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Biomedical subjects

J Hebebrand

Publications and source records attributed to J Hebebrand.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Body height, body weight and body mass index of German military recruits. Historical retrospect and current status].

Surveys of conscripts give a chance to pursue the somatic development and the nourishment situation of young men over long times. At the beginning a historical view is given of the organization and methodological basis of medical examinations of German recruits since the introduction of the general conscription at the beginning of the 19th century. Secular changes of the body height are sketched out for selected regions of Germany until the middle of the 20th century. Data of the body weight hardly exist for this time. Until now the greatest continuous documentation of data for body height and body weight is available for West Germany since 1957 and for East Germany between 1973 and the reunion in 1989. The body height of German conscripts has nearly permanently increased since 1957 and reached in 1994 a maximum with 180.0 cm. In general East German conscripts have body height data which are smaller on an average than those of West German conscripts. But in the last years a catch-up in body height could be seen. The body weight of German conscripts also shows an increase apart from some short-time exceptions. The data of West German conscripts are also higher than those of the East German conscripts. Until the reunion the West-East-differences could partly be due to the different mustering age. But the differences also continue in the nineties despite the now identical mustering age. The Body Mass Index (BMI) of the German conscripts (calculated from the average values of body height and body weight) is characterized by increments in the last years. This indicates greater changes in body weight than in body height. The BMI also shows marked West-East-differences. There is no uniform tendency in differences between urban and country side regions for body height and body weight. On the other hand until now differences between selected professional groups are existing. Especially the over-proportional increase of the number of conscripts in the higher body-weight-classes requires a further continuous analysis of the available mustering data.

Adolescent↗
PubMed2000

Candidate gene polymorphisms in eating disorders.

Anorexia nervosa and bulimia nervosa are complex disorders characterized by disordered eating behaviour. Attitudes towards weight and shape as well as the perception of body shape are disturbed. A substantial genetic influence on these disorders has been suggested by formal genetic studies. Obsessive-compulsive behaviour, perfectionism and anxious personality traits seem to occur premorbidly in several patients. Disturbances of neurotransmitter, neuropeptide and neuroendocrine systems have been reported in acutely ill and followed-up patients. Hence, these systems might be involved in the etiology of these eating disorders.Genetic studies on candidate genes have mainly focussed on the serotonergic system and on genes involved in body weight regulation. Up to now, polymorphisms and variations in various genes (e.g. genes for 5-HT receptors, leptin gene, melanocortin MC(4) receptor gene) have been assessed for association and transmission disequilibrium pertaining to anorexia nervosa and/or bulimia nervosa. Most of the studies yielded negative results. Four studies of a polymorphism (-1438 G/A) within the promoter of the 5-HT(2A) gene (5-HT(2A)) revealed an association of the A-allele to anorexia nervosa. However, three studies could not confirm this result. Furthermore, a meta-analysis did not support the positive association. Currently, combined efforts within the European Union will answer the question of whether or not the A-allele is involved in the predisposition to anorexia nervosa. A transmission disequilibrium test is being performed in about 300 trios consisting of a patient with anorexia nervosa and both parents. As candidate gene approaches did not unequivocally identify susceptibility genes (alleles) for anorexia nervosa or bulimia nervosa, systematic model-free genome-wide screenings should also be performed in order to identify currently unknown genes involved in eating disorders. This kind of approach has already been initiated for anorexia nervosa. Genetic research on eating disorders will hopefully lead to new pharmacological treatment strategies.

Animals↗
PubMed2000

Complex segregation analysis of families ascertained through Gilles de la Tourette syndrome.

Although family and twin studies suggest that genetic factors are involved in the etiology of Tourette syndrome and other related tic disorders, further evidence is needed to demonstrate that the familial transmission is consistent with known genetic factors. We performed a complex segregation analysis that allowed for a variable age of onset of Gilles de la Tourette, other tic disorders and obsessive compulsive phenotype information on 108 extended families, each ascertained through one Tourette proband by using regressive models that are able to incorporate additional explanatory variables and major gene effects. A special version of the S.A.G.E. program, REGTLhunt, was used to explore the likelihood surface of all examined models. Results indicated that the pattern of Tourette and other related tic disorders in our data sample is not consistent with Mendelian inheritance even after modelling explanatory variables such as obsessive compulsive symptomatology.

