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PubMedDate not supplied

Validity of BMI as a measure of obesity in Australian white Caucasian and Australian Sri Lankan children.

BACKGROUND: Body mass index (BMI) is used to diagnose obesity. However, its ability to predict the percentage fat mass (%FM) reliably is doubtful. Therefore validity of BMI as a diagnostic tool of obesity is questioned. AIM: This study is focused on determining the ability of BMI-based cut-off values in diagnosing obesity among Australian children of white Caucasian and Sri Lankan origin. SUBJECTS AND METHODS: Height and weight was measured and BMI (W/H2) calculated. Total body water was determined by deuterium dilution technique and fat free mass and hence fat mass derived using age- and gender-specific constants. A %FM of 30% for girls and 20% for boys was considered as the criterion cut-off level for obesity. BMI-based obesity cut-offs described by the International Obesity Task Force (IOTF), CDC/NCHS centile charts and BMI-Z were validated against the criterion method. RESULTS: There were 96 white Caucasian and 42 Sri Lankan children. Of the white Caucasians, 19 (36%) girls and 29 (66%) boys, and of the Sri Lankans 7 (46%) girls and 16 (63%) boys, were obese based on %FM. The FM and BMI were closely associated in both Caucasians (r=0.81, P<0.001) and Sri Lankans (r=0.92, P<0.001). Percentage FM and BMI also had a lower but significant association. Obesity cut-off values recommended by IOTF failed to detect a single case of obesity in either group. However, NCHS and BMI-Z cut-offs detected cases of obesity with low sensitivity. CONCLUSIONS: BMI is a poor indicator of percentage fat and the commonly used cut-off values were not sensitive enough to detect cases of childhood obesity in this study. In order to improve the diagnosis of obesity, either BMI cut-off values should be revised to increase the sensitivity or the possibility of using other indirect methods of estimating the %FM should be explored.

Adolescent↗
PubMed1990

Age-related changes in sucrase and lactase activity in the small intestine of 3- and 10-week-old obese mice (C57BL/6Jobob).

The relationship between obesity and the digestion of carbohydrates is poorly understood. Data in humans have provided conflicting results. Studies using the obese mouse (C57BL/6Jobob) suggest that obesity is associated with increased activity of intestinal alpha-disaccharidases. To evaluate the developmental pattern of these enzyme activities in obesity, we determined the activity of sucrase and lactase in the small intestine of genetically obese mice (C57BL/6Jobob) and lean littermates at 3 and 10 weeks of age. Sucrase and lactase activities were measured on intestinal homogenates from segments of the small intestine in mice maintained on standard laboratory diets during the postweaning period. Results were expressed as specific activity and total activity per intestinal segment. Obese mice did not differ from lean littermates in body weight at 3 weeks of age, but exhibited increased protein content in the proximal small intestine. Sucrase specific activity was significantly higher in the obese mice at 3 weeks of age in all intestinal segments. Sucrase total activity showed a similar pattern. At 10 weeks of age, body weights of obese mice were substantially greater than the lean littermates. Sucrase specific and total activities were also greater in the obese mice at 10 weeks of age. Lactase specific activity, however, was similar in both obese and lean mice at both ages studied. Lactase total activity was greater in the obese mice, consistent with their greater intestinal mass. These observations demonstrate that changes in the intestinal sucrase activity of the obese mouse precede the development of excessive body weight.

Age Factors↗
PubMed1993

Strategies for the molecular genetic analysis of obesity in humans.

Studies of twins, adopted children, and some human populations indicate that body composition is significantly influenced by genetic factors. However, in no specific instance in either man or animals is the precise etiology of obesity known at the molecular level. Attempts to identify the molecular basis of obesity in humans have been hampered by difficulties in measuring food intake and energy expenditure with sufficient accuracy, as well as the apparent polygenic control of body composition in man. These constraints have stimulated interest in inbred animal strains, particularly mice, that have a genetic predisposition to obesity. Using the techniques of positional cloning, molecular markers flanking two autosomal recessive mouse obesity mutants (ob and db), which demonstrate a metabolic/behavioral phenotype similar to that observed in obese humans, have been identified. These markers are being used: (1) as starting points for chromosome walks to identify these genes, (2) as an aid in identifying genetically obese rodents prior to the development of the experimentally confounding obese phenotype, and (3) to investigate the possible contribution of the ob and db gene products to obesity in families segregating an obese phenotype. Additionally, genetic crosses segregating these obesity mutations are being used to identify "polygenes" that influence the severity of obesity and type II diabetes. Such studies may ultimately lead to the characterization of genes that influence the development and severity of obesity and non-insulin-dependent diabetes (NIDDM) in humans.

