SlimLine Setpoint Theory

Transcription

1 According to the setpoint theory, there is a control system built into every person dictating how much fat he or she should carry - a kind of thermostat for body fat. Some individuals have a high setting, others have a low one. According to this theory, body fat percentage and body weight are matters of internal controls that are set differently in different people. Everyone knows a person can lose large amounts of weight in a relatively short time by simply not eating. Unfortunately, at some point the person will get extremely hungry and start eating again. Eventually, the lost weight will return. Some argue that the reason most people regain the weight lost by dieting lies in a genetically determined setpoint for body weight (or body fat) that usually differs from what the dieter would like it to be. The setpoint theory was originally developed in 1982 by Bennett and Gurin to explain why repeated dieting is unsuccessful in producing long-term change in body weight or shape. Going on a weight-loss diet is an attempt to overpower the setpoint, and the set point is a seemingly tireless opponent to the dieter. Modern research has found that whena person s weight drops by 10%, the metabolic rate drops approximately 15% to compensate. As a result, fewer calories are burned each day unless the individual increases his or her daily caloric expenditure by exercising. The proponents of setpoint theory maintain that all persons fat or thin have a well regulated internal control mechanism located deep within the lateral hypothalamus that maintains a preset level of body weight (and/or body fat) within a tight range. In a practical sense, this setpoint represents a person s body weight when he or she is not counting calories. Each time the body weight decreases below one s pre-established setpoint, internal adjustments that affect food intake and regulatory thermogenesis resist the change and conserve and/or replenish body fat. The hypothalamus (shown below) lies just beneath the thalamus in the middle of the brain. The hypothalamus houses numerous masses of nuclei which is interconnected to various places along the central nervous system. The hypothalamus is quite small yet is still able to perform vital functions which are responsible for the regulation (both directly and indirectly) of visceral organs. The hypothalalmus is also responsible for emotional and instinctual reactive processes. By accelerating and decelerating specific visceral functions, the hypothalamus is considered an autonomic nervous center. Part of its general function is the release of numerous varying hormones, including two which are released from the posterior pituitary. One of the regulation responsibilities of the hypothalamus is cardiac regulation. While it does not control whether or not the cardiac muscle beats, it does command acceleration and deceleration as it related to both emotional and physical stimuli. The posterior hypothalamus sends out impulses to increase arterial blood flow, which causes heart rate acceleration. The anterior section sends out the impulses responsible for deceleration of the arterial flow. The pulses do not go straight to the cardiac muscle but rather head to the cardiovascular centers of the medulla oblongata. The hypothalamus is also responsible for body temperature regulation. There are masses of highly specialized nuclei that are housed in the anterior section of the hypothalamus which can sense changes in the body s internal temperature. The hypothalamus sends out the necessary impulses to entice the body to sweat and lower the body s temperature when the sensors determine a high blood temperature. Heat preservation tactics are encouraged by different impulses which encourage the body to shiver, constrict the cutaneous, and cease sweating. The hypothalamus is also responsible for the body s water and electrolyte balance. Within the blood, the body has specialized receptors known as osmoreceptors which can detect electrolyte imbalances as well as indications of a lack of hydration. Page 1

2 This is known as monitoring the osmotic levels within the blood. An anti-diuretic hormone can be triggered via the posterior pituitary gland when impulses from the hypothalamus are sent out. The body is then also triggered to become thirsty. Hunger is also triggered by the hypothalamus. While it is responsible for the control over gastrointestinal activity, the hypothalamus houses a feeding center, which is a specialized segment responsible for the constant monitoring of the blood glucose, fatty acids, and amino acid levels throughout the body. Hunger is a sensation that the hypothalamus triggers when the monitored blood levels are too low, and alternatively, the mid section of the hypothalamus controls the feeding center when the body has been satiated. Sensory impulses from the GI tract also determines the hypothalamus reaction to peristaltic action and the regulation of glandular secretions. The hypothalamus is able to tell the body when it has rested enough and when it requires rest. The hypothalamus communicates constantly with other various portions of the brain to determine the level of appropriate wakefulness or sleepiness, depending on the body s needs. Within the superior portion of the hypothalamus resides the sexual sensation center. Tactile receptors in the genitalia respond to the physical sensations of sexual practice. The hypothalamus then responds with the appropriate neural activity to produce sexual pleasure and orgasms. Certain sections and masses of nuclei within the hypothalamus are responsible for the emotions the human mind reacts with. Fear, anger, pain, and joy are in part due to the responses generated via the hypothalamus. Neurosecretory chemicals are responsible for the control of various endocrine functions. Impulses from the hypothalamus are sent to the anterior or posterior portions of the pituitary gland to release various hormones in response to the body s needs. Page 2

