Self-induced Weight Loss Research Articles

Should Protocols for Weight Change During Pregnancy Include Information About the Previous Weight History of the Woman Who Is Pregnant? (P22-015-19)

ObjectivesRecent research has indicated that an increase in weight is frequently caused by prior famine or Self-Induced Weight Loss (SIWL). The purpose of the literature search was to evaluate if famine or SIWL, in a woman who is contemplating pregnancy or who is currently pregnant, could have long term effects on the child to be born. MethodsPub Med was searched using the key phrases “Pregnancy and Famine or Starvation”, and “Gestational Weight Gain”, both limited to Humans, with no limit as to dates of publication. ResultsThe earliest famine study found was published in 1976 and indicated that men born during the Dutch Famine (1944–45) had higher obesity rates if they were exposed to famine during the first half of pregnancy and lower rates if they experienced famine in the third trimester or the first few months of life. Other publications report results of pregnancy outcomes before, during, and after the Holocaust (1940–45), the Dutch Famine and famines in China (1959–61), Biafra (1968–70), and Bangladesh (1974–75). Long-term famine related problems include increased risk of overweight, obesity, Type 2 Diabetes, coronary heart disease, hypertension, and metabolic syndrome. Additional studies extend this observation to those who live in poverty with corresponding uncertainty about food resources. The most complete studies were published after 2004. Studies less than 18 months indicate that SIWL may be effective. However, with individuals followed 6 years or more either long-term weight gain occurs, or additional SIWL.Pregnancy protocols advocate specific limits to weight gain during pregnancy based on pre-pregnancy or early pregnancy BMI and recommend total weight gain ranges using usual BMI classifications. They do not ask about the weight history of the woman or if she has ever engaged in SIWL. BMI is based on height and weight and does not take into consideration the relative contribution of bone and muscle mass differentiated from fat mass. The size of the baby at birth is not an adequate indicator of actual health status. ConclusionsAn individual is conceived, lives in utero, and then is born. Caloric undernutrition in utero and during childhood can produce increased body fat and result in non-communicable diseases that are commonly related to obesity. Funding SourcesPension, University of Puerto Rico. Supporting Tables, Images and/or Graphs▪

Anorexia nervosa as differential diagnosis in underweight patients

Anorexia nervosa is a differential diagnosis in underweight patients, especially in young underweight women. Diagnostic criteria for anorexia nervosa are self-induced weight loss due to restrictive eating or purging behaviour, intense fear of gaining weight and disturbance in the way in which one`s shape is experienced, undue influence of body weight on self-evaluation and persistent lack of recognition of the seriousness of the current low body weight. Anorexia nervosa is associated with numerous medical complications.

