Teis Andersen

Body mass, fat-free body mass, and prognosis in patients with chronic obstructive pulmonary disease from a random population sample: findings from the Copenhagen City Heart Study.

RATIONALE Low body mass index (BMI) is a marker of poor prognosis in chronic obstructive pulmonary disease (COPD). In the general population, the harmful effect of low BMI is due to the deleterious effects of a low fat-free mass index (FFMI; fat-free mass/weight(2)). OBJECTIVES We explored distribution of low FFMI and its association with prognosis in a population-based cohort of patients with COPD. METHODS We used data on 1,898 patients with COPD identified in a population-based epidemiologic study in Copenhagen. FFM was measured using bioelectrical impedance analysis. Patients were followed up for a mean of 7 yr and the association between BMI and FFMI and mortality was examined taking age, sex, smoking, and lung function into account. MAIN RESULTS The mean FFMI was 16.0 kg/m(2) for women and 18.7 kg/m(2) for men. Among subjects with normal BMI, 26.1% had an FFMI lower than the lowest 10th percentile of the general population. BMI and FFMI were significant predictors of mortality, independent of relevant covariates. Being in the lowest 10th percentile of the general population for FFMI was associated with a hazard ratio of 1.5 (95% confidence interval, 1.2-1.8) for overall mortality and 2.4 (1.4-4.0) for COPD-related mortality. FFMI was also a predictor of overall mortality when analyses were restricted to subjects with normal BMI. CONCLUSIONS FFMI provides information in addition to BMI and assessment of FFM should be considered in the routine assessment of COPD.

Hepatic effects of dietary weight loss in morbidly obese subjects

This prospective study was carried out in order to evaluate the influence on liver morphology and function of a very-low-calorie formula diet. Fourty-one morbidly obese, non-alcoholic subjects had liver biopsy performed before and after a median weight loss of 34 kg. Fatty change improved (p less than 0.001), but 24% of the patients developed slight portal inflammation (p = 0.039) or slight portal fibrosis (p = 0.063). Patients developing portal fibrosis had a higher degree of fatty change at entry (p = 0.029), a more pronounced reduction of fatty change (p = 0.014) and a faster weight loss (p = 0.026). Liver biochemistry, which was of no individual diagnostic value, improved. It is concluded that morbidly obese subjects with a high degree of hepatic fatty change are at risk of developing portal inflammation and fibrosis when undergoing very fast dietary weight reductions.

Weight gain during treatment with valproate.

Abstract– An analysis was made of weight changes during treatment with valproate in 63 adult epileptic patients.

The impact of obesity, fat distribution, and energy restriction on insulin-like growth factor-1 (IGF-1), IGF-binding protein-3, insulin, and growth hormone

The aim of this study was to characterize the association between serum insulin-like growth factor-1 (IGF-1) and obesity, as well as fat distribution, before and during moderate energy restriction (1,200 kcal/d). In 51 females and nine males having a body mass index (BMI) between 27 and 39 kg/m2, relationships between serum IGF-1, IGF-binding protein-3 (IGFBP-3), insulin, growth hormone (GH), blood glucose, and anthropometric measurements of body fat were examined. The patients were studied before treatment and again after 8 and 16 weeks of dieting. Visceral adipose tissue (AT) was estimated by anthropometric computed tomography (CT)-calibrated equations. In females, IGF-1 was inversely associated with the abdominal sagittal diameter (SagD) and with the visceral AT (r = -.41, P = .006). No significant correlations were found between IGF-1 and BMI or other indices of adiposity. Weight loss caused a temporary increase in IGF-1 concentrations (P = .03) and continued decrements in blood glucose levels (P = .0004 at 16 weeks). A statistically significant inverse correlation between IGF-1 and blood glucose levels was present before (r = -.30, P = .02) and after 8 (r = -.37, P = .007) and 16 (r = .02, P = .02) weeks of dietary treatment. Both serum IGF-1 and insulin levels were positively correlated with serum IGFBP-3 levels (r = .34, P = .009 and r = .34, P = .008, respectively). We conclude that IGF-1 levels in obese females reflect the intraabdominal fat mass rather than obesity per se. IGF-1 and blood glucose levels are inversely correlated in obesity before and during energy restriction.

Metabolic changes during treatment with valproate in humans: Implication for untoward weight gain☆

This study was initiated to elucidate the mechanisms behind valproate-induced weight gain. Eight patients with epilepsy were studied with identical examination programs before and during the end of the first month of treatment with sodium valproate (VPA). The measurements included registration of food intake, indirect calorimetry, and determination of pancreatic and thyroid hormones, catecholamines, albumin, electrolytes, glycerol, and free fatty acids. Measurements were performed both at the basal condition and during a 3-hour oral glucose tolerance test (OGTT). After the start of VPA treatment, the mean levels during the OGTT of plasma glucose and catecholamines were significantly decreased by 7% and 25%, respectively (P less than .05). The mean ratio of insulin to glucagon decreased by 37% (P less than .01). During the glucose load, the decreases in free fatty acids were less pronounced after the start of VPA treatment, whereas the mean levels of glycerol were found to be unchanged. We detected no differences between the two periods with regard to total energy intake or macronutrient selection, energy expenditure, or thyroid hormones. As VPA is known to affect the concentration of carnitine in humans, it is hypothesized that a possible VPA-induced deficiency of the beta-oxidation of fatty acids is important for the development of obesity in epileptic patients in long-term treatment with VPA, but changes in catecholamines or other hormones might also be of importance.

