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Obesity in Patients with Craniopharyngioma: Assessment of Food Intake and Movement Counts Indicating Physical Activity

Department of Pediatrics, University Hospital of Bonn (K.J.H., C.R.), 53113 Bonn, Germany; Department of Pediatrics, Hospital of Oldenburg (H.L.M.), 26133 Oldenburg, Germany; Department of Pediatrics, Hospital of Murnau (E.W.), 82418 Murnau, Germany; and Department of Nutritional Psychology, University of Göttingen (V.P.), 37075 Göttingen, Germany

Address all correspondence and requests for reprints to: Christian Roth, M.D., Children’s University Hospital, Adenauerallee 119, 53113 Bonn, Germany. E-mail: croth{at}uni-bonn.de.

	Abstract

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Patients with childhood-onset craniopharyngioma (CP) often suffer from obesity. We evaluated two important etiological factors of obesity development, energy intake and physical activity. Energy intake was supposed to be high due to a disturbed hypothalamic regulation of appetite. We used a validated nutritional diary to determine the 1-wk food intake in 27 CP patients (12 with intrasellar tumors and 15 with hypothalamic tumors) and 1027 controls who were a representative sample of the 7- to 16-yr-old German population. In 2 accelerometry settings, we determined movement counts indicating physical activity. Nineteen CP patients were comparable to 26 controls for age and body mass index. One setting was a clinical one during weight reduction; the other was an out-patient setting. Daily energy intake was 1916 ± 677 kcal (mean ± SD) in intrasellar CP patients, 2075 ± 877 kcal in hypothalamic CP patients, and 2476 ± 815 kcal in non-CP controls. Patients suffering from CP showed fewer movement registrations [clinical setting, 228 vs. 298 cpm for obese controls (P = 0.01); out-patient setting, 228 vs. 282 cpm for controls (P = 0.08)]. Differences were most pronounced during leisure time (382 cpm in CP patients vs. 546 cpm in obese controls; P = 0.002; clinical setting). Our findings suggest that reduced physical activity, rather than increased energy intake, in CP patients is responsible for the obesity development noted in these subjects.

	Introduction

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CRANIOPHARYNGIOMA (CP) IS a tumor with borderline histological malignancy and a positive prognosis after complete extirpation. It is located in pituitary and hypothalamic regions and constitutes 1.2% of all brain tumors, with a yearly incidence of 1.3/million. It arises from remnants of Rathke’s pouch along the ductus glossopharyngeus and usually occurs in pediatric patients at the age of 5–14 yr and in adults at 50–74 yr (peak incidences) (1).

About 50% of patients with CP diagnosed during childhood suffer from obesity after tumor extirpation. The exact mechanisms responsible for this phenomenon are still unknown. This complication is more frequent if the tumor infiltrates hypothalamic structures (2). Augmented body energy stored as fatty tissue characterizes obesity. This presupposes a disturbed balance between energy intake and energy expenditure. In healthy subjects, a dynamic system of brain pathways regulates these parameters (3). Many aspects of energy homeostasis affect both the drive to eat and the expenditure of energy (4). Alterations in hypothalamic neuropeptides and cellular mechanisms can be responsible for obesity (5). Their complex neurohormonal consequences are not fully understood. Abnormal behavior or environmental factors may also contribute to primary obesity (6).

Adipose tissue produces leptin proportional to its mass. This hormone binds to hypothalamic receptors and informs the brain about peripheral energy reserves (7). Because of the location and treatment of the lesion in CP patients, they are at risk for disruption of the hypothalamic-adipocyte axis, which might result in disturbed regulation of appetite, leading to hyperphagia (8). Furthermore, we expected energy expenditure in CP patients to be low due to reduced drive and physical activity.

The aim of this study was to identify the mechanisms underlying the development of morbid obesity in patients with CP.

	Subjects and Methods

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Subjects and study groups

All patients with CP were chosen from the German retrospective multicenter study HIT ENDO Kraniopharyngeom (Müller, H. L., Würzburg, Germany, 1999). This study included 125 patients and now continues as a prospective study (KRANIOPHARYNGEOM 2000, www.kraniopharyngeom.com). The local standing committee on ethical practice approved all studies. We obtained written parental or patient informed consent in all cases. All body mass index (BMI) SD scores (SDS) mentioned below refer to the report by Rolland-Cachera et al. (9).

To assess energy intake, we compared 27 patients suffering from CP (8 male and 4 female patients with intrasellar CP, 7 male and 8 female patients with hypothalamic CP) with 1027 controls (487 males and 540 females). We included only patients with an exact magnetic resonance imaging classification of intrasellar vs. hypothalamic CP. The controls were a representative sample from the 7- to 16-yr-old German population, evaluated for nutritional behavior by the Department of Nutritional Psychology, University of Göttingen.