Tardy male anorexia nervosa ultimately responded to ECT

© 2015 Naguy et al; licensee Herbert Publications Ltd. This is an Open Access article distributed under the terms of Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0). This permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Correspondence Anorexia Nervosa (AN) is one of the few ‘real’ psychiatric emergencies [1], with 10-15% mortality rate; 2/3 due to medical complications and 1/3 due to suicidality. Crow et al., reported a crude mortality rate of 4% [2]. Incidence of 0.5%, female outnumbers male by a ratio of 10:1. AN is commonly thought of as a female disorder. Even though as much as 25% of the clinical population is male, research on AN in males is limited [3]. It is defined clinically with marked distortion of body image, pathologic desire for thinness, and self-induced weight loss with body mass index (BMI) of 17.5 or less. Mean age of onset is 16-17 years for females and 12 years for males [4]. A combined approach is recommended for management of AN; pharmacologic (best evidence for fluoxetine and olanzapine), psychologic (family therapy and cognitive-behavioural therapy CBT) and bibliotherapy [5]. Pharmacotherapy is generally of limited value especially acutely but might help with relapse prevention . Hospitalization is indicated in presence of serious medical sequelae [6]. Male gender and late onset (“tardy AN”) generally portend poor prognostication [7,8]. Electroconvulsive therapy (ECT) in recalcitrant AN is supported by few case reports in the literature [9]. A 42-year-old Kuwaiti gentleman was referred to us from a private facility in accompaniment of his wife, with a diagnosis of AN-restricting subtype that failed a 3 months trail of fluoxetine (Prozac®) 20 mg and cyproheptadine(Periactin®) 8 mg/d. He was also engaged in 12 sessions of weekly high-quality CBT. Extensive workup was contemplated including laboratory investigations, electrolyte panel, thyroid function (TFT), B12 and folate, toxicologic (UTox) screen, electrocardiography (ECG), electroencephalography (EEG), magnetic-resonance imaging (MRI) Brain with gadolinium (Gd ) enhancement and rheumatologic profile. Hypochromic microcytic anaemia, mild hypokalaemia, sinus bradycardia and a pattern of “pseudoatrophy” [10] were noted. Anthropometry was accomplished as well as Quetlet formula showing BMI of 17. Patient has obvious longitudinal anankastic personality traits (‘anal character’) as reported by his wife with the characteristic triad of obstinacy, parsimony and pedantism. Elaborative psychometry entailed Ideal Body Stereotype Scale-Revised, Perceived Sociocultural Pressure Scale, Eating Disorder Diagnostic Scale, Yale-Brown obsessive-compulsive scale (Y-BOCS), Beck’s depression inventory (BDI), Minnesota mutiphasic personality inventory-2 (MMPI-2) and Brown assessment of beliefs scale (BABS). Patient was partially insighted, with no depressive overlay or frank psychosis. We pushed fluoxetine to 40 mg/d and introduced olanzapine (Zyprexa®) 10 mg/d in lieu of cyproheptadine. After 4 weeks, the course was relentlessly deteriorating and the patient was losing much weight (BMI dropped to 16) and totally refusing food. He was hospitalized for intravenous (IV) drips and correction of concomitant dyselectrolaemia. He was pallid, sallow and gaunt, albeit, very resistive and disengaging. He refused to pursue with psychotropic medications. He endorsed no suicidality but was ostensibly demoralized and in marked distress. We opted for ECT on emergency basis. After 3 sessions of bitemporal modified ECT, he began to be more brightened, engaging, serene, less preoccupied, and, above all compliant with meds which then changed to fluoxetine 60 mg/d and quetiapine (Seroquel XR®) 300mg/d. We continued to a totality of 6 sessions. No cognitive side-effects were reported. CBT was reinstituted. Patient was discharged and followed up in OPD. After 2, 4, 8 and 12 weeks, he kept exponentially improving, put on 4 kgs, and faring well both socially and vocationally. Although he is still ‘obsessed’ with ‘ideal’ body weight, he is maintained on a well-balanced diet with our nutritionist, attending weekly CBT sessions and treatment-adherent. We opine that ECT remains a viable option to explore in cases of severe AN, especially in life-threatening conditions even in the absence of comorbid depression as this case illustrates. We theorize that efficacy of ECT in AN could be ascribed to presumed ‘anti-obsessional’ actions [11], independent of its antidepressant actions. Moreover, it is postulated that ECT acutely increases NE activity and endogenous opiates [12], and this could rectify the replicated findings of deficits in MHPG (methoxyhydroxyphenylglycol) and endogenous opiates activity in AN [13]. *Correspondence: ahmednagy@hotmail.co.uk

P-559 - Anorexia nervosa: report of four cases of iatrogenic onset

Anorexia nervosa is a syndrome of unknown etiology. Biological, psychological, and social components play a role in the pathogenesis of anorexia nervosa. In approximately 95 percent of cases, the eating disorder is precipitated by dieting. In 8 percent of cases, initial weight loss may be inadvertent but after some weight loss occurs for medical reasons, the patient loses weight by voluntary dieting. Even less common is an iatrogenic onset. The purpose of this article is to report four cases of iatrogenic onset of anorexia nervosa. Case study and review of the literature. The authors describe four clinical cases of patients with an onset of anorexia nervosa precipitated by iatrogenic beginning rather than the more typical onset following intentional dieting. Risk factors are non-specific and the threshold of disease varies for each patient. Iatrogenic weight loss may be as powerful a trigger as intentional dieting to initiating anorexia nervosa in predisposed individuals; self-induced weight loss may not be a necessary precursor to anorexia nervosa.

Unintentional onset of anorexia nervosa

The purpose of this article is to report a series of patients with an onset of anorexia nervosa precipitated by unintended weight loss rather than the more typical onset following intentional dieting, or the occasional iatrogenic beginning. Retrospectively, case notes of 66 consecutive outpatient evaluations at an eating disorder diagnostic clinic between 2002 and 2006 were reviewed. Five cases, 7.6%, of inadvertent onset anorexia nervosa were identified. Causes of the inadvertent weight loss were varied: the mourning of a death, a parasitic infection, medication side effects and surgery. None had intended to lose weight. We postulate that inadvertent weight loss may be as powerful a trigger as intentional dieting to initiating anorexia nervosa in predisposed individuals; self-induced weight loss may not be a necessary precursor to anorexia nervosa.

