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Obesity and hypertension.

Substantial evidence from epidemiological data supports a link between obesity and hypertension. However, the relationship between the two disorders is not straightforward and most likely represents an interaction of demographic, genetic, hormonal, renal, and hemodynamic factors. Age, race, and sex also modulate the strength of the association between obesity and hypertension. Hyperinsulinemia, which is characteristic of obesity, can contribute to the probability of developing hypertension by activating the sympathetic nervous system (SNS) and by causing sodium retention. The pressor effect of insulin in obesity may be further enhanced by the observation that its vasodilator action can be blunted in obese subjects. Preliminary data have shown that leptin, whose levels are increased in most obese individuals, can contribute to hypertension in obesity through its effects on insulin, SNS, and sodium excretion. The kidney may also have a role in the pathophysiology of hypertension in obesity. Abnormal renal sodium handling coupled with structural changes in the kidney of an obese patient can raise blood pressure. In addition, obesity is associated with distinct cardiovascular hemodynamic alterations and development of eccentric myocardial hypertrophy. Most of these obesity-associated abnormalities, as well as hypertension itself, can be reversed by weight loss. Furthermore, weight loss can prevent, or at least delay, the development of hypertension in patients with high-normal blood pressure. Weight reduction should be the first-line treatment in every obese hypertensive patient. However, the majority of patients will need pharmacologic intervention in conjunction with weight loss. Selection of antihypertensive agents in the overweight patient should take into account the mechanisms leading to hypertension and the metabolic abnormalities that characterize the obese patient.

Animals↗
PubMed2003

Are physicians equipped to address the obesity epidemic? Knowledge and attitudes of internal medicine residents.

BACKGROUND: To analyze whether internists are suited for their role in treating the growing numbers of obese patients, we surveyed residents about their knowledge and attitudes regarding obesity. Previous assessments have not analyzed familiarity with obesity measurement tools or the correlation between knowledge and attitudes. METHODS: We administered a survey to 87 internal medicine residents in two urban, university-based residency programs. RESULTS: Almost all respondents understood the medical consequences of obesity, but 60% did not know the minimum BMI for diagnosing obesity, 69% did not recognize waist circumference as a reasonable measure of obesity, and 39% incorrectly reported their own BMI. Although nearly all respondents agreed that treating obesity was important, only 30% reported treatment success. Forty-four percent felt qualified to treat obese patients, and 31% reported treatment to be futile. Knowledge and attitudes were not correlated. Rasch analysis of knowledge and attitude subscales showed satisfactory model fit and item reliability of at least 0.96. CONCLUSIONS: Despite solid knowledge of the comorbid conditions associated with obesity, residents have a poor grasp of the tools necessary to identify obesity. They also have negative opinions about their skills for treating obese patients. Residency training not only must improve knowledge of obesity measurement tools but also must address physicians' negative attitudes toward obesity treatment.

Adult↗
PubMed2000

Metabolic imprinting on genetically predisposed neural circuits perpetuates obesity.

There is an obesity epidemic in the industrialized world that is not simply explained by excess energy intake and decreased energy expenditure. Persistent obesity develops when genetically predisposed individuals are in a chronic state of positive energy balance. Once established, the obese body weight is avidly defended against both over- and underfeeding. Animal studies have shown that lean individuals who are genetically predisposed toward obesity have abnormalities of neural function that prime them to become obese when caloric density of the diet is raised. These neural abnormalities are gradually "corrected" as obesity becomes fully developed, suggesting that obesity is the normal state for such individuals. Thus, defense of the obese body weight may be perpetuated by the formation of new neural circuits involved in energy-homeostasis pathways that are not then easily abolished. Such neural plasticity can occur in both adult life and during nervous-system development. Early pre- and postnatal metabolic conditions (maternal diabetes, obesity, undernutrition) can lead genetically predisposed offspring to become even more obese as adults. This enhanced obesity is associated with altered brain neural circuitry, and these changes can then be passed on to subsequent generations in a feed-forward cycle of ever-increasing body weight. Thus, the metabolic perturbations associated with obesity during both brain development and adult life can produce "metabolic imprinting" on genetically predisposed neural circuits involved in energy homeostasis. Drugs that reduce body weight decrease the defended body weight and alter neural pathways involved in energy homeostasis but have no permanent effect on body weight or neural function in most individuals. Thus, early intervention in mothers, infants, children, and adults may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals.

