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Diarrhea and Malnutrition
Published in Fima Lifshitz, Childhood Nutrition, 2020
Andrea Maggioni, Fima Lifshitz
Anorexia is present even with mild subclinical infections,68 and the loss of appetite makes it very difficult to maintain a constant intake during the acute phase of the illness, although breast milk is rejected to a lesser extent. The anorectic effect of infection may last a few hours or extend for days or weeks. As much as 20 to 70% of the available food may be uneaten during bouts of diarrhea.69 In addition, when diarrhea strikes, there is usually restriction of solid food intake, especially feedings of animal origin which are replaced with a low-energy, low-protein diet dictated by medical or popular traditions, beliefs, or taboos to “treat” the diarrhea.20
Gastrointestinal Aspects of Eating Disorders
Published in Kevin W. Olden, Handbook of Functional Gastrointestinal Disorders, 2020
Bruce D. Waldholtz, Arnold E. Andersen
Extended medical evaluation of all anorectic patients’ disease is therefore not necessary unless they fail to gain weight or have other factors such as Hemoccult-positive stool, elevated sed. rate, or objective abdominal distension (3).
Clinical Psychopharmacology of Amphetamine and Related Compounds
Published in John Caldwell, S. Joseph Mulé, Amphetamines and Related Stimulants: Chemical, Biological, Clinical, and Sociological Aspects, 2019
While anorectic drugs have repeatedly been shown to help obese patients keep to a restricted calorie diet, and consequently lose weight, considerable misgivings have been expressed concerning the desirability of using anorectic drugs at all in obesity.84 The objections have been based on two factors: first, it is generally true that when patients stop taking their anorectic drug they tend to regain any weight they had lost (but this is true of all treatments for obesity), and secondly, the fact that some of these drugs have been abused by nonobese nonpatients has been thought to be grounds for withholding them from the obese. Our own view is that these drugs can be useful in the management of obesity but should be used only as adjuncts to a detailed dietary program. Furthermore their use should be restricted to patients whose obesity is threatening their health or well-being: in essence this means patients under the age of 50 who are at least 30% above their desirable weight, or patients who have physical or psychological problems that are thought to arise from, or are exacerbated by, their obesity. When it has been decided to prescribe an appetite suppressant, the drug should be given in adequate dosage for as long as necessary.84
The limits and challenges of antiobesity pharmacotherapy
Published in Expert Opinion on Pharmacotherapy, 2020
Kishore M Gadde, Katelyn D Atkins
In 1947, the US Food and Drug Administration (FDA) approved two branded products of desoxyephedrine (Desoxyn, Hydrin), an amphetamine, as ‘adjuncts to the dietary management of obesity’ based on an article that reported no blood pressure (BP) elevations or evidence of addiction among 110 obese patients treated with the drug [9]. Between 1956 and 1960, five amphetamine congeners were also approved [Table 1] based on safety evaluation only. In 1970, the FDA required that the manufacturers of these already marketed drugs conduct well-controlled studies and submit evidence of efficacy within a year. This ‘Amphetamine Anorectic Drug Project’ involved clinical trials that ranged in duration from 3 weeks to 6 months, mostly around 12 weeks. In the mid-70s, lacking expert consensus on what constituted clinically significant weight loss and how to determine benefit-to-risk balance, the FDA reaffirmed the approval of the previously approved amphetamines and amphetamine congeners based on a crude meta-analysis that revealed ‘trivial,’ but statistically superior weight loss relative to placebo. However, lacking adequate data on addiction potential, the FDA arbitrarily restricted their use for short-term (a few weeks) [9]. This restriction led to a fall in the use of anorectic drugs until publication of a single placebo-controlled study of 121 obese patients (less than one-third completed the study) treated with phentermine plus fenfluramine (Phen-Fen) for up to 4 years [10] led to a steep rise in their prescriptions in the mid-1990s [11].
Obesity medications in development
Published in Expert Opinion on Investigational Drugs, 2020
Candida J. Rebello, Frank L. Greenway
Peptide YY (PYY) which is released post-prandially is a well-characterized mediator of satiety and exerts its effects through the Y family of receptors. It is released from the L cells of the GI tract throughout the gut but is present in the highest concentrations in the distal regions. The most effective form is the amino-terminally truncated version, PYY3-36, since the full form binds with little affinity to the Y receptors [16]. The preferred Y2 receptor is highly expressed in orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus. Peripheral administration of PYY3-36 reduces food intake in rodents and humans [17,18]. The results in rodents could not be replicated [19] and in humans the anorectic effect was evident only at pharmacologic doses [20].
Adiponectin and resistin in acutely ill and weight-recovered adolescent anorexia nervosa: Association with psychiatric symptoms
Published in The World Journal of Biological Psychiatry, 2019
Marta Tyszkiewicz-Nwafor, Agnieszka Slopien, Monika Dmitrzak-Węglarz, Filip Rybakowski
Several studies suggest the involvement of adiponectin and resistin in the pathogenesis of obesity and its metabolic consequences (Vendrell et al. 2004). A significant inverse correlation between these two adipocytokines has been reported in the literature. It was also speculated that they share a common regulatory mechanism to mediate body metabolism. It was proposed to use the adiponectin–resistin index to assess the metabolic risk in obesity (Lau and Muniandy 2011). Thus, it can be useful to study them together. The potential role of these adipokines in the course of AN is still unclear. Decreased body fat, as well as rapid weight gain during the re-feeding of anorectic patients, can lead to dysregulation of adipokine secretion and action. We suspect that abnormal plasma levels of adipokines involved in homeostatic and non-homeostatic regulation of food intake and energy expenditure may influence certain psychopathological symptoms, such as depressed mood, disturbed body image and obsessive-compulsive symptoms. Only a few studies have examined adiponectin and resistin levels in the acute stage of adult anorexia nervosa; however, the disorder usually starts in adolescence when crucial neuroplastic processes occur (Fuhrmann et al. 2015).