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Web-based preventive interventions can reduce risk and incidence of bulimia and binge eating disorders among young high-risk women. However, their specific effects on core symptoms of anorexia nervosa (AN) are rather weak. The primary objective of this study was to evaluate the efficacy of an indicated, parent-based, Web-based preventive program Eltern als Therapeuten (E@T) in reducing risk factors and symptoms of AN. Girls aged between 11 and 17 years were screened by selected risk factors and early symptoms of AN. At-risk families were then randomized to E@T or an assessment-only control condition. Assessments took place at pre- and postintervention (6 weeks later) and at 6- and 12-month follow-up (FU). A total of 12,377 screening questionnaires were handed out in 86 German schools, and 3941 including consent returned. Overall, 477 (447/3941, 12.10%) girls were identified as at risk for AN and 256 of those could be contacted. In all, 66 families (66/256, 25.8% of those contacted) were randomized to the E@T or a wait-list control condition, 43 (43/66, 65%) participated in postassessments, and 27 (27/66, 41%) in 12-month FUs. Due to low participation and high dropout rates of parents, recruitment was terminated prematurely. At 12-month FU, girls' expected body weight (EBW) percentage was significantly greater for intervention participants compared with control participants (group by time interaction beta=21.0 [CI 5.81 to 36.13], P=.007; group by time squared interaction beta=-15.5 [CI -26.6 to -4.49], P=.007; estimated Cohen d=0.42]. No other significant effects were found on risk factors and attitudes of disturbed eating. Despite a significant increase in girls' EBW percentage, parental participation and adherence to the intervention were low. Overall, parent-based, indicated prevention for children at risk for AN does not seem very promising, although it might be useful for parents who engage in the intervention. International Standard Randomized Controlled Trial Number (ISRCTN): 18614564; http://www.isrctn.com/ISRCTN18614564 (Archived by WebCite at http://www.webcitation.org/74FTV1EpF).

Hormonal contraceptives may produce side effects that deter women from their use as a method of family planning. In nutritionally vulnerable populations these effects may be more pronounced due to micronutrient deficiencies and health status. Previous studies have been unable to resolve whether micronutrient supplementation may reduce such side effects. Aim: In a longitudinal study, 1011 women obtaining oral contraception through the public health system in rural Cambodia were allocated to either intervention or control groups, receiving either daily Vitamin B6 supplement or care as usual (without placebo). Results: The intervention participants (n = 577) reported fewer side effects in three categories: nausea/no appetite, headache, and depression compared with control group participants (n = 434). Conclusion: Women taking Vitamin B6 supplement were less likely to report side effects in a nutritionally vulnerable population. Underlying nutrition status should be considered by clinicians and reproductive health policy makers in the context of providing contraceptive services. Further investigation into micronutrient supplementation, particularly with B6, in reproductive-aged women using hormonal contraception should be conducted in other settings to determine the potential for widespread adoption.

Loss of appetite or anorexia associated with inflammation impairs quality of life and increases morbidity in many diseases. However, the exact neural mechanism that mediates inflammation-associated anorexia is still poorly understood. Here we identified a population of neurons, marked by the expression of protein kinase C-delta, in the oval region of the bed nucleus of the stria terminalis (BNST), which are activated by various inflammatory signals. Silencing of these neurons attenuates the anorexia caused by these inflammatory signals. Our results demonstrate that these neurons mediate bidirectional control of general feeding behaviors. These neurons inhibit the lateral hypothalamus-projecting neurons in the ventrolateral part of BNST to regulate feeding, receive inputs from the canonical feeding regions of arcuate nucleus and parabrachial nucleus. Our data therefore define a BNST microcircuit that might coordinate canonical feeding centers to regulate food intake, which could offer therapeutic targets for feeding-related diseases such as anorexia and obesity. Inflammation can reduce food intake. Here the authors show that the GABAergic pathway from bed nucleus of stria terminalis to lateral hypothalamus regulates the inflammation induced reduction in feeding in mice.