Animals↗
PubMed2004

[Analysis of puberal development and influence of weight loss in obese adolescent girls].

OBJECTIVES: To study several aspects of puberal development in obese adolescent girls, and the influence of weight loss on these aspects. METHODS: A longitudinal retrospective study was performed of a sample of 26 adolescent girls with normal weight and 46 obese adolescent girls at the onset of puberty. The obese teenagers were further divided into two groups (normal and obese) according to their body mass index (BMI) at the end of puberty. Height, chronological and bone age, and growth velocity were evaluated in both groups. RESULTS: Of the teenagers who were obese at the onset of puberty, 63 % remained obese at the end of puberty. The obese teenagers were significantly taller than non-obese teenagers at the onset of puberty (143.2 +/- 6.96 vs 138.9 +/- 5.95 cm, respectively; p < 0.01). However, there were no differences between the two groups in final height. No differences were found between obese teenagers who lost weight and those who did not. There were no differences in chronological or bone age throughout puberal development in any of the groups. The mean growth velocity during puberty was significantly lower in obese teenagers than in non-obese teenagers (6.18 +/- 1.94 and 6.90 +/- 127 cm/year, respectively; p < 0.02). However, there were no differences between obese teenagers who lost weight and those who did not. CONCLUSIONS: Height gain in obese girls is greater in childhood but lower in adolescence. Final height is similar in both groups. Chronological age at the onset and end of puberty and bone maturation are similar in both groups. Weight loss during puberty does not modify growth pattern during this period of development.

Adolescent↗
PubMed2000

[Epidemiology of obesity].

Obesity is a well-recognized health hazard in affluent societies. The prevalence of overweight and obesity are high and still increasing consistently in industrialized countries. The body mass index (BMI) is an internationally accepted index to estimate body weight. The recent published WHO-classification of body weight allows the worldwide comparison of obesity prevalences. The WHO-MONICA study revealed different obesity prevalences in several European countries. The lowest prevalence of obesity was found in Sweden and Northern France (7-14%) whereas the highest prevalence (40%) was reported from East-European countries. The results of the DHP-survey suggest that 50% of the adult German population are overweight and 20% are obese. Data from the MONICA-study show lower prevalences for Switzerland, where 38% of the adult population are considered to have overweight and 11% are obese. By the way the prevalence of obesity is still increasing with a renewed acceleration during the last two decades. Obesity is starting to get the status of a main health problem not only in western countries but also in less developed countries of Middle- and South-America. In Germany obesity and the obesity-related morbidity and mortality caused costs of nearly 20.7 Mrd. DM in 1995. Therefore obesity is a major economic burden for the society. Like in other developed countries the costs attributable to obesity correspond to 2-8% of total health care expenditure.

Adult↗
PubMed1999

Increased early morbidity and mortality with acceptable long-term function in severely obese patients undergoing liver transplantation.

The effect of obesity on outcomes following liver transplantation remains unclear. We reviewed our experience with 302 liver transplants in 277 patients from September 1989 to September 1996 to determine the effect of body mass on outcome. Two-hundred and seventeen transplants were performed in patients with a body mass index (BMI) < 30 kg/m2, 55 in patients with a BMI of 30-34 kg/m2 (obese), and 30 in patients with a BMI > 35 kg/m2 (severely obese). Non-weight related pre-operative demographics were similar between groups with the exception of an increased frequency of cryptogenic cirrhosis among the obese and severely obese patients. Intra-operative transfusion requirements were greater for the severely obese group (16.2 +/- 3.5 units versus 9.1 +/- 0.8 units for the non-obese, p = 0.0004), though not when normalized to body weight (0.14 +/- 0.03 units/kg versus 0.13 +/- 0.01 units/kg, p > 0.05). Post-operatively, severely obese patients had a higher rate of wound infection (20 versus 4%, p = 0.0001) and death attributed to multisystem organ failure (15 versus 2%, p = 0.0001), although overall mortality prior to discharge and total complications were not different between groups. Actual 1-yr graft survival showed a negative trend in the severely obese group (67 versus 81% for non-obese, p = 0.07), but both 3-yr graft survival and patient survival were similar to non-obese patients (p = 0.12 and 0.17, respectively by the Cox-Mantel test). Liver transplantation in severely obese patients is associated with wound infection and early death from multisystem organ failure, but has similar long-term outcomes when compared to non-obese controls.

Body Mass Index↗
PubMed2000

Familial risk of overweight and obesity in the Canadian population using the WHO/NIH criteria.