Animals↗
PubMed1992

Effect of weight reduction on resting energy expenditure, substrate utilization, and the thermic effect of food in moderately obese women.

It is not known whether the decrease in the thermic effect of food (TEF) in obesity is a consequence of obesity or a factor contributing to the development of obesity. The resting energy expenditure (REE) of 24 obese, nondiabetic, postmenopausal women was 5481 +/- 110 kJ/24 h (1310 +/- 26.4 kcal/24 h). After weight loss (12.7 +/- 0.45 kg) the REE was significantly decreased (4858 +/- 94 kJ/24 h, or 1161 +/- 22.4 kcal/24 h) and equivalent to the REE of 4866 +/- 119 kJ/24 h (1163 +/- 28.5 kcal/24 h) in 24 never-obese, postmenopausal women. The TEF, expressed as a percentage of the calories ingested, was 8.2 +/- 0.50% for obese subjects, 8.7 +/- 0.57% for postobese subjects, and 9.8 +/- 0.54% for never-obese subjects. Compared with never-obese subjects, the TEF was significantly reduced in obese subjects (P = 0.043) and remained unchanged after weight loss (P = 0.341). These findings indicate that the lower TEF in the obese subjects is uncorrected by weight loss, and thus it is a contributor to obesity rather than a consequence of obesity.

Aged↗
PubMed1998

Clustering of cardiovascular disease risk factors among obese schoolchildren: the Taipei Children Heart Study.

BACKGROUND: Childhood obesity increases the risk of obesity in adulthood and is associated with cardiovascular disease (CVD) risk factors such as hypertension, diabetes mellitus, and dyslipidemia. OBJECTIVE: We evaluated the clustering of CVD risk factors among obese schoolchildren in Taiwan. DESIGN: After multistage sampling of 85 junior high schools in Taipei, we randomly selected 1366 children (681 boys and 685 girls) aged 13.3 y (range: 12-16 y). Anthropometric, blood pressure (BP), and biochemical CVD risk factors (including blood glucose, lipid, and lipoprotein concentrations) were measured. RESULTS: Boys had a higher body mass index, systolic BP, and glucose concentrations than girls and girls had higher lipid and lipoprotein concentrations than boys. After adjustment for age, obese boys had a significantly higher BP, ratio of total to HDL cholesterol, and glucose, cholesterol, triacylglycerol, HDL cholesterol, LDL cholesterol, apolipoprotein A-I, and apolipoprotein B concentrations than nonobese boys. BP, HDL cholesterol, LDL cholesterol, and ratio of total to HDL cholesterol were significantly different between nonobese and obese girls. Approximately 70% of obese boys had one and 25% had two or more CVD risk factors other than obesity. Obese girls had a significantly higher prevalence of high BP and a higher prevalence of CVD risk factor clustering than nonobese girls. CONCLUSIONS: Boys had higher glucose concentrations and BP and lower lipid concentrations than girls. We found an association between obesity and higher BP and between obesity and blood glucose and lipid concentrations for both sexes. Clustering of CVD risk factors was especially apparent among the obese children. A clustering of CVD risk factors may begin during early adolescence among the obese.

Adolescent↗
PubMed2004

Sociodemographic and health behaviour factors associated with obesity in adult populations in Estonia, Finland and Lithuania.

