary biological role of leptin is to facilitate energy intake when energy storage is low, as opposed to slowing down over-consumption (which may contribute to obesity) when energy storage is high (Havel 2002). Leptin production is chiefly regulated by insulin-induced changes in fat cell metabolism. Havel notes that the consumption of fat (and fructose) actually results in lower circulating leptin levels, which can lead to overeating and weight gain. Thus diet, and more specifically intake of foods high in fat and fructose may have a direct connection with weight gain. In addition, with the discovery of leptin, initial hopes were that it would become the ‘anti-fat’ miracle drug. However, swallowing leptin as a pill has not shown to provide any beneficial help for the overweight, possibly because the digestion process changes this protein’s structure and function.

Adiponectin
Another specialized hormone secreted by fat is adiponectin, which is referred to as ‘the good-guy’ hormone (Liebman, 2004). Adiponectin helps insulin in sending blood glucose into the body’s cells for storage or use as fuel, thus increasing the cells’ insulin sensitivity or glucose metabolism (Havel, 2002). It also helps decreases blood levels of triglycerides by working with insulin to stimulate fat breakdown. If a person has a lot of body fat, then they typically will have lower levels of adioponectin. It is predictably low in all overweight individuals and especially low in persons with insulin resistance (a cellular condition where glucose is inhibited in entering the muscle cell). However, as of yet, science has not begun attempts of administering adiponectin as a pharmacological agent for weight loss.

Immune Hormones
It is now known that fat tissue produces a number of immune system hormones such as tumor necrosis factor-alpha, interleukin-6, plasminogen activator inhibitor 1, angiotensin II and other cytokines (Havel 2002). Cytokines, which are hormone-like proteins, function largely as inflammatory proteins, reacting to areas of infection or injury in the body. However, persons with excess fat appear to have an over-reaction of the release of these inflammatory proteins. It has been proposed that this is caused by the low oxygen content in the clusters of adipocytes, which are somewhat distant from the tissue vascular supply (Trayhurn, 2005). This topic of inflammation is one of the most critical in obesity biology. Both obesity and diabetes are associated with chronic low-grade inflammation (Trayhurn, 2005). As well, inflammation is now understood to be a key facet in heart disease. The release of these inflammatory proteins may inflame arterial plaque, causing the plaque to rupture, and thus leading to a heart attack or stroke (Liebman, 2004). Trayhurn notes that with weight loss, there is a corresponding decrease in the circulating levels of these inflammatory proteins. As well, it appears that these fat tissue derived inflammatory hormones may play a causal role in the development of insulin resistance (Trayhurn).

The Gut Hormones: How You Know its Time to Eat and When You’ve Eaten Enough
Grehlin
Another component of the energy reserve regulation in the body involves some of the hormones that control feeding and appetite, which are located in the gastrointestinal tract, including the pancreas. Specific hunger signals trigger eating, while satiety messages inhibit appetite. These distinct hormones are often referred to as the ‘gut hormones’, of which grehlin has been proposed to be particularly associated with obesity (Druce et al., 2005). Grehlin, secreted by the stomach, plays a major role in appetite regulation. It is referred to as the ‘hormone of hunger” and has an opposite association to body mass index (Druce et al., 2005).
Working in a positive feedback loop, high levels of grehlin during a fasted state promote increased food intake, while lower levels of grehlin are observed after eating a meal. However, when obese individuals lose weight, this often results in an elevation of grehlin, also promoting food intake, and thus may be a physiological reason there is difficulty in maintaining the new found weight with dieters. In addition, it appears that food does not suppress grehlin levels in obese individuals, again contributing to overeating.


Peptide YY
When your body feels you have eaten enough, the hormone peptide YY (and other satiety hormones) is released from the intestines. It is particularly stimulated by lipids and carbohydrates (Druce et al., 2004). This gut hormone is proposed to work with the central nervous system to regulate the cessation of appetite as you eat. Thus, when released it provides an awareness of satiety and fullness (Druce et al. 2004).

Fat Cells Behaving Badly
It is well-established that fat deposition is highly linked to a person’s health. Fat deposited in the hips and thighs, referred to as gynoid fat appears to be quite benign and metabolically inactive. Contrariwise, fat around the internal organs of the abdomen (the trunk area) is referred to as android or visceral fat. Visceral fat has the highest correlation to high blood pressure, diabetes and high blood triglycerides. It is much more metabolically active, producing more of the inflammatory proteins. It is interesting to observe that with exercise, it is the visceral fat that is often the first to disappear. The distribution of fat depots on the body is considered to be predominantly genetically determined.

Fitness professionals can utilize waist circumference measurement to establish health risk. The waist measurement is made at the narrowest part of the torso between the ribs and iliac crest. With waist circumference, the National Cholesterol Education Program recommends using a waist circumference of >88cm (or >35 inches) for women and >100 (or >39 inches) cm for men, to evaluate obesity as a risk factor to metabolic diseases and coronary heart disease (Heyward, 2002).