3 For example, with low calorie diets the resting metabolism slows and the individual often becomes obsessed with food. Eventually the person becomes unable to control the urge to eat, so he or she often binges and regains all the weight (or fat) that was previously lost. When the person overeats and gains body fat above his or her normal level, the body once again resists this change by increasing resting metabolism and causing the person to lose interest in food. The ideal approach to weight control would be a safe method that lowers or raises the set point rather than simply resisting it. So far no one knows for sure how to change the set point, but some theories exist. Of these, regular exercise including thermal therapy which raises heart rate and metabolic rate-- is the most promising. Studies have shown thata sustained increase in physical activity lowers the setpoint (Wilmore et al. 1999). FDA-approved antiobesity drugs may also lower a person s setpoint. Dieting, on the other hand, exerts no influence. According to the setpoint theory, the setpoint itself keeps weight fairly constant, presumably because it has more accurate information about the body s fat stores than the conscious mind can obtain. At the same time, this system pressures the conscious mind to change behavior, producing feelings of hunger or satiety. Studies show that a person s weight at the setpoint is optimal for efficient activity and a stable, optimistic mood. When the setpoint is driven too low, depression and lethargy may set in as a way of slowing the person down and reducing the number of calories expended. The setpoint, it would appear, is very good at supervising fat storage, but it cannot tell the difference between dieting and starvation. The dieter who begins a diet with a high setpoint experiences constant hunger presumably as part of her body s attempt to restore the status quo. Even dedicated dieters often find that they cannot lose as much weight as they would like. After an initial, relatively quick loss, dieters often become stuck at a plateau and then lose weight at a much slower rate, although they remain as hungry as ever. Dieting research demonstrates that the body has more than one way to defend its fat stores. Long-term caloric deprivation, in a way that is not clear, acts as a signal for the body to turn down its metabolic rate. Calories are burned more slowly, so that even a meager diet almost suffices to maintain weight. The body reacts to stringent dieting as though famine has set in. Within a day or two after semi-starvation begins, the metabolic machinery shifts to a cautious regimen designed to conserve the calories it already has on board. Because of this innate biological response, dieting becomes progressively less effective, and (as generations of dieters have observed) a plateau is reached at which further weight loss seems all but impossible. The only way to combat this plateau is to engage in regular physical exercise including thermal therapy sessions. Food Intake Related Hormones: Leptin and Ghrelin Energy intake and body weight are tightly regulated at a consistent set point by control systems in the hypothalamus. These hypothalamic circuits receive feedback from peripheral signals. Discovery of the hormone leptin, which could regulate satiety, energy expenditure, and weight gain, added complexity to these relationships. Leptin is produced by adipocytes and is thought to feed back through the hypothalamic receptors to regulate weight gain and energy expenditure. Normally, leptin blunts the urge to eat when caloric intake is sufficient to maintain ideal fat stores. Normal levels of leptin signal the hypothalamus to maintain food intake so body weight remains stable. Low levels of leptin signal the brain to increase the appetite in order to increase levels of body fat. Leptin can also elevate the metabolic rate. Ghrelin has been discovered to be the antithesis of leptin. Ghrelin is a powerful appetite-stimulating hormone secreted primarily by the stomach and duodenum. Ghrelin increases hunger through its action on hypothalamic feeding centers, and it strongly stimulates growth hormone secretion. Page 3