OBJECTIVE: To determine the familial risk of overweight and obesity in Canada. RESEARCH METHODS AND PROCEDURES: The sample was comprised of 15,245 participants from 6377 families of the Canada Fitness Survey. The risk of overweight and obesity among spouses and first-degree relatives of individuals classified as underweight, normal weight, pre-obese, or obese (Class I and II) according to the WHO/NIH guidelines for body mass index (BMI) was determined using standardized risk ratios. RESULTS: Spouses and first-degree relatives of underweight individuals have a lower risk of overweight and obesity than the general population. On the other hand, the risk of Class I and Class II obesity (BMI 35 to 39.9 kg/m2) in relatives of Class I obese (BMI 30 to 34.9 kg/m2) individuals was 1.84 (95% CI: 1.27, 2.37) and 1.97 (95% CI: 0.67, 3.25), respectively, in spouses, and 1.44 (95% CI:1.10, 1.78) and 2.05 (95% CI: 1.37, 2.73), respectively in first-degree relatives. Further, the risk of Class II obesity in spouses and first-degree relatives of Class II obese individuals was 2.59 (95% CI: -0.91, 6.09) and 7.07 (95% CI: 1.48, 12.66) times the general population risk, respectively. DISCUSSION: There is significant familial risk of overweight and obesity in the Canadian population using the BMI as an indicator. Comparison of risks among spouses and first-degree relatives suggests that genetic factors may play a role in obesity at more extreme levels (Class II obese) more so than in moderate obesity.

Adolescent↗
PubMed2001

Childhood obesity: the health issue.

Overweight and obesity in children is epidemic in North America and internationally. Approximately 22 million children under 5 years of age are overweight across the world. In the United States, the number of overweight children and adolescents has doubled in the last two to three decades, and similar doubling rates are being observed worldwide, including in developing countries and regions where an increase in Westernization of behavioral and dietary lifestyles is evident. Comorbidities associated with obesity and overweight are similar in children as in the adult population. Elevated blood pressure, dyslipidemia, and a higher prevalence of factors associated with insulin resistance and type 2 diabetes appear as frequent comorbidities in the overweight and obese pediatric population. In some populations, type 2 diabetes is now the dominant form of diabetes in children and adolescents. Disturbingly, obesity in childhood, particularly in adolescence, is a key predictor for obesity in adulthood. Moreover, morbidity and mortality in the adult population is increased in individuals who were overweight in adolescence, even if they lose the extra weight during adulthood. Although the cause of obesity in children is similar to that of adults (i.e., more energy in vs. energy utilized), emerging data suggest associations between the influence of maternal and fetal factors during intrauterine growth and growth during the first year of life, on risk of later development of adult obesity and its comorbidities. In addition, recent data suggest that varying biological responses in different racial/ethnic groups differently contribute to overweight, obesity, and their comorbidities. Although differences in gene-nutrient interactions may contribute, the role of varying cultural and socioeconomic variables still needs to be determined to understand these disparities. Novel approaches in the prevention and treatment of childhood overweight and obesity are urgently required. With the strong evidence that a lifecycle perspective is important in obesity development and its consequences, consideration must be focused on prevention of obesity in women of child-bearing age, excessive weight gain during pregnancy, and the role of breast-feeding in reducing later obesity in children and adults. Consideration must be given to family behavior patterns, diet after weaning, and the use of new methods of information dissemination to help reduce the impact of childhood obesity worldwide.

Adolescent↗
PubMed2006

Prevalence of obesity in elementary schoolchildren living in Northeast Attica, Greece.

OBJECTIVE: To assess the prevalence of obesity and obesity trend in schoolchildren living in Northeast Attica, Greece. RESEARCH METHODS AND PROCEDURES: Mean (standard deviation) and median weight and BMI were calculated in 4131 (2054 boys and 2077 girls) 6- to 11-year-old Greek schoolchildren living in Northeast Attica between November 2003 and April 2004. Two hundred thirty-six (95 boys, 141 girls) immigrant children also participated in the study. The secular trend for obesity was determined comparing our data with those of a similar study performed in 1994. RESULTS: Of boys, 27.8% were overweight, and 12.3% were obese. For girls, the corresponding values were 26.5% for overweight and 9.9% for obesity. There was an increase in the prevalence of overweight and obesity in the last 10 years in both sexes. For boys, overweight increased by 4.2% and obesity by 2.9%, whereas, for girls, overweight increased by 3.8% and obesity by 1.6%. Overweight and obesity were less prevalent in the immigrant children compared with their Greek peers. For immigrant boys, overweight was 15.9% and obesity was 7.9%, and for immigrant girls, overweight was 15.2% and obesity was 8.7%. DISCUSSION: Greek schoolchildren living in Northeast Attica present a high prevalence of overweight and obesity and a positive secular change in the prevalence of obesity.

