Fast Eating Is Associated with Increased BMI among High-School Students

Fast self-reported eating rate (SRER) has been associated with increased adiposity in children and adults. No studies have been conducted among high-school students, and SRER has not been validated vs. objective eating rate (OBER) in such populations. The objectives were to investigate (among high-school student populations) the association between OBER and BMI z-scores (BMIz), the validity of SRER vs. OBER, and potential differences in BMIz between SRER categories. Three studies were conducted. Study 1 included 116 Swedish students (mean ± SD age: 16.5 ± 0.8, 59% females) who were eating school lunch. Food intake and meal duration were objectively recorded, and OBER was calculated. Additionally, students provided SRER. Study 2 included students (n = 50, mean ± SD age: 16.7 ± 0.6, 58% females) from Study 1 who ate another objectively recorded school lunch. Study 3 included 1832 high-school students (mean ± SD age: 15.8 ± 0.9, 51% females) from Sweden (n = 748) and Greece (n = 1084) who provided SRER. In Study 1, students with BMIz ≥ 0 had faster OBER vs. students with BMIz < 0 (mean difference: +7.7 g/min or +27%, p = 0.012), while students with fast SRER had higher OBER vs. students with slow SRER (mean difference: +13.7 g/min or +56%, p = 0.001). However, there was “minimal” agreement between SRER and OBER categories (κ = 0.31, p < 0.001). In Study 2, OBER during lunch 1 had a “large” correlation with OBER during lunch 2 (r = 0.75, p < 0.001). In Study 3, fast SRER students had higher BMIz vs. slow SRER students (mean difference: 0.37, p < 0.001). Similar observations were found among both Swedish and Greek students. For the first time in high-school students, we confirm the association between fast eating and increased adiposity. Our validation analysis suggests that SRER could be used as a proxy for OBER in studies with large sample sizes on a group level. With smaller samples, OBER should be used instead. To assess eating rate on an individual level, OBER can be used while SRER should be avoided.     

Cause and treatment of anorexia nervosa

The hypothesis that eating disorders are caused by an antecedent mental disorder, presently believed to be an obsessive compulsive disorder, has been clinically implemented during many years but has not improved treatment outcome. Alternatively, eating disorders are eating disorders and the symptoms of anorexic patients and probably bulimic patients as well, are epiphenomena which emerge as a consequence of starvation. This hypothesis is supported by the observations of the effects of a 6 month long period of semi-starvation on healthy human volunteers, which demonstrated not only the emergence of psychiatric symptoms but also the reduction in eating rate which is typical of anorexia nervosa patients. On this framework training anorexic patients how to eat may be a useful intervention. We report that anorexic patients, either with a body mass index<14 or >15.5 display the same pattern of eating behavior, with a low level of intake, a slow eating rate and a high level of satiety. They also have the same, high level of psychiatric symptoms, including obsessive compulsive symptoms. Training patients to eat more food at a progressively higher rate reverses these symptoms and patients remain free of symptoms during an extended period of follow-up. It is suggested that the pattern of eating behavior mediates between the starved condition and the psychopathology of anorexia nervosa.     

Linear eaters turned decelerated: Reduction of a risk for disordered eating?

It has been suggested that restrained eating is a cognitive strategy that an individual uses for control of food intake. If losing control, the restrained eater enters a state of disinhibition and is therefore thought to be at risk for developing eating disorders and obesity. Restrained eaters eat at a constant rate and can therefore also be referred to as linear eaters. Here, we have tested the hypothesis that restrained eating is a state that can be modified by teaching linear eaters to eat at a decelerated rate. Seventeen female linear eaters scored high on a scale for restrained eating. When challenged to eat at an increased rate, a test of disinhibition, the women overate by 16% on average. The women then practiced eating at a decelerated rate by use of feedback from a training curve displayed on a computer screen during the meals. The training occurred three times each week and lasted eight weeks. When re-tested in the absence of feedback, the women ate at a decelerated rate, they did not overeat in the test of disinhibition and they scored lower on the scale for restrained eating. It is suggested that restrained eating is a state that can be reduced by training.     