Adolescent↗
PubMed2000

Significant association between a silent polymorphism in the neuromedin B gene and body weight in German children and adolescents.

Neuromedin B has been shown to exert an inhibiting effect on food consumption in rats. The corresponding gene NMB maps to chromosome 15q22.3-q23, a region expected to contain a gene for the Bardet-Biedl syndrome type 4 (BBS4). Based on its map position and the putative function of the encoded peptide, NMB can be considered as a candidate gene both for BBS4 and the development of human obesity. To examine its involvement in these phenotypes, we determined the genomic structure of human NMB, and performed a mutation screen in its coding region. In genomic DNA of six BBS4 patients and in a large population sample, two sequence variants were detected: a g.253C-->A transversion creating a P73T substitution and a g.401G-->A silent mutation changing the stop codon TGA into stop codon TAA. A case-control study with 92 extremely obese patients and 94 underweight students revealed a significant association between the g.401G-->A polymorphism and body weight (adjustedp = 0.03), which was confirmed in a validation sample consisting of 95 extremely obese patients, and 95 normal weight and 48 underweight individuals (Mann-Whitney p = 0.02). These results suggest a contribution of NMB or a gene in its close vicinity to genetic weight control in humans.

Adolescent↗
PubMed2000

["Cyclic vomiting" in childhood and adolescence].

The clinical picture of the "cyclical vomiting syndrome" is discussed in the case of a 5 1/2-year-old child. The core symptom of this recurrent disorder is vomiting that occurs in regular cycles and while the patient is in a state of complete well-being, and which is hard to influence. The symptoms, the differential diagnosis, and the therapy of this disorder, which occurs primarily in childhood, are discussed along with the close etiological relationship to infantile migraine. The diagnosis of "psychogenic vomiting" is addressed critically, since it is frequently applied in Germany to disorder pictures that are similar to cyclical vomiting.

Adrenergic Uptake Inhibitors↗
PubMed2000

Epidemic obesity: are genetic factors involved via increased rates of assortative mating?

OBJECTIVE: Prevalence rates of obesity have been increasing in several countries over the past two decades. Mainly secular changes in energy intake and expenditure have been invoked to underly the increasing rates; genetic factors have not been considered because of the very recency of this phenomenon. We hypothesize that genetic factors might very well be involved via an increased rate of assortative mating between obese individuals. We speculate that the recent upsurge in social stigmatization of obese individuals underlies the hypothesized increase in assortative mating. DESIGN: To accumulate evidence for our hypothesis we analysed deduced rates of assortative mating among parents of extremely obese children and adolescents, who belonged to two different large study groups (n = 201 and n = 270). For this purpose we calculated parental body mass indices (BMIs) based on (a) measured current heights and weights, (b) self-reported current heights and weights, and finally (c) measured current heights and recalled weights at ages 20 and 30, respectively. BMI centiles were determined which in turn were attributed to the respective BMI decile. Deduced rates of assortative mating were evaluated in bivariate histograms of the paternal and maternal BMI deciles. RESULTS: High rates of assortative mating were observed as deduced from the bivariate histograms, which revealed a fairly consistent pattern. Thus, in the first study group almost 35% of the parental pairs had a BMI in the tenth decile; over 50% of the mothers and fathers had a BMI in this top decile. Recalled parental BMIs at ages 20 and 30 also clustered in the upper decile. These results were basically replicated in the second study group. In addition, parental loading on the tenth decile was shown to be higher for the subgroup of children and adolescents who had a BMI equal to or exceeding the highest BMI of the population-based age and gender matched control group. CONCLUSIONS: Our results indicate that assortative mating is common among parents of extremely obese children and adolescents, ascertained between 1995 and 1997. In addition, the parental loading on the tenth decile is most prominent for the most obese children. Whereas we are unable to document an increased rate of assortative mating, we interpret our results as being consistent with the hypothesis that an increased rate of assortative mating has contributed to the recent rise in obesity rates in several countries. Thus, assortative mating warrants further studies to assess its impact on obesity prevalence rates through both genetic and non-genetic mechanisms. Our results suggest that assortative mating might especially increase the rates for extreme obesity.