To assess movement counts indicating physical activity, two settings with different groups of patients were included. The first was an out-patient setting of normal daily life. We compared 9 patients with CP (mean age, 19.2 yr; range, 11–23 yr; mean BMI, 2.9 ± 3.0 SDS; range, -0.3 to 8) with 11 controls (mean age, 18.5 yr; range, 12–27 yr; mean BMI, 2.7 ± 2.7 SDS; range, -0.5 to 7.2). The second setting was a clinical one consisting of in-patients at Children’s Hospital Murnau. These patients were studied during a weight reduction program. In the morning, patients went to the clinic’s internal school; in the afternoon, the program was made up of sports and other activities. Ten patients suffered from CP. With the exception of 1 overweight 7-yr-old CP girl with a BMI of 1.5 SDS, all of them were obese (mean age, 13.7 yr; range, 7–20 yr; mean BMI, 4.2 ± 2.1 SDS; range, 1.5–8.6). We compared them with 15 obese control subjects (mean age, 14.1 yr; range, 7–17 yr; mean BMI, 5.2 ± 1.9 SDS; range, 2.1–8.3). In both settings, age, sex, and BMI were comparable between CP patients and controls.

We assessed CP patients for hormonal deficiencies as follows: ACTH/cortisol: ACTH, serum cortisol in the morning, cortisol in 24-h urine, cortisol 1-d profile in saliva; TSH/thyroid hormones: T₃, T₄, TSH basal, and TSH after stimulation; sex hormones: estradiol/testosterone, LH/FSH after LH-releasing hormone stimulation; GH: growth rate, GH after stimulation of less than 10 ng/ml; and antidiuretic hormone (ADH): serum and urine osmolarity.

All out-patients had ADH and ACTH deficiencies. In addition, all but one had deficiencies in GH and TSH. All eight adolescent or adult out-patients had LH/FSH deficiency (not relevant for the one out-patient who was still at prepubertal age). All hospitalized patients exhibited TSH and ADH deficiencies, and all but one had ACTH deficiency in addition. Six patients had poor growth rates and were diagnosed with GH deficiency. All five hospitalized adolescent or adult patients were LH/FSH deficient. Five hospitalized patients were at prepubertal age. We substituted hormonal deficiencies with hydrocortisone, L-T₄, and sexual hormones depending upon bone age and growth prediction. We used testosterone depot (Testoviron, Schering Deutschland GmbH, Berlin, Germany) in male patients and estrogen/gestagen tablets (Presomen compositum, Solvay Arzneimittel GmbH, Hannover, Germany), 1.25 mg conjugated estrogens/d; Cycloprogynova, Schering Deutschland GmbH, 2 mg estradiol valerate/d; Leios, Wyeth Pharma GmbH, Münster, Germany, ethinyl estradiol 0.2 mg/d) in female patients. ADH was given intranasally as arginine vasopressin (Minirin, Ferring Arzneimittel GmbH, Kiel, Germany) or as Minirin tablets. Further substitutions were administered to patients with known GH deficiency (four of six in the clinical setting and five of eight in the out-patient setting; see Table 1).

One-week food intake under normal everyday conditions was reported by a validated nutritional diary (Pudel 1998 Essen und Trinken. Tagebuch für eine Woche. Göttingen: Ernährungspsychologische Forschungsstelle der Universität Göttingen and Bauhaus für Kommunikation GmbH, diary for 1 wk, eating and drinking, developed by Pudel in 1998 at Department of Nutritional Psychology, University of Göttingen, Germany). The Pudel booklet illustrates normal-sized servings of the 156 most common foodstuffs with color photos. Each item of food eaten was indicated in a scale beside these photos. We determined the following parameters: daily energy intake (kilocalories); percentages of carbohydrate, protein, and fat intake; and daily fiber intake representing energy density.

Assessment of movement counts indicating physical activity

Movement counts indicating physical activity were measured by accelerometry (Actiwatch Activity Monitoring System, Cambridge Neurotechnology, distribution in Germany by med-NATIC GmbH, Munich, Germany). To avoid any influence of the monitoring technique on activity, the watch-size device was worn on the dominant wrist.

The out-patient setting assessed movement counts during normal daily life with a free choice of use for 48 h. In the clinical setting, movement counts were measured for 24 h during a weight reduction program at Murnau Children’s Hospital. There, each day consisted of a defined time spent with sports and other activities. We collected each patient’s total average of movement counts. Each time an activity began, patients pressed the button on the Actiwatch and recorded the type of activity in a questionnaire. This allowed us to assess time spent at school/work, sleeping time, and leisure time separately in a second analysis. Leisure time was defined as all time not spent at school/work or sleeping, thus including sedentary activities as well as sports. All measurements were obtained between May and July 2001.