A sex difference in the response to fasting

We determined whether women and men would alter their pattern of food intake after they had deprived themselves of food. We found that women consumed 12% less food after fasting and that men ate 28% more food after fasting. Serving more food on the test day did not increase food intake of women. Women, who ate at a nearly constant rate (linear eaters), consumed less food than those eating at an initially high speed which decreased over the course of the meal (decelerated eaters). Women decreased their food intake after fasting as their eating pattern became more linear. After fasting, men increased their food intake, and the rate at which they ate became more decelerated. Food intake of both women and men was normalized after fasting by providing feedback that encouraged them to eat according to the pattern they showed in the non-fasted condition. The results support the hypothesis that linear eating, and the dieting that elicits linear eating, are risk factors for the development of the abnormal linear eating pattern that characterizes patients with anorexia nervosa. The data also provide additional support for the use of behavioral feedback to normalize the pattern of eating for individuals who have difficulty maintaining their body weight.     

How eating affects mood

IOAKIMIDIS I, M. ZANDIAN, F. ULBL, C. BERGH, M LEON, AND P. S?DERSTEN. How eating affects mood. PHYSIOL BEHAV 2011 (000) 000-000. We hypothesize that the changes in mood that are associated with eating disorders are caused by a change in eating behavior. When food is in short supply, the rhythm of the neural network for eating, including orbitofrontal cortex and brainstem, slows down and we suggest that this type of neural activity activates a partially overlapping neural network for mood, including dorsal raphe serotonin projections to the orbitofrontal and prefrontal cortex. As a consequence, people who restrict the amount of food that they consume, either by choice or by their limited access to food, become preoccupied with food and food-related behavior. Most eating disorders emerge from a history of dietary restriction and we suggest that disordered eating consequent upon food restriction produces the altered mental state of patients with eating disorders. Based on the present hypothesis, eating disorders are not the result of a primary mental disorder. Rather, this notion suggests that the patients should be treated by learning to eat an appropriate amount of food at an appropriate rate.     

Bendamustine therapy in patients with relapsed or refractory Waldenström's macroglobulinemia

We report the treatment outcome for 30 relapsed/refractory Waldenström's macroglobulinemia (WM) patients following bendamustine-containing therapy. Treatment consisted of bendamustine (90 mg/m² I.V. on days 1, 2) and rituximab (375 mg/m² I.V. on either day 1 or 2) for 24 patients. Six rituximab-intolerant patients received bendamustine alone (n = 4) or with ofatumumab (1000 mg I.V. on day 1; n = 2). Each cycle was 4 weeks, and median number of treatment cycles was 5. At best response, median serum IgM declined from 3980 to 698 mg/dL (P < .0001), and hematocrit rose from 31.9% to 36.6% (P = .0002). Overall response rate was 83.3%, with 5 VGPR and 20 PR. The median estimated progression-free survival for all patients was 13.2 months. Overall therapy was well tolerated. Prolonged myelosuppression was more common in patients who received prior nucleoside analogues. Bendamustine is active and produces durable responses in previously treated WM, both as monotherapy and with CD20-directed monoclonal antibodies.     

Factors influencing the quality of life of young patients with diabetes

Background: Diabetes is a significant challenge for pediatric health care professionals because it affects youths’ psychoemotional functioning and, consequently, the quality of life (QOL). The aim of the present study was to evaluate the QOL in young patients with diabetes, as well as the factors affecting it. Methods: The study was conducted from April to September 2008 in 98 young patients, 11–18 years of age, who were under the supervision of Diabetological Center, General Pediatric Hospital (Athens, Greece). The Diabetes Quality of Life for Youths Questionnaire was used to evaluate the QOL of youths with diabetes. Results: The mean QOL score was 97.5. There was a negative correlation between the QOL and age (P = 0.02), the duration of diabetes (P = 0.05), body mass index (BMI; P = 0.04), and comorbidities (P = 0.03). In contrast, there was a positive correlation between QOL and increased metabolic control (P = 0.03), participating in sports activities (P = 0.007), and a greater number of insulin infusions (P = 0.04). Conclusions: The QOL of young diabetics was influenced by demographic, somatometric, and other characteristics of diabetes. Increased metabolic control, participating in sports activities, and a greater number of insulin infusions resulted in better QOL. Increased patient age, duration of diabetes, HbA1c values, BMI, and the coexistence of various health problems, as well as the use of an insulin pump, decreased QOL.     