Body Mass Index↗
PubMed2006

A comparison of weight histories in women with class III vs. class I-II obesity.

OBJECTIVE: To describe the weight histories of women with extreme or class III obesity (BMI >or= 40 kg/m(2)) in comparison with a sample of women with class I-II obesity (BMI < 40 kg/m(2)) and to provide reliability data for a clinical instrument that assesses weight history. RESEARCH METHODS AND PROCEDURES: Female patients (N = 149) with extreme obesity seeking bariatric surgery and 90 class I-II obese women seeking behavioral treatment completed the Weight and Lifestyle Inventory (WALI), a self-report instrument that assesses age of onset of obesity, maximum weight at different ages, family weight history, and weight changes related to pregnancy. Test-retest reliability data were obtained by administering the WALI to a subsample (n = 58) of class I-II obese participants at their initial visit and at another pretreatment visit 1 to 2 weeks later. RESULTS: Patients with extreme obesity had a significantly younger age of onset of obesity, were significantly heavier at all age ranges, reported significantly more weight gain with their first pregnancy, and had significantly heavier parents and siblings as compared with less obese patients. There were no significant differences between groups with respect to weight gain during second pregnancies or postpartum weight retention. Robust test-retest correlations were obtained for the weight history items on the WALI. DISCUSSION: Patients with extreme obesity report more indicators of a genetic predisposition to obesity as compared with less obese patients. The WALI appears to be a reliable instrument for the assessment of weight history in obese patients.

Adolescent↗
PubMed2024

Obesity: exploring its connection to brain function through genetic and genomic perspectives.

Obesity represents an escalating global health burden with profound medical and economic impacts. The conventional perspective on obesity revolves around its classification as a "pure" metabolic disorder, marked by an imbalance between calorie consumption and energy expenditure. Present knowledge, however, recognizes the intricate interaction of rare or frequent genetic factors that favor the development of obesity, together with the emergence of neurodevelopmental and mental abnormalities, phenotypes that are modulated by environmental factors such as lifestyle. Thirty years of human genetic research has unveiled >20 genes, causing severe early-onset monogenic obesity and ~1000 loci associated with common polygenic obesity, most of those expressed in the brain, depicting obesity as a neurological and mental condition. Therefore, obesity's association with brain function should be better recognized. In this context, this review seeks to broaden the current perspective by elucidating the genetic determinants that contribute to both obesity and neurodevelopmental and mental dysfunctions. We conduct a detailed examination of recent genetic findings, correlating them with clinical and behavioral phenotypes associated with obesity. This includes how polygenic obesity, influenced by a myriad of genetic variants, impacts brain regions associated with addiction and reward, differentiating it from monogenic forms. The continuum between non-syndromic and syndromic monogenic obesity, with evidence from neurodevelopmental and cognitive assessments, is also addressed. Current therapeutic approaches that target these genetic mechanisms, yielding improved clinical outcomes and cognitive advantages, are discussed. To sum up, this review corroborates the genetic underpinnings of obesity, affirming its classification as a neurological disorder that may have broader implications for neurodevelopmental and mental conditions. It highlights the promising intersection of genetics, genomics, and neurobiology as a foundation for developing tailored medical approaches to treat obesity and its related neurological aspects.

Humans↗
PubMed2006

Comparison between bioelectrical impedance analysis and body mass index methods in determination of obesity prevalence in Ahvazi women.