BACKGROUND: The aim of this study was to analyse the pattern of sociodemographic variations in the prevalence of obesity in Estonia, Finland and Lithuania. In addition, the association between obesity and selected health behaviours was examined. METHODS: Cross-sectional surveys were conducted among representative national samples of adult populations in 1994, 1996 and 1998. The number of participants aged 20-64 was 3759 in Estonia, 9488 in Finland and 5635 in Lithuania. The data were obtained from mailed questionnaires (covering sociodemographic characteristics, health behaviour indicators, and self-reported height and weight). Obesity was defined as BMI > or = 30 kg/m2. RESULTS: The prevalence of obesity among men and women was 10% and 15% in Estonia, 11% and 10% in Finland, and 10% and 18% in Lithuania respectively. The prevalence of obesity increased only among Estonian men. Obesity was more prevalent among those aged over 50 in all three countries. It was also more prevalent among the less educated women in all countries and among the less educated men in Finland. Obesity was less prevalent among daily smokers among Estonian men and women and Lithuanian men. Physically inactive Estonian women and Finnish men and women were more likely to be obese. CONCLUSIONS: A significant association was found between low educational level and obesity in women in all the countries, but this association was found for men only in Finland. In Finland obesity was also more consistently associated with indicators of unhealthy behaviour than in Estonia and Lithuania. Thus, even though the social gradient of obesity was broadly similar in all the countries studied, differences emerged with regard to the behavioural correlates of obesity.

Adult↗
PubMed1981

Effects of obesity, food restriction and pregnancy on fetal and maternal weight and on body composition in rats.

The effects of obesity and food restriction on fetal and maternal body weight and on maternal body composition were determined in pregnant and nonpregnant rats. Obesity was induced by several weeks of ad libitum feeding of a varied diet of retail food products which continued until experimental day 5 (gestational age in pregnant groups). From day 5 all groups were fed a standard diet. Ad libitum-fed obese pregnant rats gained less weight during pregnancy than non-obese rats. All rats which were 60% food restricted lost body weight. Weight loss in obese rats was due to loss of body fat whereas non-obese rats lost lean tissue as well. Obese pregnant rats ended the food restriction period 62 g heavier than non-obese restricted pregnant rats and had the same carcass weight and composition as ad libitum fed non-obese nonpregnant rats. Fetal and placental weight was reduced 25 percent by food restriction in obese as well as non-obese groups. These results indicate that during food restriction the fetal rat cannot parasitize maternal nutrient stores to prevent growth retardation, even if the mother is obese.

Animals↗
PubMed1992

Dynamic and static phases of severe dietary obesity in sheep: food intakes, endocrinology and carcass and organ chemical composition.

The chronology of changes in body weights, food intakes and plasma concentrations of selected metabolic hormones and metabolites were determined in sheep during the induction (dynamic) and static phases of diet-induced obesity. Lean adult Dorset ewes weighing 47 kg were fed a pelleted hay-grain diet at maintenance (lean; n = 7) or were fed the same diet ad libitum to a maximum intake of 3 kg.sheep-1.d-1 (obese; n = 8) for 78 wk. Body weight of obese sheep doubled (97 vs. 47 kg) by wk 42 of ad libitum intake. Average daily intakes of dry matter (12.8 g/kg) and digestible energy (165 kJ/kg) were comparable in maintenance-fed lean sheep and ad libitum-fed obese sheep consuming maintenance after wk 50, which began the static phase of obesity. Fasting plasma concentrations of insulin in the obese sheep increased steadily from 50 +/- 6 pmol/L at wk 0 to a sustained plateau of 249 +/- 21 pmol/L after wk 30. Plasma levels of glucose, immunoreactive glucagon and thyroid hormones were consistently greater (P less than 0.05) in obese sheep than in lean sheep after wk 2, 3 and 25, respectively, of the experiment. Concentration of lipid (49 vs. 25%) in the carcass stripped of internal fat was greater (P less than 0.01) in obese sheep than in lean sheep, but concentration of protein (10.4 vs. 15.3%) was less in the heavier carcass (58 vs. 24 kg) of the obese sheep. We conclude that hyperinsulinemia and abnormal fuel metabolism are early events during dynamic obesity and these defects persist throughout the static phase of obesity. Maintenance energy requirements relative to unit body weight (W1.0) seem similar in lean and dietary obese sheep.

Adipose Tissue↗
PubMed1987

Obesity in black women.