Histone deacetylase inhibitors demonstrate significant preclinical activity as single agents, and in combination with bortezomib in Waldenström's macroglobulinemia

We studied the role of histone deacetylase inhibitors in Waldenstrom's macroglobulinemia (WM). Gene expression profiling of bone marrow CD19+ cells from 30 patients and 10 healthy donors showed overexpression of HDAC4, HDAC9, and Sirt5, with validation of HDAC9 overexpression by q-PCR in primary and BCWM.1 cells. Suberoylanilide hydroxamic acid, trichostatin A, panobinostat, and sirtinol demonstrated dose-dependent killing of BCWM.1 cells. TSA showed the greatest potency with IC50 of 70 nM. Importantly, HDAC9 activity was decreased following TSA treatment suggesting an essential role for this HDAC in WM therapy. The combination of bortezomib plus HDAC inhibitors resulted in at least additive tumor cell killing in BCWM.1 cells. TSA and bortezomib-induced apoptosis depended on a similar set of caspase activation, whereas their effect on cell cycle regulators was distinctly different. These results provided a framework for examining HDAC inhibitors as monotherapy, as well as combination therapy with bortezomib in WM.     

IgA and IgG hypogammaglobulinemia in Waldenstr?m’s macroglobulinemia

Background

Hypogammaglobulinemia is common in Waldenström’s macroglobulinemia. The etiology of this finding remains unclear, but it has been speculated to be based on tumor-induced suppression of the ‘uninvolved’ immunoglobulin production

Design and Methods

We evaluated the incidence of IgA and IgG hypogammaglobulinemia in 207 untreated patients with Waldenström’s macroglobulinemia and investigated the associated clinicopathological findings and impact of therapy. We also sequenced eight genes (AICDA, BTK, CD40, CD154, NEMO, TACI, SH2D1A, UNG) implicated in immunoglobulin deficiency in 19 Waldenström’s macroglobulinemia patients with IgA and/or IgG hypogammaglobulinemia.

Results

At baseline 63.3%, 58.0% and 49.3% of the 207 patients had abnormally low serum levels of IgA, IgG, or both. No association between IgA and IgG hypogammaglobulinemia and disease burden, serum IgM levels, β₂-microglobulin, International Prognostic Scoring System score, or incidence of recurrent infections was observed, although the presence of adenopathy and/or splenomegaly was associated with a lower incidence of hypogammaglobulinemia. Lower IgA and IgG levels were associated with disease progression in patients managed with a ‘watch and wait’ strategy. IgA and/or IgG levels remained abnormally low despite response to treatment, including complete remissions. A missense mutation in the highly conserved catalytic site of UNG was observed in a patient with hypogammaglobulinemia, warranting further study of this pathway in Waldenström’s macroglobulinemia.

Conclusions

IgA and IgG hypogammaglobulinemia is common in Waldenström’s macroglobulinemia and persists despite therapeutic intervention and response. IgA and IgG hypogammaglobulinemia does not predict the risk of recurrent infections in patients with Waldenström’s macroglobulinemia, although lower levels of serum IgA and IgG are associated with disease progression in Waldenström’s macroglobulinemia patients being managed with a ‘watch and wait’ strategy.     

Osseous metaplasia: case report and review

OBJECTIVE: To discuss, through the experience of a case report and extensive literature review, the best practices for the diagnosis and treatment of osseous metaplasia, which is the cause of secondary infertility. DESIGN: Case report. SETTING: In vitro fertilization unit in Athens. PATIENT(S): A 40-year-old woman with a 10-year history of secondary infertility. INTERVENTION(S): Hysteroscopic diagnosis and removal of the bony fragment. MAIN OUTCOME MEASURE(S): Elimination of secondary infertility caused by osseous metaplasia. RESULT(S): After treatment, the woman underwent an IVF program and a healthy neonate was born with cesarean section. CONCLUSION(S): Hysteroscopy remains the best practice for the diagnosis and removal of endometrial ossifications, causing secondary infertility.