Statistics

Statistical analysis was performed using commercial software programs (Statistica, SAS, SPSS, Chicago, IL; Microsoft-Excel) and was supervised by the department of Statistical Mathematics at University of Göttingen. Results are given as the mean ± SD. Statistical differences between groups were computed by analysis of covariance (significance level, P < 0.05). For the nutritional diaries, data were analyzed by analysis of covariance including the factors age, sex, BMI, and group classification (i.e. intrasellar craniopharyngioma, hypothalamic craniopharyngioma, or controls). For accelerometry data, influence of age and BMI (covariables) as well as sex and group classification (factors) were analyzed.

	Results

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Nutritional diaries

Overall, 48% of CP patients included in this part of the study filled in the nutritional diary. We found significant differences between the groups for total energy intake (P = 0.002): In 12 patients suffering from intrasellar CP, daily energy intake was 1916 ± 677 kcal. In 15 patients suffering from hypothalamic CP, daily energy intake was 2075 ± 877 kcal. In controls, daily energy intake was 2476 ± 815 kcal. In all groups, younger children’s energy intake was significantly lower (P = 0.001). There was no significant influence on energy intake for sex, group and sex, or BMI. The influence on percentage of fat intake was significant for the factor group only (P = 0.0007): mean fat intake was 35.0% of total energy intake (intrasellar CP) vs. 33.0% (hypothalamic CP) vs. 37.9% (controls). Mean intake of carbohydrates was 50.9% (intrasellar CP) vs. 53.6% (hypothalamic CP) vs. 51.6% (controls). Influence on carbohydrate intake was significant for age (P = 0.005, with younger children showing higher percentage of carbohydrates) and BMI (P = 0.002, higher percentage of carbohydrates in children with lower BMI). Mean protein intake was 15.3% (intrasellar CP) vs. 13.9% (hypothalamic CP) vs. 14.5% (controls). Influence on protein intake was significant only for BMI (P < 0.0001, higher percentage of proteins correlated with higher BMI). Mean fiber intake was 17.6 g/d (intrasellar CP) vs. 18.5 g/d (hypothalamic CP) vs. 19.8 g/d (controls). None of the analyzed factors significantly influenced dietary fiber intake. Table 2 compares these results.

The results are summarized in Table 3. Patients suffering from CP showed significantly less movement registrations. In the clinical setting during weight reduction (n = 25), CP patients’ 24-h average was 228 cpm compared with 298 cpm in obese controls (P = 0.01). The difference was particularly obvious during leisure time, including all activities other than school and sleeping (382 cpm in CP patients vs. 546 cpm in obese controls; P = 0.002). At school, the difference was inconspicuous (CP patients, 312 cpm; obese controls, 331 cpm).

Analysis of covariance also revealed a significant influence of age on total movement counts in the ambulatory setting (P = 0.04), with younger subjects showing higher activity levels. Age also significantly influenced movement counts during school in the clinical setting (P = 0.03), with higher activity observed in younger patients. There were no other significant influences; in particular, there was no significant influence of BMI on any category of movement counts.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Up to 52% of patients with craniopharyngioma diagnosed and treated in childhood suffer from obesity as a complication (2). In the current study we assessed possible etiological factors of obesity development in patients with childhood-onset CP. First, we investigated energy intake, which was not augmented. Second, reduced movement counts in accelerometry indicated a reduced physical activity in patients with CP.

For analysis of nutritional diaries, we separated patients with defined intrasellar tumors from patients with hypothalamic tumors. Hypothalamic tumor localization represents a risk factor for obesity in CP patients (2). In a previous study we found evidence for leptin resistance only in CP patients with hypothalamic tumors (8) and therefore assumed a high energy intake, especially in our hypothalamic tumor group. Surprisingly, our results did not demonstrate increased total energy intake in patients with either hypothalamic or intrasellar CP. Energy intake and percentage of fat intake were significantly lower than even those in controls. The low compliance of CP patients (48%) may have constituted a potential bias, although the results from patients who filled in the diary were plausible and consistent. At the time of our retrospective analysis, obesity possibly existed in an already static state. Once manifested in a dynamic phase, obesity does not need further hyperalimentation to persist. Further investigation of this static to dynamic phase in prospective studies might prove interesting. Nevertheless, our present results are consistent with earlier reports of nearly normal caloric intake in patients with hypothalamic obesity and the hypothesis of disturbed expenditure of energy in these patients (10, 11).