The marked excess of obesity among black women in the United States poses several interesting questions which provide the framework for this review: Is the apparent high prevalence of obesity in black women a valid finding? If so, does it show the expected disease and disease risk associations? Can the contributory genetic and environmental variables be identified? Regarding the validity issue, the high prevalence of obesity in black women seems to be neither artifactual nor primarily an indirect effect of socioeconomic status. On the issue of racial comparability of disease risks among women, the available evidence is less conclusive. Obesity appears to have qualitatively similar health consequences for black women and white women but may be less strongly related to some disease risks (for example, hypertension) in black women than in white women. Obesity risks of black women may, however, be enhanced by the presence of multiple risk factors. On the question of causes, no clear mechanism for the excess obesity in black women can be identified. There is some evidence to support hypotheses based on dietary, lifestyle, and metabolic influences. Genetic factors cannot be ruled out. Several relevant future research possibilities can be suggested. Epidemiologic studies of both genetic and environmental influences in female obesity are needed. Studies among black females might further specify patterns of body weight and body fat distribution according to degree of European admixture and developmental variables such as caloric exposure in utero and in early infancy. Studies to establish more clearly the relative risks of various health outcomes for obese black women are needed to assist in setting public health priorities. For example, what are the attributable and absolute risks of overweight or obesity compared with other risk factors that are potential intervention targets? Studies are needed to define effective means of preventing and treating obesity among black women. Effective interventions are likely to be culture-specific. Definitive comparisons of black women and white women on environmentally mediated aspects of obesity might contribute to models of obesity in the general population and might also elucidate points at which black women and white women diverge. For example, short-term prospective studies are needed to better specify the natural history of weight gain and weight loss among females of both races during critical periods such as adolescence, post partum, lactation and post lactation, and during major life stresses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Insulin-mediated sympathetic stimulation: role in the pathogenesis of obesity-related hypertension (or, how insulin affects blood pressure, and why).

Thus, the evidence summarized here supports an important role for insulin and the sympathetic nervous system in the pathogenesis of obesity-related hypertension. Is it possible that insulin-mediated sympathetic stimulation contributes a pro-hypertensive effect in non-obese as well? It seems possible in young borderline hypertensives where sympathetically mediated thermogenic mechanisms are potent enough to compensate for the increased caloric intake, thereby enabling these young hypertensives to avoid obesity. This is consistent with an observation made in the original Framingham cohort that not only did obesity predict the eventual development of hypertension, but hypertension, as well, predicted the eventual development of obesity. A reasonable interpretation of these data suggests that as subjects age and the effectiveness of thermogenic mechanisms wanes, obesity might develop as a consequence of increased caloric intake no longer effectively buffered by the increased SNS activity. It is important to note that the mechanisms described here exert a pro-hypertensive effect and cannot properly be considered to 'cause' hypertension. Hypertension is rarely the consequence of a single mechanism. It is also true, as pointed out convincingly by Julius and his colleagues, that enhanced sympathetic activity, as a primary factor, can be associated with both hypertension, insulin resistance and, possibly, obesity [39]. And, finally, it should be noted that the mechanism described here is not the only mechanism linking obesity and hypertension. A rapidly emerging body of evidence indicates that leptin, the polypeptide product of the ob/ob gene secreted from adipose tissue, exerts potent central neural effects on both appetite and sympathetic activity. Leptin levels, elevated in obese humans, have the potential to increase both sympathetic activity and blood pressure [40-43]. A more comprehensive summary of the relationships between hypertension and obesity may, therefore, involve insulin and leptin, as well as the SNS, as represented in the schema presented in Figure 7. Both leptin and insulin may, therefore, be considered as compensatory mechanisms recruited to restore energy balance, with the SNS as one of the effector arms. Viewed in this way, obesity-related hypertension is inextricably linked to the metabolic economy of the obese.

Animals↗
PubMed2000

Relationship of obesity and specimen weight to complications in reduction mammaplasty.