Secondary hyperparathyroidism of morbid obesity regresses during weight reduction

In order to test the relation between obesity and the secondary hyperparathyroidism found in markedly overweight subjects, 24 morbidly obese patients were studied before and after a weight loss of 35.9 kg obtained by a nutritionally adequate, intermittent very-low-calorie diet. Overweight was reduced from 98 +/- 34% to 44 +/- 19%. Serum total calcium did not change, but serum ionized calcium (Ca2+) increased from 1.22 +/- 0.04 mmol/L to 1.25 +/- 0.04 mmol/L (P less than .001). A corresponding fall was observed in serum parathyroid hormone (s-PTH), which decreased from 47.2 +/- 21.7 pmol/L to 35.2 +/- 19.4 pmol/L (P = .01). The change of s-PTH was positively associated with the reduction of body weight (r = .50, P less than .05) and with the reduction of overweight (r = .55, P less than .01). Regarding calcium binding substances, serum albumin remained low. The initially lowered serum phosphate and bicarbonate both rose (P less than .001). Plasma lactate and plasma free fatty acids (FFAs) decreased (P less than .001). The study supports our hypothesis that the change profile of calcium complexing anions in obesity interferes with the tubular reabsorption of calcium, which in turn lowers serum Ca2+, thus promoting hyperparathyroidism. Along with weight loss, concentrations of calcium complexing anions returns towards normal values and the secondary hyperparathyroidism regresses.

Change in fat-free mass assessed by bioelectrical impedance, total body potassium and dual energy X-ray absorptiometry during prolonged weight loss

A total of 16 obese women (body mass index (BMI) 30-43 kg m(-2)) participated in a weight reduction study. Before and after a weight loss of 11.7 +/- 7.4 kg (mean +/- SD), body composition was assessed by dual energy X-ray absorptiometry (DXA), and total body potassium counting (TBK). These measurements were compared with bioimpedance analysis (BIA) by applying 11 predictive BIA equations published in the literature. Predictive equations for the present study population were developed, with the use of fat-free mass (FFM) as assessed by TBK and DXA as references in multiple regression analysis. The results of the BIA equations varied widely; FFM was generally overestimated by BIA as compared with DXA and TBK before and after weight loss. During weight loss, the FFM did not change, as estimated by DXA (1.3 +/- 2.3 kg, p > 0.05) and TBK (0.9 +/- 2.9 kg, p > 0.05). The recorded change in impedance (R) was also insignificant. Three BIA equations from the literature, which were not specific for the degree of obesity in the present study group, predicted changes in FFM (from 0.5 + 3.6 to 2.4 +/- 4.4kg, p > 0.05) that were comparable with those estimated by the reference methods. Eight equations from the literature, which included equations specific for the degree of obesity in the study group, and the group specific equations developed for the present population predicted significant changes in FFM during weight loss (from 2.3 +/- 3.0 to 5.0 +/- 3.0 kg, p < 0.05). We conclude that in obesity most predictive equations are unable to predict static body composition and are not reproducible for individuals over time. However, a significant or insignificant change in R (without accompanying predictive equations) may be used to indicate whether FFM is lost or preserved in groups of obese subjects.

Obstetric risks in obesity. An analysis of the literature.

In order to evaluate the obstetric risks in obesity a partly computerized literature search was performed. Irrespective of language, papers published between 1960 and 1982 were included, provided that they were original and controlled studies on obstetric complications among women with a stated degree of overweight. Out of 143 publications 26 fulfilled the criteria and were included. They revealed information on 10,440 cases. Most reported subjects were only moderately obese. Thirty-seven complications were stated in one or more publications as being significantly more prevalent among obese women compared with lean controls. However, as data were often scarce or highly conflicting, it is concluded that an increased risk is only sufficiently documented with regard to a minority of these complications. They are: preeclampsia as well as each separate element of this disorder, diabetes mellitus, varicose veins, and the need for caesarean section. The significantly increased birth weight of the infants did not induce increase of labor complications.

Plasma fibronectin concentrations in morbidly obese patients

Plasma fibronectin concentrations and liver morphology were investigated in 45 morbidly obese subjects (median overweight 88%) and in 42 normal weight controls, matched for sex and age. A significantly (P less than 0.01) raised plasma fibronectin concentration (median 464 mg/l, range 276-862 mg/l) was found in the obese subjects when compared with concentrations in the controls (median 348 mg/l, range 164-536 mg/l). Plasma fibronectin concentrations of the obese patients correlated significantly to their degree of overweight (r = 0.33, P less than 0.05) as well as to the degree of fatty change found in their liver biopsies (r = 0.33, P less than 0.05). Significantly (P less than 0.05) elevated plasma fibronectin concentrations even in obese subjects without hepatic fatty change indicate that liver fat accumulation is no prerequisite of the obesity-related elevation of plasma fibronectin. Raised plasma fibronectin concentration in obesity may more readily be explained by an increased fibronectin formation by lipocytes.

Does Calcium Supplementation Reduce the Risk of Urinary Oxalate Calculi after Jejunoileal Bypass for Morbid Obesity

Twelve patients having received an end-to-side jejunoileal bypass operation for morbid obesity 6-10 years previously were studied over three periods of 2 weeks each. The first period was used for baseline observations without any treatment. For the second period patients were randomly assigned to equimolar (75 mmol/day) oral calcium supplements administered either as a slow-release or as a bolus calcium preparation. During the third period these treatments were crossed over. The calcium preparations used caused equal reductions in frequency of bowel movements. Both preparations increased serum calcium and serum phosphate, but significance (p < 0.05) was reached only during supplementation with the slow-release preparation. Despite the intended raising of serum calcium levels, none of the preparations influenced the 24-hour urine oxalate to creatinine ratio or the urine stone index. There are several other reasons for supplying extra calcium after intestinal bypass procedures, but our data do not support the concept of preventing renal stone formation by means of calcium supplementation.