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Secondary Causes of Obesity

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Secondary Causes of Obesity REVIEW Secondary causes of obesity Jocelyne G Karam & While the rising epidemic of obesity is primarily attributed to sedentary lifestyle, poor Samy I McFarlane† dietary habits and the aging of the population, secondary causes of obesity generally go †Author for correspondence undetected and untreated. These include endocrinological disorders, such as Cushing’s State University of New York, Division of Endocrinology, syndrome, polycystic ovary syndrome, hypogonadism and hypothyroidism, as well as Diabetes and Hypertension, genetic, syndromic and drug-related obesity. We present an overview of the major Department of Medicine, disorders associated with obesity, highlighting the pathophysiologic mechanisms and Box 50 Health Science Center at Brooklyn Kings County discussing diagnostic and treatment strategies that are most helpful to practicing Hospital Center, physicians in recognizing and treating these generally underdetected and 450 Clarkson Avenue, undertreated disorders. Brooklyn, NY 11203, USA Tel.: +1 718 270 3711; Fax: +1 718 270 6358; During the past few decades, prevalence of obes- recognized by physicians and specific therapeutic Email: smcfarlane@ downstate.edu ity has dramatically increased in the Western strategies should be planned in conjunction with world, including the USA where obesity has cur- diet and exercise. rently reached epidemic proportions. A compar- In this review, we provide the readers with a ison of data from two National Health and general overview of the secondary causes of obesity, Nutrition Examination Surveys (NHANES) has highlighting the pathophysiology, the clinical diag- shown that among US adults, the prevalence of nosis and the therapeutic options of each disorder. obesity increased from 15% (in the 1976–1980 Obesity is a state of excessive body weight asso- survey) to 32.9% (in the 2003–2004 survey) [1]. ciated with adverse health risks such as diabetes, Data from the 2003–2004 survey estimate that hypertension, hyperlipidemia and coronary approximately 66% of US adults are overweight artery disease. In 1997 and 1998, The WHO and or obese and 17.1% of US children and adoles- the National Heart Lung and Blood Institute of cents are also overweight [1]. This sharp increase the National Institute of Health advocated the in the prevalence of obesity correlates with a pro- use of a specific BMI threshold of 30 to diagnose portional increase in obesity-associated comor- obesity and 25 to diagnose overweight [5,6]. The bidities, such as Type 2 diabetes, hypertension BMI is calculated by dividing a person’s weight in and cardiovascular disease (CVD) [2], and a sig- kg by height in m2. nificant rise in healthcare costs related to Furthermore, it appears that fat distribution obesity [3]. The economic burden of obesity in plays a key role in determining the associated the USA was estimated to be US$117 billion in health risks. Central or android obesity is associ- 1998, with obesity accounting for approximately ated with greater risk of adverse health effects 5.7% of the US National Health expenditure [3]. than lower-body or gynecoid obesity [7]. There- The relatively rapid and dramatic increase in fore, waist circumference measurement has been the prevalence of obesity has been largely attrib- a useful clinical tool in risk stratification of over- uted to a changing lifestyle that promotes weight in moderately obese patients increased caloric intake and reduced physical (BMI 25–35). A waist circumference greater than activity. A high-fat diet, excessive consumption 40 inches (102 cm) in men and 35 inches (88 cm) of sugar-sweetened beverages and increased fast in women is linked to higher CVD risks and food intake might all contribute to the continuing should lead to more aggressive weight reduction increase in prevalence of obesity [4]. strategies in overweight patients. Although most cases of weight gain are indeed Interpretation of BMI values may also change Keywords: endocrinologic related to increased caloric intake and sedentary with ethnicities. For example, android obesity obesity, genetic obesity, lifestyle, obesity can also be secondary to known leading to increased cardiovascular risk is clearly obesity, overweight, secondary obesity, syndromic obesity and possibly treatable neuroendocrine or genetic present in Asian individuals with lower BMI disorders that affect appetite, metabolism, (not in overweight and obesity categories), sug- part of energy balance and fat distribution (Box 1). gesting a lower BMI cut-off for definition of Although rare, these conditions should be obesity in this population [8]. 