A prospective study of changes in bone turnover and bone density associated with regaining weight in women with anorexia nervosa

Anorexia nervosa (AN) is a condition of self-induced weight loss, associated with an intense fear of gaining weight. Previous studies have shown that bone density may increase with regaining and maintaining normal weight; however, relatively little is known about the changes in bone metabolism that occur during weight restoration. We describe the effect of weight restoration and maintenance of weight over 1 year on bone mineral density (BMD) and bone turnover. We recruited women from the eating disorders services at the South West London and St George's Mental Health NHS Trust, and the Priory and Charter Nightingale Hospitals in London, UK. Details of their AN, fracture history, menstrual history and exercise were obtained by interview and case note review. Morning samples of blood and second void urine were taken for biochemical analysis. BMD was measured by DXA at the lumbar spine (LS), femoral neck (FN), distal radius (RD) and total body bone mineral content (BMC). Patients then entered the treatment program, which includes re-feeding, dietary education and psychotherapy. Over a period of 42 months, we recruited 55 women who agreed to participate in this study and underwent baseline investigations. Of these, 15 (27%) subjects achieved and then maintained their target weight for the duration of the study. At baseline for all subjects (n=55) estradiol levels were lower than the normal reference ranges (both follicular and luteal phases) in 91% of the women. Bone specific alkaline phosphatase (BSAP) concentrations were lower than the premenopausal reference range in 55% of women, and urinary deoxypyridinoline (DPD) was above the premenopausal reference range in 78% of women. Baseline lumbar spine BMD was positively related to BMI (Pearson's r=0.29, P=0.04) and inversely related to bone turnover markers: urinary DPD (Pearson's r=-0.39, P=0.01 and serum BSAP (Pearson's r=-0.3, P=0.06). The 15 patients who regained and maintained weight were followed-up for a mean duration of 69 weeks (SD 7.3, range 54 to 84 weeks). Mean BMI increased from 14.2 (1.7) to 20.2 (0.77) kg/m2 and remained stable throughout follow-up. Menstruation resumed in 8 of the 15 women. Total body BMC and LS BMD increased significantly over the duration of follow-up (by 4.3% each), but FN BMD and distal radius remained stable. Lumbar spine bone area also increased significantly, whereas FN and distal radius did not. These changes were associated with a significant increase in BSAP (P=0.01), and a non-significant trend for a decrease in DPD (P=0.10). Our findings suggest that when women are at low body weight they are in a hypo-estrogenic state, which is associated with imbalance of bone turnover (high bone resorption and low bone formation). This is reversed with weight gain and persists as target weight is maintained and is associated with increases in BMC and BMD.

Separation-induced body weight loss, impairment in alternation behavior, and autonomic tone: effects of tyrosine

We have investigated the effects of tyrosine on alternation behavior and hippocampal adrenergic and cholinergic tone in a model of self-induced weight loss caused by separation stress. Separation decreased body weight in mice ( P<.001) and spontaneous alternations in the T-maze ( P<.001). This impairment was associated with depletion of both norepinephrine (NE, P<.001) and dopamine ( P<.01) while increasing MHPG ( P<.05) and the ratio of MHPG/NE ( P<.05). Increasing tyrosine availability restored performance to control levels ( P<.001) and repleted dopamine ( P<.05) and presumably also NE (indicated by increases in both MHPG, P<.001, and MHPG/NE, P<.05). Stress increased adrenergic α 2-receptor density ( P<.001) without changing its K d and the B max and K d of β-receptors, suggesting that it decreased NE transmission through action on α 2-receptors. The balance between β- and α 2-receptors appeared to be related to alternation behavior as shown by the decrease ( P<.01) and increase ( P<.05) in their ratios induced by stress and tyrosine, respectively. With regard to cholinergic tone, separation stress increased M1 receptor density ( P<.05) and its mRNA signal ( P<.001). Tyrosine further increased M1 receptor density of stressed mice ( P<.05). Tyrosine might be a potential therapy for cognitive and mood problems associated with the maintenance of a reduced body weight in the treatment of obesity and in the extreme case of anorexia nervosa.

Structural and functional changes in skeletal muscle in anorexia nervosa.