BACKGROUND: Obesity has an increasing trend worldwide. Recently, application of body mass index (BMI) cutoff points of obesity classification for all population studies has been questioned. On the other hand, bioelectrical impedance analysis (BIA) is a safe, accurate, reliable and inexpensive method for screening the overweight and obesity in such studies. OBJECTIVES: There were three objectives followed in this research: to determine the prevalence of obesity and overweight in married women using BMI and BIA methods; to evaluate the correlation between these methods; and to compare the women's obesity degrees according to their educational levels. METHOD: Six hundred and thirty-seven healthy married women 18-40 years aged, who had referred to 14 health centers of the city of Ahvaz (center of Khouzestan province, south-west of Iran) were recruited in a cross-sectional design, and their socio-economic and anthropometric questionnaires were completed by the trained students. Body fat percent (%BF) and body fat mass (BFM) were measured using BIA method. BMI>25 and >30 kg/m(2) were used as criteria for determining the overweight and obese women, respectively. %BF>35% was regarded as cutoff for defining obesity. RESULTS: Mean age+/-s.d. of the women was 26.9+/-5.8 years and majority of them were housewives with secondary educational level. Their BMI, %BF, waist-to-hip ratio, and mid-upper arm circumference means were: 25.9(4.7) kg/m(2), 27.6(7.3)%, 0.75(0.08) and 27.9(3.9) cm, respectively. Central obesity was prevalent in 21.2% of the subjects. Prevalence of obesity determined by BMI and BIA methods was 18.3 and 15.5% and women within normal ranges were detected in 44.7 and 46% of the subjects by these methods, respectively. However, thin (underweight) women were 2.6 and 14.6% of the subjects studied, respectively. About one half of the women were overweight or obese. BMI was statistically correlated with BFM (r=0.86; P<0.0001) and %BF (r=0.77; P<0.0001). Women with higher educational levels had lower body fat percentage and BMI than the other subjects with lower degrees (P<0.05). CONCLUSION: Obesity and overweight is prevalent in about one-half of the Ahvazian married women and more than one-fifth of the subjects have central obesity. BIA and BMI methods can similarly detect the normal and obese married women but they are different in determining the underweight female subjects. Women with higher educational grades tend to have lower BMI levels.

Adolescent↗
PubMed1997

Muscle amino acid pattern in obese rats.

OBJECTIVE: To determine how the ability of skeletal muscle to manage amino acids is conditioned by obesity. The test was performed in two different models of obese rats: diet-obese rats and genetically obese rats. SUBJECTS: Lean and genetically obese (fa/fa) male Zucker rats were used. DESIGN: For up to 60 d of life lean animals were fed with standard chow pellet or with a hypercaloric cafeteria diet. Genetically obese rats were fed with standard chow pellet during the same period. MEASUREMENTS: Amino acid concentration in the femoral artery and vein and leg blood flow were measured. Free amino acid concentration, protein and nitrogen content and enzyme activities were determined in whole leg muscle. RESULTS: Amino acid availability was increased in diet-obese animals and remained unchanged in the genetically obese group. The genetically obese groups had a lower protein content and unchanged concentration of amino acids in leg muscle. Furthermore, total nitrogen remained unchanged in these animals and they showed an increased activity in alanine aminotransferase and glutamine synthetase. The leg muscle of the diet-obese rats took up several amino acids (Ala, Arg and Val) or released others (mainly Gln and Gly). Conversely, genetically obese rats took up many amino acids and did not release any. CONCLUSIONS: We conclude that in nutritionally obese rats there is an increased availability of amino acids in skeletal muscle. This augmented availability propitiates the increase in the uptake of many amino acids. In genetically obese rats, the lack of variation in amino acid availability points to a possible hereditary alteration that increases the capacity of different amino acid transport systems. Furthermore, the diminished protein content of fa/fa muscle is not due to a lower availability and intracellular pool of amino acids.

Amino Acids↗
PubMed1998

Combined effect of obesity and aging on feeding-induced monoamine release in the rostromedial hypothalamus of the Zucker rat.

OBJECTIVE: The obesity of the Zucker rat is associated with numerous metabolic and neurochemical disturbances involving the central transmitters regulating feeding behaviour. Among them, the release of satiety-related monoamines from the median hypothalamus in response to a meal is enhanced in obese, as compared to normal, rats as though larger amounts of these amines were necessary to bring about satiety in obese rats. Besides, the obese Zucker rat has often been described as shorter-living than its lean congener. One of the reasons for the shorter longevity of the obese rat was investigated in this study: it could be an aggravation of its obesity-related central disturbances with age. METHODS: We assessed the response to a meal of the hypothalamic monoamines, dopamine and serotonin, in young (four month old) and old (twelve month old) lean (Fa-Fa) and obese (fa-fa) Zucker rats. The in vivo technique of microdialysis was used to combine behavioural recordings and continuous neurochemical assays. RESULTS: The exacerbation of monoamine release observed in young obese rats in response to a meal was no longer found in old obese rats. Serotonin increase during a meal weakened with aging, especially in obese rats. Dopamine (DA) response to a meal was completely reversed in old obese rats, with a decrease instead of the increase observed in the three other groups. CONCLUSION: The decrease of monoaminergic response to a meal with age is apparently the opposite to the enhanced release related to obesity. However, this does not correspond to an amelioration of the hyperphagia of the obese rats with age, as we could observe in parallel behavioural experiments, but rather to a decrease in neurotransmitter metabolism and thus in neuronal functioning.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Growth hormone in obesity.