During the past decades, malnutrition has attracted increasing scientific attention and is by now regarded as a true geriatric syndrome characterized by multifactorial causality, identified by symptoms and accompanied by frailty, disability and poor outcome. This viewpoint summarizes our present knowledge and the usual current handling of malnutrition in older people and highlights the urgent need for action in this field. Age-related changes in the complex system of appetite regulation, resulting in the so-called anorexia of aging, predispose older adults to a decrease in food intake which may lead to malnutrition, if additional risk factors like health or social problems occur. Consequently, malnutrition is widespread in the older population, notably in those who are institutionalized. Despite the fact that effective interventions are available, prevention and treatment of malnutrition do not currently receive appropriate attention. As an important first step towards better awareness, screening for malnutrition should become a mandatory integral part of the comprehensive geriatric assessment. Furthermore, practical local guidelines should be implemented in all geriatric hospital wards and nursing homes in order to improve nutritional care in the daily routine. Important to note is that reasonable nutritional management is not possible without qualified staff in adequate numbers allowing appropriate individual nutritional care. Regarding future research, studies at the cellular, metabolic and clinical levels and the linking of information from different research approaches are required to better understand the transition from good nutritional health and independence of old people to malnutrition, functional impairment and poor health. In parallel to well-designed observational and intervention studies, standardized documentation of nutritional information in daily routine would enable the uniform collection of data for research as well as for political decisions. In summary, the time is ripe for better inclusion of nutrition in geriatric health care. This will not only bring about improved nutritional status and outcome, and thus individual benefit for the affected person, but also economic benefits both for the institution and the health-care system.

Enough is enough Appetite is regulated — at least in part — in the hypothalamus, the brain region that links the nervous and endocrine systems. A screen for appetite-regulating molecules has now identified a fragment of the protein nucleobindin 2, dubbed nesfatin-1, as a satiety molecule produced in the hypothalamus. When nesfatin-1 is injected into the brain, rats eat less and lose weight. When nesfatin-1 is blocked, animals eat more. Nesfatin-1 is therefore a possible target for antiobesity drugs. A secreted protein, nesfatin-1, is expressed in the hypothalamus and induces the feeling of being full. In rats, its injection into the brain decreases food intake, but blocking its action stimulates appetite. The brain hypothalamus contains certain secreted molecules that are important in regulating feeding behaviour 1 , 2 , 3 . Here we show that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats. Intracerebroventricular (i.c.v.) injection of NUCB2 reduces feeding. Rat cerebrospinal fluid contains nesfatin-1, an amino-terminal fragment derived from NUCB2, and its expression is decreased in the hypothalamic paraventricular nucleus under starved conditions. I.c.v. injection of nesfatin-1 decreases food intake in a dose-dependent manner, whereas injection of an antibody neutralizing nesfatin-1 stimulates appetite. In contrast, i.c.v. injection of other possible fragments processed from NUCB2 does not promote satiety, and conversion of NUCB2 to nesfatin-1 is necessary to induce feeding suppression. Chronic i.c.v. injection of nesfatin-1 reduces body weight, whereas rats gain body weight after chronic i.c.v. injection of antisense morpholino oligonucleotide against the gene encoding NUCB2. Nesfatin-1-induced anorexia occurs in Zucker rats with a leptin receptor mutation, and an anti-nesfatin-1 antibody does not block leptin-induced anorexia. In contrast, central injection of α-melanocyte-stimulating hormone elevates NUCB2 gene expression in the paraventricular nucleus, and satiety by nesfatin-1 is abolished by an antagonist of the melanocortin-3/4 receptor. We identify nesfatin-1 as a satiety molecule that is associated with melanocortin signalling in the hypothalamus.