4 In addition, ghrelin suppresses fat utilization in adipose tissue and communicates the state of energy balance in the body to the brain. Ghrelin administration has caused weight gain in rodents and humans resulting from increased food intake and reduced fat utilization. Leptin deficiency may be a cause of obesity. However, common adult obesity is related to elevated leptin levels, possibly indicative of leptin resistance. Fasting plasma ghrelin concentrations are decreased in obesity and are negatively correlated with body mass index. These results raise the possibility that ghrelin and leptin are part of a dynamic feedback system in the regulation of body weight. Changes in plasma ghrelin and serum leptin concentrations might produce important differences in food intake and energy balance and play a significant role in the pathogenesis of obesity. Food Intake Is Improved by Repeated Thermal Therapy Sessions It has been observed that appetite loss in patients with chronic heart failure was improved by thermal therapy. The improvement of appetite loss after thermal therapy may be associated with plasma ghrelin and serum leptin concentrations. The plasma ghrelin and serum leptin concentrations, daily caloric intake, feeding behavior, and body weight and body fat have been investigated in normal-weight patients with appetite loss after 2 weeks of thermal therapy. Feeding behavior was evaluated by the presence of appetite, hunger, taste, pleasure in eating, and deliciousness. High scores indicate problems in feeding behavior. It has been found that repeated thermal therapy increased plasma ghrelin concentrations and daily caloric intake and improved feeding behavior. However, serum leptin concentrations, body weight, and body fat did not change after repeated thermal therapy sessions. These findings suggest that improvement of daily caloric intake and feeding behavior in normal-weight patients with appetite loss might be related to increased plasma ghrelin concentrations. Effects of Repeated Thermal Therapy Sessions for Obese Patients Obesity represents a global epidemic and is one of the leading causes of lifestyle-related diseases and death worldwide. Hyperphagia, weight gain, and increased adiposity occur after continuous systemic ghrelin administration in experimental animals. Ghrelin stimulates appetite and food intake potently in humans. As such, ghrelin would be an important new target for the development of treatments for obesity. In obese patients, plasma ghrelin concentrations are low and serum leptin concentrations are high. The effects of 2-week thermal therapy on plasma ghrelin and serum leptin concentrations and feeding behavior in 10 obese patients (body mass index > 30, mean age 46 ± 5 years, five men and five women) have been examined. The patients took the same meals of 1800 cal/d during this 2-week period. Plasma ghrelin and serum leptin concentrations and feeding behavior did not change after 2 weeks of thermal therapy, unlike in the normal-weight group. It is reported that plasma ghrelin falls in response to food intake in non-obese subjects but not in obese subjects. These results indicate that the responses of plasma ghrelin to food intake and repeated thermal therapy sessions are different between non-obese and obese subjects. The low plasma ghrelin concentrations in obese patients may represent a physiological adaptation to the positive energy balance associated with obesity. The lack of response to plasma ghrelin concentrations after repeated thermal therapy sessions in obese patients suggests that the sensitivity to circulating ghrelin may be decreased. Furthermore, the obese subjects, having sufficient energy stores, may have maximally suppressed ghrelin secretion, failing to respond to thermal therapy. Interestingly, the body weight and body fat in obese patients significantly decreased after 2 weeks of thermal therapy. The acceleration of appetite and abnormal feeding behavior such as Page 4

5 eating a snack between meals and overeating did not appear. These results suggest that repeated thermal therapy sessions decreased body weight and body fat in obese patients without increasing plasma ghrelin concentrations and decreasing serum leptin concentrations. It has been shown that repeated thermal therapy sessions have proven to be effective in the treatment of obesity. One case in which thermal therapy sessions proved to be very effective involved an obese patient who could not take any exercise because of severe knee joint pain resulting from osteoarthritis. The patient s body weight and body fat percentage decreased significantly after 10 weeks of regular thermal therapy sessions and a dietary limit of 1600 calories per day. The patient s body weight decreased from kg to kg and body fat percentage decreased from 46% to 35% over the 10 week period. The thermal therapy sessions also had the positive effect of improving the patient s mood including anxiety, anger, and irritability. There was no acceleration of appetite or abnormal feeding behavior during the 10 week treatment period. Page 5