Adolescent↗
PubMed2000

Rates of psychiatric disorders in a clinical study group of adolescents with extreme obesity and in obese adolescents ascertained via a population based study.

OBJECTIVE: To compare rates of DSM-IV psychiatric disorders between (1) a clinical study group of extremely obese adolescents and young adults, (2) gender-matched population-based obese controls and (3) a population-based control group of the same age range. DESIGN: Rates of psychiatric disorders were assessed in (1) the clinical study group of obese adolescents and (2) the population based sample of obese adolescents, and compared to (3) a large population-based control group using a standardized psychiatric interview. SUBJECTS: (1) Clinical study group: 30 female and 17 male extremely obese adolescents and young adults (age range: 15-21 y; mean BMI:42.4 kg/m2). (2) Thirty females and 17 males with the highest BMI (age range 15-21 y; mean BMI: 29.8 kg/m2) of a population-based control group encompassing 1655 (805 males) adolescents and young adults. (3) The population based control group excluding the 30 females and 17 males with the highest BMI (n = 1608; 788 males). MEASUREMENTS: Munich-Composite International Diagnostic Interview (M-CIDI) allowing for DSM-IV diagnoses. RESULTS: High rates of mood, anxiety, somatoform and eating disorders were detected in the clinical sample of obese adolescents which exceeded those observed in population controls (all P-values < 0.01). Rates between population-based obese adolescents and young adults and population controls did not differ. In most patients the psychiatric disorders set in after onset of obesity. 57% and 35% of the female and male patients, respectively, reported eating binges with lack of control. However, less than one-half of these patients qualified for a DSM-IV diagnosis of an eating disorder. CONCLUSIONS: Extremely obese adolescents and young adults who seek long-term inpatient treatment have a high lifetime prevalence for affective, anxiety, somatoform and eating disorders. Because the mean BMI of the clinical study group was considerably higher than that of the obese population controls, we were not able to clarify whether the high rate of psychopathology in the study group was related to the extreme obesity or to their treatment-seeking behavior.

Adipose Tissue↗
PubMed2000

Leptin suppresses semi-starvation induced hyperactivity in rats: implications for anorexia nervosa.

Semi-starvation induced hyperactivity (SIH) occurs in rodents upon caloric restriction. We hypothesized that SIH is triggered by the decline in leptin secretion associated with food restriction. To test this hypothesis, rats, which had established a stable level of activity, were treated with leptin or vehicle via implanted minipumps concomitantly to initiation of food restriction for 7 days. In a second experiment treatment was initiated after SIH had already set in. In contrast to the vehicle-treated rats, which increased their baseline activity level by 300%, the development of SIH was suppressed by leptin. Furthermore, leptin was able to stop SIH, after it had set in. These results underscore the assumed major role of leptin in the adaptation to semi-starvation. Because SIH has been viewed as a model for anorexia nervosa, we also assessed subjective ratings of motor restlessness in 30 patients with this eating disorder in the emaciated state associated with hypoleptinemia and after increments in leptin secretion brought upon by therapeutically induced weight gain. Hypoleptinemic patients ranked their motor restlessness higher than upon attainment of their maximal leptin level during inpatient treatment. Thus, hypoleptinemia might also contribute to the hyperactivity frequently associated with anorexia nervosa.

Animals↗
PubMed2000

Time relationship between circadian variation of serum levels of leptin, insulin and cortisol in healthy subjects.

BACKGROUND: Leptin is involved in the regulation of eating behavior. Its serum levels are determined by fat mass but a diurnal rhythm is also described. It is not clear whether leptin levels are also controlled in vivo by hormonal stimuli, like insulin or cortisol. METHODS AND RESULTS: This possible temporal relation was investigated by serial measurements during 24 h (group A) and 46 h (group B) in 15 healthy volunteers and another 10 subjects (group C) while fasting for 72 h. Maximal leptin levels were observed at 4:00 a.m. and 4:00 p.m. in subjects on a normal diet. During 24 h starvation (group B), there was a 40% decrease of mean leptin concentration when compared to baseline values. In group C, the leptin concentration under starvation dropped to 25% of basal levels after 72 h. Pooled data from group A and the nonfasting data from group B showed an insulin increase preceding leptin increase by 6 h (r = 0.405, p < 0.0001), while cortisol decreased 4 h (r = 0.361, p < 0.001) after leptin decrease. CONCLUSION: Starvation results in a fall of circulating leptin, ending leptin rhythmicity. Food intake is causally involved in the fluctuation of leptin levels in serum. Presumably this effect is mediated by insulin, while cortisol does not seem to affect leptin release directly in vivo.