The Treatment of Obesity
It is powerful to recognize that small changes in weight result in consequential health benefits. Studies show that a 5-10% loss of initial body weight is associated with meaningful improvements in cholesterol levels, hypertension and glucose metabolism (Fabricatore and Wadden, 2003). In fact, Fabricatore and Wadden note that the recent Diabetes Prevention Program study showed that a 4-year lifestyle intervention of physical activity and diet designed to induce a loss of 7% in body weight resulted in experimental subjects having a 58% lowered risk of developing type 2 diabetes, as compared to a control group. And, this preventive effect was seen to hold for members of all racial, ethnic and genders in this 3,200 subject study. Since obesity and type 2 diabetes health consequences seem to parallel each other closely, Fabricaore and Wadden have summarized the guidelines from the National Heart, Lung, and Blood Institute and the North American Association for the Study of Obesity and suggest that the three lifestyle modification components of a successful obesity treatment program include dietary intervention, behavioral therapy and physical activity.

Lifestyle Modification––This Change is for the Long Journey
Central to lifestyle modification is the understanding that changes being made represent a change in the way one lives their life. All too often, some individuals view a weight loss programs as a discrete period of time where a person goes on a diet, takes classes in group X, or secures a personal trainer for a period of time to get in shape. As well, others will attempt diet strategies with very unrealistic expectations for weight loss, and give up when these hopes are not met. Encouragement and education needs to be stressed that lifestyle modifications are being introduced as a means to establish a new way of life for the client, and not just a temporary quick fix for some loss of weight. Fitness professionals and personal trainers are encouraged to emphasize the overall health benefits of lifestyle modifications as opposed to allowing students and clients to dwell on issues of personal appearance.

Dietary Intervention
Over the last 5 decades there has been a remarkable increase in the various types of diets. Many clients will have tried, with no sustained success, two or more of these fad diets by the time the fitness professional begin to work with the student. In essence, the goal of the weight loss dietary intervention is to keep the dietary content nutritionally correct for health concerns, while introducing some doable ways of reducing calorie intake. As acknowledged earlier, modern society has influenced our food consumption so dramatically that attaining this goal can be easily sabotaged. Fabricaore and Wadden (2003) also note that obese individuals tend to underestimate how much they eat by approximately 30 – 50%. Thus, concern for accurate self-monitoring is central for life long-term success of the dietary intervention. Evidence suggests that low- and moderate-fat, calorie restricted diets promote weight loss and are nutritionally sound (Boucher, Shafer, and Chafffin, 2001). Boucher et al. add that the substantiation is lacking for high-protein, high-fat, low-carbohydrate weight loss approaches. According to the Position Statement on the Appropriate Intervention Strategies for Weight Loss and Prevention of Weight Regain for Adults by ACSM (Jackicic et al., 2001), the absolute dietary energy intake should be adjusted based on the body to elicit an energy deficit of 500-1000 kcals per day. In addition, ACSM recommends reducing dietary fat intake to < 30% of total energy intake. Therefore, with this deficit, a minimum weight loss of 1 to 2 lbs per week would be realistic.

Behavioral Therapy
The behavioral approaches to weight loss are quite vast. Costain and Croker (2005) summarize that the behavioral therapy evidence suggests the following techniques may be incorporated to help clients attain long-term weight control.
1) Proper assessment of the readiness to change of clients
2) Teaching accurate self-monitoring of food consumption
3) Realistic goal setting
4) Dietary change
5) Increase physical activity
6) Stimulus control: This is learning how to avoid triggers such as the sight of food and wanting to eat, or dealing with cravings for food.
7) Cognitive restructuring: This behavioral technique involves learning how to replace unhealthy or negative thoughts and “self-talk” about weight loss with positive affirmations.
8) Relapse management: Relapse management education attempts to provide client awareness that lapses and relapses are a normal part of behavior change. This strategy helps to relieve the stress of ‘being a diet failure’ some individuals experience when they miss an exercise session or overindulge in a meal.
9) Establish ongoing support: Ongoing support involves creative communication techniques such as email, phone, and websites that provide maintenance support to clients in an effort to sustain the lifestyle changes that have been made.