Growth hormone (GH) secretion, either spontaneous or evoked by provocative stimuli, is markedly blunted in obesity. In fact obese patients display, compared to normal weight subjects, a reduced half-life, frequency of secretory episodes and daily production rate of the hormone. Furthermore, in these patients GH secretion is impaired in response to all traditional pharmacological stimuli acting at the hypothalamus (insulin-induced hypoglycaemia, arginine, galanin, L-dopa, clonidine, acute glucocorticoid administration) and to direct somatotrope stimulation by exogenous growth hormone releasing hormone (GHRH). Compounds thought to inhibit hypothalamic somatostatin (SRIH) release (pyridostigmine, arginine, galanin, atenolol) consistently improve, though do not normalize, the somatotropin response to GHRH in obesity. The synthetic growth hormone releasing peptides (GHRPs) GHRP-6 and hexarelin elicit in obese patients GH responses greater than those evoked by GHRH, but still lower than those observed in lean subjects. The combined administration of GHRH and GHRP-6 represents the most powerful GH releasing stimulus known in obesity, but once again it is less effective in these patients than in lean subjects. As for the peripheral limb of the GH-insulin-like growth factor I (IGF-I) axis, high free IGF-I, low IGF-binding proteins 1 (IGFBP-1) and 2 (IGFBP-2), normal or high IGFBP-3 and increased GH binding protein (GHBP) circulating levels have been described in obesity. Recent evidence suggests that leptin, the product of adipocyte specific ob gene, exerts a stimulating effect on GH release in rodents; should the same hold true in man, the coexistence of high leptin and low GH serum levels in human obesity would fit in well with the concept of a leptin resistance in this condition. Concerning the influence of metabolic and nutritional factors, an impaired somatotropin response to hypoglycaemia and a failure of glucose load to inhibit spontaneous and stimulated GH release are well documented in obese patients; furthermore, drugs able to block lipolysis and thus to lower serum free fatty acids (NEFA) significantly improve somatotropin secretion in obesity. Caloric restriction and weight loss are followed by the restoration of a normal spontaneous and stimulated GH release. On the whole, hypothalamic, pituitary and peripheral factors appear to be involved in the GH hyposecretion of obesity. A SRIH hypertone, a GHRH deficiency or a functional failure of the somatotrope have been proposed as contributing factors. A lack of the putative endogenous ligand for GHRP receptors is another challenging hypothesis. On the peripheral side, the elevated plasma levels of NEFA and free IGF-I may play a major role. Whatever the cause, the defect of GH secretion in obesity appears to be of secondary, probably adaptive, nature since it is completely reversed by the normalization of body weight. In spite of this, treatment with biosynthetic GH has been shown to improve the body composition and the metabolic efficacy of lean body mass in obese patients undergoing therapeutic severe caloric restriction. GH and conceivably GHRPs might therefore have a place in the therapy of obesity.

Body Composition↗
PubMed2001

Endocrine, metabolic and nutritional factors in obesity and their relative significance as studied by factor analysis.

OBJECTIVE: To evaluate different aspects of obesity, such as body fat distribution, plasma hormone and lipid profiles, adipose tissue composition and dietary intake in an obese population in order to identify the most important factors that contribute to obesity. DESIGN: Eighty-five obese subjects, 30 men and 55 women (age, 30-70 y; body mass index (BMI), 27-35 kg/m2), were studied using anthropometric measurements, computed tomography, adipose tissue composition, serum hormone and lipid profiles and nutritional evaluations. To determine to what extent individual factors contributed to the general process of obesity, the data were subjected to a factor analysis. RESULTS: Three patterns of anthropometric and computed tomography data emerged that accounted for 69% of the variance. Factor 1 defined abdominal obesity and explained 30% of the total variance, factor 2 (gynoid obesity) accounted for 26%; and factor 3 (subcutaneous fat) explained 13% of the total variance. When other factors associated with obesity, such as lipid profile, hormonal profile and fat composition, were introduced, obesity itself, especially abdominal obesity, remained the principal factor, accounting for 23% of total variability. All factors were of secondary importance when dietary characteristics were introduced. In the overall factor analysis, more than 40% of the variability in obesity was related to dietary habits, particularly fat intake, followed by energy and saturated fatty acids intake. CONCLUSION: Even though obesity is a multifactorial phenomenon, the results suggest that dietary intake, especially fat intake, is the most important factor contributing to obesity. Secondary factors include endocrine and metabolic factors.