Circadian Rhythm↗
PubMed2000

Independent confirmation of a major locus for obesity on chromosome 10.

Linkage results obtained in genome-wide scans for complex phenotypes require confirmation in independent samples. Recently, linkage of obesity to chromosome 10p12 with a maximal multipoint LOD score of 4.85 was reported upon use of an affected sib-pair approach including nuclear families in which the adult index case had a BMI > or = 40 kg/m2 and at least one further sibling had a BMI > or = 27 kg/m2 (Hager et al., 1998, Nat Genet 20:304-8). To attempt to replicate this linkage finding we genotyped 11 markers spanning approximately 23 cM from 10p13 to 10ql1 in a total of 386 individuals stemming from 93 nuclear families with two or more young obese offspring with a BMI > or = 90th age percentile. The highest multipoint maximum likelihood binomial (MLB) LOD score using the extreme concordant sib-pair approach in which one sib had a BMI > or = 95th percentile, and other sibs a BMI > or = 90th percentile was 2.32. Six markers yielded nominal p-values < 0.05, the highest two point MLB-LOD score of 2.45 (nominal p = 0.0004) was obtained for the marker TCF8. Transmission disequilibrium tests for the most frequent parental allele yielded no nominal p-value < 0.05. The linkage results confirm the presence of a major susceptibility locus for obesity in a region near the centromere on chromosome 10.

Adult↗
PubMed2000

Longitudinal changes of circadian leptin, insulin and cortisol plasma levels and their correlation during refeeding in patients with anorexia nervosa.

OBJECTIVE: To study the longitudinal changes in plasma levels of leptin, insulin and cortisol during the transition from the state of starvation to the state of refeeding focussing on diurnal secretion characteristics and their temporal relationships. DESIGN: Leptin, insulin and cortisol were measured every 2h for 24h during acute starvation (T1). Sampling was repeated after reaching half the target-body mass index (BMI) (T2) and again at target-BMI (17. 5kg/m(2); T3). The temporal relationships between the diurnal secretion patterns were assessed by cross-correlation analysis. RESULTS: Although BMIs at T1 were uniformly low, leptin levels varied widely within a range clearly below normal levels (0.03-1. 7microg/l). With increasing body fat during the course of refeeding, mean leptin levels increased from 0.64microg/l (range: 0.27-1. 73microg/l) (T1) to 1.61microg/l (range: 0.36-4.2microg/l) (T2) and to 3.67microg/l (range: 0.7-9.8microg/l) (T3). Circadian leptin secretion patterns showed maximal values uniformly around 0200h and minimal values around 0800h at all stages of the study. At all three weight levels, plasma leptin levels were highest between midnight and the early morning hours and lowest around the late morning hours. Refeeding neither profoundly changed secretion patterns of leptin nor did it change the positive, time-delayed relationship between leptin and insulin with increments in insulin secretion preceding those of leptin by 6h. A temporal relationship between leptin and cortisol could not be demonstrated in the state of semistarvation but emerged after a substantial weight gain; at that time, leptin increases preceded cortisol increases by 8h. CONCLUSIONS: Absolute leptin, insulin and cortisol levels are profoundly changed during starvation in anorectic patients, while refeeding, paralleled by a BMI gain, reverses these changes. During refeeding the relationship between leptin and cortisol changed profoundly, showing no significant correlation in the state of starvation, whereas at T3 after refeeding a strong inverse relationship could be observed. Leptin and insulin did not correlate significantly at any of the three stages studied.

Adult↗
PubMed2000

Resting metabolic rate, body composition, and serum leptin concentrations in a free-living elderly population.