Physical Activity
Although there are different physical activity and exercise approaches to weight control that are evidence-based and highly praised, such as the 10,000 steps a day model or the >2000 kilocalories per week target goal, the ‘accumulated time’ approach will be highlighted here for designing weight management programs. The accumulated time approach addresses the fact that energy expenditure in weight loss is actually a cumulative phenomenon, including both low-intensity activities of daily life, such as stair climbing and housecleaning, and more vigorous exercise like swimming, elliptical training and cycling. For weight management goals in overweight and obese persons, the evidence suggests that gradually progressing to 60 minutes per day of accumulated exercise is recommended. There appears to be an optimal dose from approximately &Mac179; 200 minutes/week up to &Mac179; 280 minutes/week (Jackicic, and Gallagher, 2003). Jackicic and Gallagher add that these greater weekly volumes of exercise tend to lead to less food consumption in individuals, thus the exercise and the decreased food consumption facilitates weight loss goals. The ACSM position stand for weight loss and prevention of weight regain recommends progressing to 200-300 minutes of accumulated exercise per week. It is important to note that although resistance exercises are highly recommended for enhanced muscular strength, muscular endurance, bodily function and a host of other health benefits, it is the cardiovascular exercise that elicits the needed energy expenditure deficits for weight loss and prevention of weight regain (Jackicic et al., 2001). The data indicate that a moderate intensity of exercise is the preferred level of exertion. This is approximately 60-70% of maximal oxygen capacity and a 11-13 ratings on the perceived exertion scale (6 to 20 unit scale) (Jackicic, and Gallagher, 2003).

The Obesity Alarm: Is Help on Its Way?
On a weekly basis we read or hear new alarms about the increasing incidence and the possible associations of obesity to health diseases such as diabetes, heart disease and hypertension. However, sound intervention strategies to combat obesity are quickly diffused with trendy diets, quick weight loss schemes and new diet books not based upon solid research. From the basic energy balance perspective, obesity may be considered a breakdown in our biological regulatory system in balancing the physical activity we perform to the food we eat. Although this article clearly shows some possible flaws in some of our physiological mechanisms involved with energy balance, appetite and insulin resistance, the influence of our changing and ‘toxic’ environment may be the underlying focus that needs to be our center of attention. It has taken several decades for our obesity epidemic to manifest itself. With the appropriate interventions, will it take this long to reverse? Research is quite extensive in trying to identify the link of certain genes to obesity as well as new drugs for treatment for obesity. With 65% of our population overweight and or obese, would it be conceivable to think that we could (or would) put that many of our population on a drug treatment, if it were available? The obesity alarm has sounded, but we have yet to respond in any organized national strategy. What factors in our environment can be changed to encourage us to move more and eat less (and make healthy food options)? Just as the fitness industry has evolved tremendously in the last few decades to bring exercise techniques and programs to new levels of excellence, maybe one of our new directions will be to develop and introduce some viable national strategies to combat weight gain. The challenge is in front of us and fairly noted, there are numerous colleagues in the field confronting this problem. Resolving the obesity epidemic may very well include the combined talents of the dedicated leaders in the fitness industry working with researchers, clinicians, physicians and public health advocates to create not one, but several innovative approaches and initiatives to deal with this health pandemic.

References
Boucher, J.L,, Shafer, K.J., and Chafffin, J.A. (2001). Weight loss, diets, and supplements: Does anything work? Diabetes Spectrum, Vol. 14, No. 3, pp 169-175.
Costain, L. and Croker, H. (2005). Helping individuals to help themselves. Proceedings of the Nutrition Society, Vol. 64, pp 89-96.
Druce, M.R., Small, C.J., Bloom, S.R. (2005). Minireview: Gut peptides regulating satiety. Endocrinology, Vol. 145, No. 6, 2660-2665.
Fabricatore, A.N., and Wadden, T.A. (2003). Treatment of obesity. Clinical Diabetes, Vol. 21, No. 2, pp 67-72.
Havel, P.J. (2002). Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin. Current Opinion in Lipidology, 2002, Vol. 13, 51-59.
Heyward, V. (2002). Advanced Fitness Assessment and Exercise Prescription (4th Edition). Human Kinetics.
Hill, J.O., Wyatt, H.R., Reed, G.W., and Peters, J.C. (2003). Obesity and the environment: Where do we go from here? Science. Vol. 299, 853-855.
Jakicic, J.M., Clark, K., Coleman, E., Donnelly, J.E., Foret, J., Melanson, E., Volek, J., and Volpe, S.L. (2001). Appropriate Intervention Strategies for Weight Loss and Prevention of Weight Regain for Adults. Medicine & Science in Sports & Exercise, Vol. 33, 2145-2156.
Jackicic, J.M. and Gallagher, K.I. (2003). Exercise considerations for the sedentary, overweight adult. Exercise and Sport Sciences Reviews. Vol. 31, No. 2, pp. 91-95.
Liebman, B. (2004). Fat: More than just a lump of lard. Nutrition Action Health Letter, Vol. 31, No. 8, pp. 1, 3-6.
Loos, R.J.F. and Bouchard, C. (2003). Obesity––is it a genetic disorder? Journal of Internal Medicine. Vol. 254, 401-425.
Trayhurn, Paul. (2005). The biology of obesity. Proceedings of the Nutrition Society.Vol. 64, pp. 31-38.
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