Adipose Tissue↗
PubMed2001

Psychoneuroendocrine characteristics of common obesity clinical subtypes.

OBJECTIVE: To relate psychological profiles, cerebral asymmetry and the hypothalamus-pituitary-adrenal axis (HPA) reactivity to clinical characteristics of common obesity. METHODS: Sixty consecutive adult female overweight and obese patients attending the outpatient endocrine department were included in this study. Clinical evaluation specifically selected a priori the following indexes: obesity age of onset, parenthood obesity, carbohydrate craving, binge eating with purging, obesity degree (defined by the body mass index (BMI)--weight (kg)/height (m(2))), body fat distribution (defined by the abdominal--thigh ratio (A/T)) and initial weight loss after medical treatment. Psychological evaluation was performed with the Minnesota Multiphasic Personality Inventory (MMPI). In the last 30 patients, the Edinburgh Inventory of Manual Preference (EIMP) and the corticotrophin-releasing hormone (CRH) test were also performed. RESULTS: Clinical characteristics defined a priori were independent variables as evaluated by contingency table analysis. Factorial analysis of variance (ANOVA) revealed a significantly different MMPI profile, according to parental obesity, with post-hoc significantly higher scores on the hypochondriasis (Hs), paranoia (Pa), psychasthenia (Pt) and schizophrenia (Sc) scales in patients with obese parents. Obese patients presented significantly higher dichotomized manual preference indexes in relation to overweight patients. Parental obesity, binge eating behaviour with purging, body fat distribution and the dichotomized manual preference index were independent significant factors for the ACTH response in the CRH test, together explaining 41% of the response variability. Age of onset of obesity and the dichotomized manual preference index were independent and significant factors for the cortisol response, together explaining 37% of its variability. A non-normal distribution was found for the ACTH response: high- and low-responders presented significantly different MMPI profiles, with high-responders presenting higher scores on all clinical scales except masculinity/femininity (Mf). CONCLUSION: Overweight/obese subjects with parental obesity present a distinctive personality profile and a higher ACTH response in the CRH test. Cerebral asymmetry may be a relevant factor for obesity development and is associated with the HPA reactivity. HPA reactivity is a sensitive index integrating clinical, psychological and neural asymmetric factors. International Journal of Obesity (2001) 25, 24-32

Adipose Tissue↗
PubMed2001

Obesity and selected co-morbidities in an urban Palestinian population.

OBJECTIVE: To assess the prevalence of obesity and central obesity in an urban Palestinian population and their associations with selected co-morbidities, including diabetes, hypertension and dyslipidaemia. DESIGN: A population-based cross-sectional survey in an urban Palestinian community. SUBJECTS: Men and women aged 30-65 y residing in the urban community, excluding pregnant women. MEASUREMENTS: According to WHO guidelines, obesity for men and women was defined as BMI> or =30 kg x m(-2), while pre-obesity was defined as BMI 25-29.9 kg x m(-2). Central obesity was defined as a waist-to-hip ratio (WHR) of >0.90 in men and >0.85 in women. RESULTS: The prevalence of obesity in this population was high at 41% (49% and 30% in women and men, respectively). Central obesity was more prevalent among men (59% compared to 25% in women). After adjusting for the effects of age, sex, smoking and each other, obesity and central obesity were found to be significantly associated with diabetes, low HDL-cholesterol and elevated triglycerides in separate logistic regression analyses. Central obesity was also significantly associated with hypertension (OR 2.26, 95% CI 1.30-3.91). CONCLUSION: Obesity and central obesity are prevalent in the urban Palestinian population. Their associations with diabetes, hypertension, and dyslipidaemia point to a potential rise in cardiovascular disease (CVD). An understanding of the reasons behind the high prevalence of obesity is essential for its prevention as well as for the prevention of the morbidities to which it may lead.

Adult↗