Obesity and specimen weight have both been associated with a higher incidence of complications for patients undergoing reduction mammaplasty. However, obesity has been arbitrarily and inconsistently defined, and the degree of obesity has not been considered in these previous studies. Because insurance companies are increasingly demanding weight loss before authorizing surgery, the relationship of obesity and breast size to complications is of great importance. Upon critical review of the literature, a number of fundamental questions remain unanswered. If complications are more frequent in the obese patient, are these complications directly proportional to the degree of obesity? Also, if the patient is required to lose weight before surgery, is weight loss effective in reducing complication rates? In an attempt to clarify these issues, 395 patients who underwent reduction mammaplasty over a 10-year period were reviewed retrospectively. Patients were arbitrarily divided into five groups in which, depending on their degree of relative obesity, they were classified as less than 5 percent, 5 to 10 percent, 10 to 15 percent, 15 to 20 percent, or greater than 20 percent above average body weight. To evaluate the relationship of specimen weight to complications, patients were also arbitrarily divided into five groups according to weight of the breast reduction specimen, which was classified as less than 300 g, 300 to 600 g, 600 to 900 g, 900 to 1200 g, and greater than 1200 g reduction per breast. Complications were then divided into local and systemic and major and minor. When bilateral reductions alone were analyzed (n = 267), there was a statistically significant increase in complication rate in the obese (p = 0.01). However, when the obese population was further subdivided according to their degree of obesity (less than 5 percent, 5 to 10 percent, 10 to 15 percent, 15 to 20 percent, and greater than 20 percent above average body weight), no further correlation was found. However, the relationship between specimen weight per breast and complications was much stronger with a direct correlation existing between increasing specimen weight and the incidence of complications. Although this study has shown that patients who are average body weight have fewer complications than obese patients after breast reduction surgery, it has not shown an increasing incidence of complication with increasing degrees of obesity. The implications of these findings and their relationship for denying patients surgery on the basis of weight alone are discussed in detail.

Adolescent↗
PubMed2001

Outcome comparison between free and pedicled TRAM flap breast reconstruction in the obese patient.

Obesity can be a contraindication for TRAM flap breast reconstruction. This study reviewed the authors' experience with free TRAM and pedicled TRAM flap breast reconstruction in the obese patient to examine the complication rates associated with each reconstructive method and to determine whether TRAM flap reconstruction can safely be used in these high-risk patients. The records of 221 consecutive TRAM flap reconstructions were reviewed. Preoperative risk factors for morbidity were noted, as well as the incidence of TRAM flap success, operative time, length of hospital stay, and postoperative complications. Patients were categorized as obese if their body mass index was greater than 25.8 kg/m2. Data were tabulated using contingency tables and analyzed using chi-squared statistics. Multiple logistic regression was used to determine risk factors for flap complications. Of the 221 patients studied, 114 patients were found to be obese (body mass index >25.8 kg/m2). Of these 114 patients, 78 were reconstructed with free TRAM flaps and 36 were reconstructed with pedicled flaps. In these obese patients, the average body mass index was 32 kg/m2 in the free TRAM and 30 kg/m2 in the pedicled TRAM flap reconstructions. There were no significant differences between groups with regard to age or preoperative risk factors. Length of hospital stay and operative time did not differ significantly between the two reconstructive methods. The average duration of follow-up was 24 months in both groups. Complications occurred in 26 percent of free TRAM flap reconstructions and 33 percent of pedicled reconstructions. There was no significant difference between reconstructive methods with regard to overall complication rates. Increasing body mass index was found to have a significant effect on free TRAM flap complications (p = 0.008) but not on pedicled TRAM flap complications. There were no partial or total flap losses in obese free TRAM flap patients; however, there was one case of total flap loss and four cases of partial flap loss in the obese pedicled TRAM flap group. The incidence of flap loss was significantly higher when pedicled TRAM flaps were used for reconstruction in obese patients (p = 0.04). Obese patients who underwent reconstruction with pedicled TRAM flaps were more likely to experience a complication if they also smoked (p = 0.001). There was no significant difference in operating time or length of stay when pedicled and free TRAM flap reconstructions in obese patients were compared. There were more cases of flap necrosis in the pedicled TRAM flap group. Free TRAM flaps may provide some benefit in reducing partial flap loss in obese patients, but overall complication rates were not significantly different between reconstructive methods. Of 114 patients, there was only one case of total reconstructive failure. From these findings, it seems that the free or pedicled TRAM flap can be used successfully for breast reconstruction in the majority of patients with obesity. Surgeons should use the technique with which they are most familiar to obtain consistent results.

Body Mass Index↗
PubMed2002

Association between obesity and functional status in patients with spine disease.