OBJECTIVE: The present study investigated the relationship between serum leptin concentrations and resting metabolic rate (RMR) in a large study group of elderly individuals with special consideration of body composition and body fat distribution as possible confounders. DESIGN AND METHODS: The subjects were 122 women (age: 69+/-6 years, body mass index (BMI): 26.3+/-3.6 kg/m(2)) and 82 men (age: 69+/-5 years, BMI: 26.0+/-2.6 kg/m(2)). RMR was measured by indirect calorimetry and body composition by the bioelectrical impedance method. Serum leptin levels were determined by radioimmunoassay. RESULTS: There was a strong correlation between fat mass (FM) and serum leptin levels in both sexes. An age-related decline in leptin levels adjusted for FM was observed only in the women. After adjustment of RMR for both fat-free mass (FFM) and FM, leptin levels were not associated with RMR. In stepwise multiple regression analysis, FFM was the main predictor of RMR, explaining 35.8% and 47.6% of the variance of RMR in men and women respectively. FM did not explain variance in RMR in men, but accounted for 2.6% of the variance in RMR in women. Waist-hip-ratio and age influenced RMR only in males, explaining 5.7% and 4.0% of the variance in RMR respectively. CONCLUSION: Leptin is not a significant predictor of RMR in the elderly, but body composition and distribution of body fat are significantly associated with RMR.

Age Factors↗
PubMed1999

No evidence for involvement of polymorphisms of the dopamine D4 receptor gene in anorexia nervosa, underweight, and obesity.

Family and twin studies suggest a genetic contribution to the etiology of anorexia nervosa (AN) and obesity. Genes involved in weight regulation can be considered as candidate genes for AN. The dopaminergic system has been implicated in weight regulation; previous results had suggested a possible involvement of the dopamine D4 receptor gene (DRD4). We screened for alleles of two different polymorphisms (13-bp deletion, 48-bp repeat) in the DRD4. For association tests, allele frequencies were compared between 109 inpatients with AN, 82 underweight students, and 327 extremely obese children and adolescents. For application of transmission disequlibrium tests (TDT) we additionally genotyped 57 and 137 trios comprising a patient with AN or an extremely obese child or adolescent, respectively, and both parents. All genotyping was performed with polymerase chain reaction fragment length polymorphism analyses. None of the association tests or TDT rendered nominal P values below 0.1. An influence of alleles of the DRD4 on the development of AN, underweight, or extreme early onset obesity was not detected. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:594-597, 1999.

Adolescent↗
PubMed1999

Tourette syndrome and the norepinephrine transporter gene: results of a systematic mutation screening.

Tourette syndrome (TS) is a complex inherited neuropsychiatric disorder characterized by multiple motor and phonic tics. Involvement of central norepinephrine mechanisms is suggested by central norepinephrinic hyperactivity in patients with TS and by the therapeutic effects of the presynaptic alpha2-adrenergic agonist clonidine. The norepinephrine transporter gene (NET) was systematically screened by single-strand conformation analysis for genetic variants, including the whole coding region and adjacent exon-intron boundaries in 43 patients with TS and 46 healthy controls. We detected 12 DNA sequence variants, among them four missense mutations (Val69Ile, Thr99Ile, Va1245Ile, and Gly478Ser). The observed missense mutations may alter conformational rearrangements during gating of the transporter, assembly of subunits, and norepinephrine-specific uptake affinity. Allele frequency and genotype distribution of the genetic variants showed no differences between TS patients and controls. No mutation of likely functional significance was found that distinguished TS patients from healthy controls, indicating that genetic variants of the NET gene are not causally related to Tourette syndrome.

Adolescent↗
PubMed1999

The relationship between premorbid body weight, weight loss, and weight at referral in adolescent patients with anorexia nervosa.

OBJECTIVE: The purpose of this study was to investigate the relationship between premorbid weight and weight upon referral for inpatient treatment in patients with anorexia nervosa (AN). METHOD: Forty-nine consecutively ascertained female inpatients with AN were asked to recall their premorbid body weights as well as their ages at onset of the illness. Premorbid body mass indexes (BMIs) and BMI percentiles were calculated for 42 of the patients and related to the BMIs upon initial referral for inpatient treatment. RESULTS: Low premorbid BMI centiles were associated with a low BMI at referral. Vice versa, patients with an above average premorbid body weight had a higher BMI at referral. The largest absolute weight losses also occurred in those patients who had an above average premorbid body weight. DISCUSSION: In conclusion, premorbid body weight explains a proportion of the variance of body weight at referral.

Adolescent↗