For the first time our study documented reduced accelerometric movement counts per minute, indicating lower physical activity in patients with CP compared with controls with comparable BMI. Accelerometry, an objective method with minimal discomfort to assess physical activity, was developed and evaluated by Westerterp in large populations for time periods long enough to represent normal daily activity (12). The method was also used by Tulen et al. (13) and Benefice and Cames (14). Because we wanted to record physical activity during walking as well as in the sitting position without disturbing daily activities, we used motion sensors on the wrist. Accelerometer counts cannot be equated with activity energy expenditure, which differs depending upon body weight. To ensure statistically sound measurements, we tested CP patients and controls for comparability. In this part of the study statistical limitations did not allow us to subdivide CP patients by their tumor localization. Accurate assessment of total energy expenditure, also including resting energy expenditure, by indirect calorimetry would have caused unnecessary discomfort to the patients.

Several factors may explain the reduced physical activity among our patients who had reduced rates of movement counts. Neurological and visual deficits present in some patients may have accounted for a restricted repertoire of movements. In addition, it is conceivable and in some instances probable that complications of CP impact the patient’s physical activity. For example, disturbed melatonin production results in increased daytime sleepiness (15). Infiltration of hypothalamic structures possibly affects the control of somatomotoric programs or neurohormonal balance. Moreover, disturbed regulation among hypothalamus, pituitary, and peripheral hormonal production necessitates diverse hormonal substitution. If the hypothalamic-pituitary-thyroid axis’s substitution by T₄ is insufficient, typical symptoms of hypothyroidism are weariness and weight gain. Hypocortisolism resulting from insufficient substitution of the hypothalamic-pituitary-adrenal axis reduces activity. Overdosing with hydrocortisone, low levels of testosterone, and low levels of GH are all associated with fatigue, a condition that, when chronic, can lead to obesity. In the current study two patients in the clinical setting received hydrocortisone doses above the recommended 15 mg/m²·d. This was necessary to enable them to participate in the weight reduction program that included sports. It is well known that some CP patients have normal growth patterns, although they have GH deficiency (16, 17). More than 6 of 10 patients in the clinical setting may have had GH deficiencies, although invasive tests to determine GH deficiency were not warranted in the patients who grew within the percentiles. All other hormonal deficiencies were adequately supplemented).

In attempt to understand the CP/obesity phenomenon, it is important to bear in mind that hypothalamic regulation also concerns the autonomic nervous system. Sympathetic nervous system activity showed a correlation with spontaneous physical activity (18) and basal metabolism, with a decrease representing a risk factor for obesity (19). Monroe et al. (20) demonstrated a direct influence of sympathetic activity on resting metabolic rate in healthy human adults. Schöfl et al. (21) demonstrated an impairment of counterregulatory sympathoadrenal activation in patients with hypothalamic CP. In a recent study dextroamphetamine stabilized weight gain and improved activity in children who had experienced obesity after surgical resection for CP (22). Defective sympathetic regulation may be one cause of disturbed autonomic system activity. Another cause may be associated with the vagus nerve, the most important pathway of efferent signaling in hypothalamic regulation of energy balance according to Lustig (10). He speculated that disinhibited parasympathetic activity caused by hypothalamic lesions induces postprandial insulin hypersecretion from pancreatic ß cells, resulting in augmented energy storage. He effectively treated some patients suffering from hypothalamic obesity with the somatostatin agonist octreotide. Octreotide blocks the somatostatin receptor, leading to decreased insulin secretion from the ß cell. Treated patients experienced improved insulin response to glucose, weight loss or lack of weight gain, appetite suppression and reduced energy intake, increased reported physical activity, and decreased leptin levels (10).

Based on the findings of our study, reduced physical activity, rather than hyperphagia, appears to be the major factor accounting for obesity in CP patients. Further studies to accurately assess energy homeostasis and responsible autonomic nervous system parameters are warranted. In particular, studies are needed to determine the effects of early administration of drugs, such as dextroamphetamine, that are able to improve sympathetic tone and physical activity (19). Moreover, influences on parasympathetic pancreatic insulin secretion, such as octreotide, warrant further investigation (10). In combination with other effective weight control measures, e.g. physical activity, such drugs may contribute to the effective prevention of obesity in patients treated for childhood craniopharyngioma.

	Acknowledgments

 
We are grateful to M. Lakomek (Göttingen, Germany) for his support of this study, and to M. Neff-Heinrich (Göttingen, Germany) and B. Gohlke (Bonn, Germany) for editing the manuscript.

	Footnotes

 
Abbreviations: ADH, Antidiuretic hormone; BMI, body mass index; CP, craniopharyngioma; SDS, SD score.

Received November 14, 2002.

Accepted July 19, 2003.

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This Article Abstract Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Harz, K. J. Articles by Roth, C. Search for Related Content PubMed PubMed Citation Articles by Harz, K. J. Articles by Roth, C.