STUDY DESIGN: A cross-sectional study of 15,974 patients with spine disease from 26 members of the National Spine Network. OBJECTIVES: To use functional status measures and clinical parameters to evaluate the association between obesity and health status among patients with spine conditions. SUMMARY OF BACKGROUND DATA: With 22.5% of Americans overweight, obesity is a significant health concern. However, the functional impact caused by obesity in spine patients remains unknown. METHODS: Functional status was measured on 15,974 patients on an initial visit using a general physical health measure (SF-36 Physical Component Summary score) and a disease-specific measure (Oswestry Disability Index). Obesity was measured using body mass index (kg/m2). Patients were categorized into four groups according to body mass index: normal range (<25.0 kg/m2, n = 5732), Grade 1 obesity (25.0-29.9 kg/m2, n = 5845), Grade 2 obesity (30.0-39.9 kg/m2, n = 3836), and Grade 3 obesity (>/=40.0 kg/m2, n = 561). The associations between SF-36 Physical Component Summary and Oswestry Disability Index scores and body mass index were evaluated in a multivariate linear regression model. Clinical presentation data were derived from patient and clinician reports and were compared across body mass index categories. RESULTS: In the four obesity categories, the PCS scores were 32.6 (normal range body mass index), 30.8 (Grade 1), 28.2 (Grade 2), and 25.9 (Grade 3) (P < 0.001). The SF-36 Physical Component Summary score of the general U.S. population is 50.0. The Oswestry Disability Index scores across the four body mass index groups were 39.0, 41.6, 46.6, and 52.2, respectively (P < 0.001). Compared with nonobese patients, obese patients were more likely to have radicular pain and neurologic signs (P < 0.01). Furthermore, obese patients had more comorbidities and were more likely to be receiving worker's compensation. After adjusting for clinical and demographic factors, each increased level of obesity was associated with a 1-1.5-point worsening in both the SF-36 Physical Component Summary and Oswestry Disability Index scales (P < 0.05). CONCLUSIONS: General and disease-specific functional health status was significantly worse for patients with a higher body mass index. Obese patients also displayed more severe pain symptoms than nonobese spine patients.

Body Mass Index↗
PubMed2006

Is obesity overrated as a "risk factor" for poor outcomes in chronic occupational spinal disorders?

STUDY DESIGN: Prospective cohort study. OBJECTIVE: To investigate whether obesity is a risk factor for poor socioeconomic outcomes in patients with chronic occupational spinal disorders beginning an interdisciplinary functional restoration program. SUMMARY OF BACKGROUND DATA: Obesity is known as a risk factor for a multitude of physical and mental health disorders. A classification system can define obesity based on body mass index (BMI). Limited evidence is available on the effect of obesity on rehabilitation from chronic occupational spinal disorders. METHODS: A large cohort of chronic occupational spinal disorder patients with extended disability (average 16 months) following work-related injuries (n = 2483) were divided into 5 groups based on BMI. Socioeconomic outcomes were identified through a 1-year post-rehabilitation structured telephone interview. Patients were also assessed before and after intervention with validated questionnaires measuring pain intensity, functional deficits, and depression. The interdisciplinary functional restoration program was individualized for length of disability and severity of physical and psychological deficits. RESULTS: The prevalence of obesity in this population was high. Only 22% of patients were "normal" (BMI <25), while 43% were obese (BMI >30). There was a significant linear trend for males to be progressively less represented as obesity increased. There was also a significant trend for hypertension to be associated with greater levels of obesity. However, there were no significant differences in site of injury, disability duration, or attorney representation among the groups. Most importantly, there were no statistically significant differences in all but 1 of the socioeconomic outcomes among any of the obese groups and the normal weight patients. There was a trend toward higher pretreatment and posttreatment functional assessment scores (i.e., greater perception of disability), and a linear trend for higher pretreatment depression ratings across BMI groups, although they all improved at comparable rates after treatment. CONCLUSIONS: Obesity is more prevalent and severe in chronic occupational spinal disorders when entering a functional restoration program as the final step in a prolonged treatment regimen. We conclude that obesity, even gross obesity, has no significant impact on outcomes of an interdisciplinary functional restoration program for patients disabled an average of 16 months.

Adult↗
PubMed2006

Morbid obesity is an independent determinant of death among surgical critically ill patients.

