Obesity and the Metabolic Syndrome
I. Introduction
In industrialized nations, the prevalence of obesity has reached epidemic proportions. It is associated with increased morbidity and mortality and is the leading cause of preventable death in the United States.
II. Definition
Obesity refers to an excess of body fat.
A.
In healthy individuals, body fat accounts for approximately 25% of body weight in women and 18% in men.
B.
Overweight refers to weight above some reference norm, typically standards derived from actuarial or epidemiological data. In most cases, increasing weight reflects increasing obesity.
C.
Body mass index (BMI) is calculated by dividing weight in kilograms by height in meters squared. Although there is debate about the ideal BMI, it is generally thought that a BMI of 20 to 25 kg2 represents healthy weight, a BMI of 25 to 27 kg2 is associated with somewhat elevated risk, a BMI above 27 kg/m2 represents clearly increased risk, and a BMI above 30 kg/m2 carries greatly increased risk.
III. Epidemiology
A.
In the United States, over 50% of the population is overweight (defined as a BMI of 25.0 to 29.9 kg/m2), whereas 30% are obese (defined as a BMI >30 kg/m2). Extreme obesity (BMI ≥40 kg/m2) is found in about 3% of men and 7% of women.
B.
The prevalence of obesity is highest in minority populations, particularly among non-Hispanic black women.
C.
More than one half of these individuals 40 years of age or older are obese and more than 80% are overweight.
D.
The prevalence of overweight and obesity in children and adolescents in the United States has also increased substantially. About 18% of adolescents and about 10% of 2- to 5-year-olds are overweight.
IV. Etiology
Persons accumulate fat by eating more calories than are expended as energy, thus intake of energy exceeds its dissipation. If fat is to be removed from the body, fewer calories must be put in or more calories must be taken out than are put in. An error of no more than 10% in either intake or output would lead to a 30-pound change in body weight in 1 year’s time.
A. Satiety.
The feeling that results when hunger is satisfied is satiety. A metabolic signal derived from food receptor cells, probably in the
hypothalamus, produce satiety. Studies have shown evidence for dysfunction in serotonin, dopamine, and norepinephrine involvement in regulating eating behavior through the hypothalamus. Other hormonal factors that may be involved include corticotrophin releasing factor, neuropeptide Y, gonadotropin-releasing hormone, and thyroid-stimulating hormone. A new substance, obestatin, made in the stomach, is a hormone that, in animal experiments, produces satiety and may have potential use as a weight-loss agent in humans.
hypothalamus, produce satiety. Studies have shown evidence for dysfunction in serotonin, dopamine, and norepinephrine involvement in regulating eating behavior through the hypothalamus. Other hormonal factors that may be involved include corticotrophin releasing factor, neuropeptide Y, gonadotropin-releasing hormone, and thyroid-stimulating hormone. A new substance, obestatin, made in the stomach, is a hormone that, in animal experiments, produces satiety and may have potential use as a weight-loss agent in humans.
Eating is also affected by cannabinoid receptors, which, when stimulated, increases appetite. Marijuana acts on that receptor, which accounts for the “munchies” associated with marijuana use. The drug rimonabant is an inverse agonist to the cannabidiol receptor, meaning that it blocks appetite. It may have clinical use.
B. Olfactory system.
The olfactory system may play a role in satiety. Experiments have shown that strong stimulation of the olfactory bulbs in the nose with food odors by use of an inhaler saturated with a particular smell produces satiety for that food. This may have implications for therapy of obesity.
V. Factors that Contribute to Obesity
A. Genetic factors.
About 80% of patients who are obese have a family history of obesity, although no specific genetic marker of obesity has been found. Studies show that identical twins raised apart can both be obese, an observation that suggests a hereditary role.
B. Developmental factors
Obesity that begins early in life is characterized by adipose tissue with an increased number of adipocytes (fat cells) of increased size. Obesity that begins in adult life, on the other hand, results solely from an increase in the size of the adipocytes. In both instances, weight reduction produces a decrease in cell size.
The distribution and amount of fat vary in individuals, and fat in different body areas has different characteristics. Fat cells around the waist, flanks, and abdomen (the so-called potbelly) are more active metabolically than those in the thighs and buttocks.
A hormone called leptin, made by fat cells, acts as a fat thermostat. When the blood level of leptin is low, more fat is consumed; when it is high, less fat is consumed.
C. Physical activity factors.
The marked decrease in physical activity in affluent societies seems to be the major factor in the rise of obesity as a public health problem. Physical inactivity restricts energy expenditure and may contribute to increased food intake. Although food intake increases with increasing energy expenditure over a wide range of energy demands, intake does not decrease proportionately when physical activity falls below a certain minimum level.
D. Brain-damage factors.
Destruction of the ventromedial hypothalamus can produce obesity in animals, but this is probably a very rare cause
of obesity in humans. There is evidence that the central nervous system, particularly in the lateral and ventromedial hypothalamic areas, adjusts to food intake in response to changing energy requirements so as to maintain fat stores at a baseline determined by a specific set point. This set point varies from one person to another and depends on height and body build.
of obesity in humans. There is evidence that the central nervous system, particularly in the lateral and ventromedial hypothalamic areas, adjusts to food intake in response to changing energy requirements so as to maintain fat stores at a baseline determined by a specific set point. This set point varies from one person to another and depends on height and body build.
E. Health factors
In only a small number of cases of obesity, the consequence is identifiable illness. Such cases include a variety of rare genetic disorders, such as Prader-Willi syndrome, as well as neuroendocrine abnormalities. Hypothalamic obesity results from damage to the ventromedial region of the hypothalamus (VMH), which has been studied extensively in laboratory animals and is a known center of appetite and weight regulation. In humans, damage to the VMH may result from trauma, surgery, malignancy, or inflammatory disease.
Some forms of depression, particularly seasonal affective disorder, are associated with weight gain. Most persons who live in seasonal climates report increases in appetite and weight during the fall and winter months, with decreases in the spring and summer. Depressed patients usually lose weight, but some gain weight (e.g., atypical depression).
F. Other factors
Clinical disorders. A variety of clinical disorders are associated with obesity. Cushing’s disease is associated with a characteristic fat distribution and moonlike face. Myxedema is associated with weight gain, although not invariably. Other neuroendocrine disorders include adiposogenital dystrophy (Fröhlich’s syndrome), which is characterized by obesity and sexual and skeletal abnormalities.
Psychotropic drugs. Long-term use of steroid medications is associated with significant weight gain, as is the use of several psychotropic agents. Patients treated for major depression, psychotic disturbances, and bipolar disorder typically gain 3 to 10 kg, with even larger gains with chronic use. This can produce the so-called metabolic syndrome discussed later.Related posts:
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