10.2217/14750708.4.5.641 © 2007 Future Medicine Ltd ISSN 1475-0708 Therapy (2007) 4(5), 641–650 641 REVIEW – Karam & McFarlane Box 1. Endocrine and genetic causes At a physiological level, the principal gluco- of obesity. corticoid, cortisol, contributes significantly to the regulation of protein, carbohydrate, lipid and Endocrine causes nucleic acid, enhancing the production of blood • Hypothyroidism glucose by antagonizing the secretion and action • Cushing disease of insulin, increasing peripheral protein break- • Polycystic ovaries down and enhancing the activation of lipo- • Growth hormone deficiency protein lipase in adipocytes, which in turn • Hypothalamic obesity increases fat accumulation [9]. Glucocorticoids • Hypogonadism are also required for the differentiation of adi- • Insulinoma pose stromal cells to mature adipocytes. The • Pseudohypoparathyroidism action of cortisol on adipose tissue varies in dif- Genetic causes ferent parts of the body, decreasing peripheral Monogenic obesity: adipose tissue mass and expanding abdominal and interscapular fat. • Leptin and leptin receptor deficiency Furthermore, the highly expressed • POMC deficiency β • Melanocortin Receptor 4 deficiency 11 -hydroxysteroid-dehydrogenase-1 in omen- • Prohormone convertase deficiency tal adipose tissue is believed to enhance the local • BDNF and TrkB insufficiency effect of cortisol on adipose tissue by converting • SIM 1 insufficiency inactive cortisone to active cortisol [10]. Hypercortisolism in Cushing’s syndrome Syndromic obesity: results in central obesity, with fat accumulation • Prader–Willi syndrome in the face (moon face), neck, dorsocervical area • Bardet–Biedl syndromes (buffalo hump), supraclavicular area (fat pads), • Beckwith–Wiedemann syndrome retroorbital space (exophthalmos), trunk and • Alstrom–Hallgren syndrome abdomen, with sparing or wasting of the • Carpenter syndrome extremities, characterizing the typical central fat • Cohen syndrome distribution of the syndrome [11]. In addition to the gradual obesity that develops in 80–90% of Pathophysiology of obesity individuals, patients with Cushing’s syndrome The development of obesity requires a period of may present with hypertension, impaired glu- positive energy balance where energy intake cose tolerance, proximal muscle weakness, thin- exceeds energy expenditure, manifesting clearly in ning of the skin, increased tendency to bruise, obese individuals with high caloric intake and sed- red or violacious striae, hypokalemia, oste- entary lifestyle. Energy expenditure is divided into oporosis with vertebral compression fracture or basal metabolic rate, energy expended in activity aseptic necrosis and menstrual irregularities and thermic effect of food. Moreover, to maintain with signs of androgen excess in women. energy balance, the organism should be able to Hyperpigmentation in this context reflects sig- assess its own energy stores, the caloric content of nificantly elevated ACTH levels, favoring the the diet and the current balance status of the body, etiologic diagnosis of ectopic ACTH secretion, and be able to adjust hormone levels, energy and to a lesser degree Cushing’s disease. Chil- expenditure and consumption behaviors accord- dren with Cushing’s syndrome characteristically ingly. A defect at any energy balance level may present with abnormal weight gain and poor result in positive balance and obesity, as seen in linear growth [12]. most cases of secondary obesity (Figure 1). A widely used screening test for Cushing’s syn- drome is the overnight 1 mg low-dose dexameth- Endocrine causes of obesity asone suppression test where at 8 am the cortisol Cushing’s syndrome value is expected to be lower than 2 µg/dl Cushing’s syndrome results from prolonged (55 nmol/l) in normal subjects who had received exposure to glucocorticoid excess deriving from dexamethasone 1 mg at 11 pm. However, owing four potential sources: pituitary tumors (Cush- to relatively high rates of false-negative and false- ing’s disease), adrenal tumors, ectopic adreno- positive results, a 24 h urine-free cortisol test is corticotropic hormone (ACTH) secretion and, considered a more accurate diagnostic approach, most commonly, exogenous glucocorticoids, followed if necessary, by late-evening plasma or including oral, topical or inhaled steroids. salivary cortisol level [13,14]. Acute or chronic 642 Therapy (2007) 4(5) futurefuture sciencescience groupgroup Secondary causes of obesity – REVIEW Figure 1. Endocrinologic etiologies of obesity and related pathophysiology. Hypothyroidism Growth hormone Cushing Energy expenditure Glycosaminoglycans deficiency Fat tissue modulation Fat deposition Polycystic ovary Hypogonadism syndrome Fat redistribution Energy balance disruption polyphagia Lipolysis GH Hypothalamic Energy intake PHP obesity Insulinoma PHP: Pseudohypopparathryoidism. illnesses, depression and alcohol abuse can result expenditure [18]. Thyroid
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