OBJECTIVE: To determine whether extreme obesity (morbid obesity; body mass index > or =40 kg/m(2)) is an independent risk factor for death among critically ill patients; this objective is most salient in the subset of patients who sustain a prolonged intensive care unit stay during which the burdens of care imposed by obesity and its consequences would become most apparent. DESIGN: Cohort analysis of data from the Project Impact database used to catalog admissions and outcomes to a surgical intensive care unit, with predetermined end point analyses of outcomes. SETTING: Surgical intensive care unit serving Tufts-New England Medical Center, a tertiary care and university medical center in Boston. PATIENTS: All critically ill surgical patients admitted to the Tufts-New England Medical Center surgical intensive care unit from January 1998 to March 2001. INTERVENTIONS: Intensive care unit and hospital mortality and lengths of stay were compared with body mass index subclassified into five groups: underweight, normal weight, overweight, obese, and extremely obese. Data were examined for all admissions during the study period and for a predetermined subgroup with a prolonged intensive care unit stay (> or =4 days). MEASUREMENTS AND MAIN RESULTS: The prevalence of obesity in the surgical intensive care unit was 26.7%; extreme obesity was observed in 6.8%. In the full cohort of patients (n = 1373), median length of stay was short (2 days) and there were no differences in mortality in patients among any of the body mass index classes. In the subgroup of prolonged stay patients (n = 406), intensive care unit and hospital mortality rates were significantly increased in extremely obese patients compared with all other patients (intensive care unit, 33.3% vs. 12.3%, p = .009; hospital, 33.3% vs. 16%, p = .045). Multivariate analysis showed that extreme obesity was an independent predictor of death in surgical critically ill patients with prolonged intensive care unit stay after controlling for age, gender, and severity of illness. The odds of death increased 7.4 times in patients with morbid obesity. CONCLUSIONS: Morbid obesity (body mass index > or =40 kg/m(2)) is an independent risk factor for death in surgical patients with catastrophic illness requiring prolonged intensive care. The prevalence of obesity is growing, both in the intensive care unit and in the general population. The increased risk of complications and death in this population mandates that we adapt customized processes of care to specifically address this unique and very challenging subset of patients.

Critical Care↗
PubMed2006

Obesity and traumatic brain injury.

BACKGROUND: As obesity continues to run rampant in our society, an understanding of its adverse effect after traumatic injury is starting to unfold. We hypothesize that obesity negatively impacts head-injured patients, and the current study intends to compare obese and lean patients with traumatic brain injury (TBI). METHODS: This is a retrospective study evaluating all blunt trauma patients with TBI admitted to the intensive care unit (ICU) in our urban, Level I trauma center from 1998 until 2003. Body mass index (BMI) was used to categorize patients as either lean (BMI <30 kg/m2) or obese (BMI > or =30 kg/m2). Admission demographics, type and severity of head injury, and associated injuries were recorded for each patient. Primary outcome was mortality, while secondary outcomes were cause of death, complications, and for survivors, days of mechanical ventilation, ICU length of stay, and hospital length of stay. Obese and lean patients were compared using univariate analysis and multivariate stepwise logistic regression. In addition, a subgroup analysis of patients with isolated head injury was performed. RESULTS: There were 690 patients with TBI admitted to the ICU during the study period, with 129 (19%) obese patients (BMI = 34 +/- 5 kg/m2) and 561 (81%) lean patients (BMI = 24 +/- 4 kg/m2). The two groups were similar with the exceptions that obese patients were older (46 +/- 20 years versus 39 +/- years, p < 0.01), had lower admission systolic blood pressure (125 +/- 38 mm Hg versus 134 +/- 30 mm Hg, p = 0.01), and more often sustained an associated chest injury (46% versus 35%, p = 0.03). Obese patients with TBI had a trend toward more complications (34% versus 28%, p = 0.17) and a higher mortality (36% versus 25%, p = 0.02). However, stepwise logistic regression failed to identify obesity as an independent risk factor for either morbidity or mortality. In addition, obese patients with isolated head injury had no increase in complications or death. CONCLUSIONS: Although obese patients suffer more complications and higher mortality than lean patients after TBI, this adverse effect seems to be due to age, lower admission blood pressure, and more associated chest injury, rather than a direct result of the obese state.

Adult↗
PubMed2004

Maternal obesity as an independent risk factor for caesarean delivery.