D-methionine is a sulfur-containing amino acid that can act as a potent antioxidant. Anorexia and nephrotoxicity are side effects of cisplatin. The protective effects of D-methionine on cisplatin-induced anorexia and renal injury were investigated. The model of chronic cisplatin administration (5 mg/kg body weight) involved intraperitoneal injection on days 1, 8, and 15 and oral D-methionine (300 mg/kg body weight) coadministration daily for 20 days. On the 21st day of treatment, food intake and body weight in the cisplatin-treated group significantly decreased by 52% and 31%, respectively, when compared with a control group. D-methionine coadministration with cisplatin decreased food intake and body weight by 29% and 8%, respectively. In cisplatin-treated rats, white blood cell, mean corpuscular volume, and platelet values significantly decreased, while mean corpuscular hemoglobin concentration significantly increased by 8.6% when compared with control rats. Cisplatin administration resulted in significantly decreased feeding efficiency, elevated renal oxidative stress, and reduced antioxidative activity. Leukocyte infiltration, tubule vacuolization, tubular expansion, and swelling were observed in the kidneys of cisplatin-treated rats. Oral D-methionine exhibited an antianorexic effect, with improvement in food intake, feeding efficiency, and hematological toxicities, as well as a protective effect against nephrotoxicity by elevated antioxidative activity. D-methionine may serve as a chemoprotectant in patients receiving cisplatin as part of a chemotherapy regimen.

Loss of muscle mass related to anti-cancer therapy is a major concern in cancer patients, being associated with important clinical endpoints including survival, treatment toxicity and patient-related outcomes. We investigated effects of voluntary exercise during cisplatin treatment on body weight, food intake as well as muscle mass, strength and signalling. Mice were treated weekly with 4 mg/kg cisplatin or saline for 6 weeks, and randomized to voluntary wheel running or not. Cisplatin treatment induced loss of body weight (29.8%, P < 0.001), lean body mass (20.6%, P = 0.001), as well as anorexia, impaired muscle strength (22.5% decrease, P < 0.001) and decreased glucose tolerance. In addition, cisplatin impaired Akt-signalling, induced genes related to protein degradation and inflammation, and reduced muscle glycogen content. Voluntary wheel running during treatment attenuated body weight loss by 50% (P < 0.001), maintained lean body mass (P < 0.001) and muscle strength (P < 0.001), reversed anorexia and impairments in Akt and protein degradation signalling. Cisplatin-induced muscular inflammation was not prevented by voluntary wheel running, nor was glucose tolerance improved. Exercise training may preserve muscle mass in cancer patients receiving cisplatin treatment, potentially improving physical capacity, quality of life and overall survival.

SummaryIntroduction. Clinical observations of cancer patients treated with selinexor have reported high incidence of nausea and anorexia. The study objective was to investigate the adoption of prophylactic olanzapine for the prevention of nausea, vomiting and anorexia in cancer patients receiving selinexor and standard chemotherapy. Methods. We retrospectively reviewed supportive care interventions in patients receiving selinexor and recorded frequency of adverse events (NCI-CTAE). Association between categorical variables were analyzed using Fisher’s exact tests; repeated measures analysis was performed to assess weight changes over time. Results. Of 124 evaluable patients, 83 (66.9%) were female, 93 were white (75.0%), and the most common cancer was ovarian (N = 30, 24.2%). One hundred and four patients (83.9%) received olanzapine, of which 93 (89.4%) were prophylactically treated, the majority (86.5%) receiving low 2.5 mg daily dose. Other anti-emetics included ondansetron in 90 patients (72.6%), dexamethasone prescribed in 50 patients (40.3%) and metoclopramide in 49 patients (39.5%), while aprepitant/fosaprepitant (N = 2, 1.6%) were prescribed infrequently. Cancer patients receiving prophylactic olanzapine (N = 93) compared to patients who never received olanzapine (N = 20) had more Grade 1 + anorexia (31.2% vs 20.0%), less nausea (53.8% vs 70.0%), less vomiting (33.3% vs 40.0%), and increased hyperglycemia (29.0% vs 10.0%), but differences were non-statistically significant. In addition, there was minimal weight loss over time in both groups and no statistically significant differences in weight loss between groups. Conclusion. Prophylactic olanzapine decreased nausea, vomiting and maintained weight over 3 months but did not prevent anorexia in patients receiving selinexor and chemotherapy. Low dose olanzapine was well tolerated but associated with hyperglycemia.