The present study was aimed to investigate pregnancy outcome among obese women and specifically the correlation between maternal obesity and incidence of caesarean section (CS) while controlling for the potential confounding effects of other variables associated with obesity. A population-based study was performed comparing all pregnancies of obese (maternal pre-pregnancy body mass index (BMI) of 30 kg/m2 or more) and non-obese patients, between the years 1988 and 2002. Patients with hypertensive disorders and diabetes mellitus as well as patients lacking prenatal care were excluded from the analysis. Stratified analyses, using the Mantel-Haenszel technique, and a multiple logistic regression model were performed to control for confounders. During the study period there were 126,080 deliveries meeting the inclusion criteria, of which 1769 (1.4%) occurred in obese patients. Using a multivariable analysis, the following conditions were significantly associated with maternal obesity: failure to progress during the first stage (odds ratio (OR) = 3.1; 95% confidence interval [CI] 2.5, 3.8; P < 0.001), fertility treatments (OR = 2.0; [95% CI 1.6, 2.5]; P < 0.001), previous CS (OR = 1.7; [95% CI 1.5, 1.9]; P < 0.001), malpresentations (OR = 1.4; [95% CI 1.2, 1.6]; P < 0.001), recurrent miscarriages (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001) and fetal macrosomia (OR = 1.4; [95% CI 1.2, 1.7]; P < 0.001). Higher rates of caesarean deliveries were found among obese parturients (27.8% vs. 10.8%; OR = 3.2; [95% CI 2.9, 3.5]; P < 0.001). When controlling for possible confounders, using the Mantel-Haenszel technique, the association between maternal obesity and CS remained significant. No significant differences were noted between the groups regarding perinatal complications such as perinatal mortality, congenital malformations, shoulder dystocia and low Apgar scores. In conclusion, a significant association was found between obesity and CS even after the exclusion of hypertensive disorders and diabetes mellitus. Importantly, obesity alone was not associated with adverse perinatal outcome. Obstetricians should be encouraged to allow obese patients not suffering from diabetes or hypertensive disorders an adequate trial of labour.

Abortion, Spontaneous↗
PubMed2006

Dietary therapy for obesity is a failure and pharmacotherapy is the future: a point of view.

1. We confront an escalating epidemic of obesity. The precipitating factors are undoubtedly environmental and include increasingly immobilizing occupations and technologies and an abundance of food in many societies. This understanding has led to the view that the obesity epidemic is entirely environmental and that obesity should be treated primarily by behavioural (particularly dietary) therapy. That is, a prominent view is that common human obesity is an environmental disease and is not, like hypertension and hypercholesterolaemia, a complex, multifactorial disease resulting from the interaction of genetic and environmental variance. 2. In the first part of the present article, I argue that this view has obscured a strong genetic-biological contribution to body mass and adiposity in humans. This is supported by studies of adopted children and twins and by rare Mendelian forms of human obesity. 3. In the second part of the present article, I argue that behavioural therapy for maintenance of weight loss is, overall, a failure. The overwhelming majority of people who lose weight by dieting regain it in several years. Many have blamed this on patients' lack of will-power and discipline, but there is mounting evidence that biological mechanisms contribute substantially to relapse from weight loss during dietary therapy. These include a compensatory decrease in energy expenditure during dieting and compensatory adaptations that would be expected to increase appetite. 4. We live in an era of evidence-based medicine; the evidence does not support the efficacy of diet therapy for maintenance of weight loss in obesity. This has been true for decades, despite efforts to improve behavioural therapy. Despite what we want to happen, this will not likely improve, because the failure of diet therapy for the maintenance of weight loss in obesity is probably primarily biological, not behavioural. 5. In the third part of the article, I argue that drugs will increasingly dominate the treatment of obesity. We are in the midst of a revolution in understanding the biological regulation of appetite and metabolism that began with the pioneering discovery of leptin. In my judgement, this will lead inevitably to the development of safe, effective therapy for obesity. 6. This transformation from behavioural to pharmacological therapy proved true with hypertension and hypercholesterolaemia. Pharmacological therapy for hypertension and hypercholesterolaemia followed the discovery of the pathways regulating arterial pressure and cholesterol biosynthesis, respectively, and behavioural therapy for these diseases is now secondary. Despite the skepticism, I predict that the same transformation will occur in the treatment of obesity. This is not to argue against the need for environmental modification to slow the escalating epidemic of obesity, but it is to suggest that future effective treatment of common human obesity should recognize the limitations of dietary therapy for maintenance of weight loss and the promise of pharmacological therapy.

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