Protein-energy malnutrition in anorexia nervosa is an under-recognised cause of muscle dysfunction. To characterise the skeletal myopathy that occurs in patients with severe anorexia nervosa, muscle function and structure were comprehensively examined in eight young adult female patients with severe (40%) self-induced weight loss. All of the patients showed impaired muscle function on strength and exercise measurement. The maximum voluntary contraction force for the patient group was significantly less than predicted values. Electromyography revealed myopathy in five of the patients, four of whom also had electro-physiological evidence of neuropathy. However, muscle biopsy specimens consistently showed myopathic changes with severe type 2 fibre atrophy but with no evidence of neuropathic changes. Ultrastructurally, there was separation and segmental loss of myofibrils and most biopsy samples contained abundant glycogen granules; we have previously reported that one of the most consistent biochemical abnormalities in these patients is impaired ischaemic lactate responses to forearm exercise. The result of severe protein-energy malnutrition on the musculo-skeletal system is a metabolic myopathy. Although the patients admitted to a variety of abnormal dieting behaviours, such as over-exercising and self-induced vomiting, no association was found between any of these and quantitative histological changes in the muscle biopsy samples. It is recommended that myopathy in anorexia nervosa be treated by instituting an appropriate refeeding programme.

Separation as a New Animal Model for Self-Induced Weight Loss

van Leeuwen, S. D, O. B. Bonne, Y. Avraham and E. M. Berry. Separation as a new animal model for self induced weight loss. Physiol Behav 62(1) 77–81, 1997.—Animal models for weight loss are generally either stress mediated or following diet restriction (DR) schedules. We investigated weight loss in mice subjected to activity stress (ACT), DR schedules of 40, 60 and 100% of daily requirements, and propose a new model for animal weight loss based upon separation. Mice were separated (SEP) from each other by perspex partitioning for 23 h per day, with free access to food for one hour. No significant differences in weight loss were found between the ACT, SEP and 40‰ groups. However, mean food intake in the 40‰ group was half that of the ACT group (p < 0.001) and significantly less (p < 0.01) than the SEP group, which consumed amounts equivalent to 65‰ of daily requirement. Separation of mice increases metabolic demands and may be used as a new, easily performed, animal model for weight loss.

Anorexia nervosa in Hong Kong: a Chinese perspective

A prospective study of sixteen Chinese anorexic patients in Hong Kong indicates that they were single young females who came from lower social class, exhibited severe self-induced weight loss, rigid maintenance of low body weight and amenorrhea. Weight reduction was primarily by dietary restriction. The typical bulimic syndrome and major depression were uncommon. There were multiple aetiological factors, but no pre-morbid obesity and little pressure to pursue slimness for beauty. Instead of displaying an intense fear of obesity and a distorted body image, patients more commonly attributed poor food intake to abdominal bloating. As such, they only partially fulfilled current criteria for diagnosis. It is argued that such clinical patterns arise logically from their sociocultural backgrounds, but may gradually change with Westernization.

Steroids and neuroendocrine function in anorexia nervosa

Anorexia nervosa is a primarily psychiatric syndrome of self-induced weight loss due to an intense fear of becoming obese. Numerous endocrine abnormalities occur in anorexia nervosa patients, and in many respects these alterations reflects the endocrinology of reduced energy intake. However, the basic mechanisms of those alterations are far from being understood. In an attempt to understand the disrupted mechanisms of the hypogonadotropic hypogonadism of the anorectic state, we studied 10 anorectic women in the acute phase of their illness; all met the DSM III criteria. On each patient, two tests were performed with either saline as control or infusion of the opioid antagonist naloxone, and both LH and FSH levels were measured. Four mg of naloxone as bolus was used, followed by a naloxone infusion of 2 mg/h for 4 h. Compared with the pattern of normal women, naloxone did not increase in the anorectic patients either LH or FSH levels nor pulsatility. This result suggests that endogenous opioid peptides are not implicated in the low gonadotropic situation of anorexia nervosa. An alternative explanation could be that the low estrogenic “milieu” of these patients could mask the opioid action. To test this second possibility, another group of 7 anorectic women after partial weight recovery were challenged with estrogen administration. Compared with the pattern of normal women volunteers, all the anorectic patients but one presented an abnormal response in both LH and FSH levels after estrogen administration. In fact, the negative feedback and the delayed positive feedback of LH after estrogen were absent in these patients. Interestingly enough, the only patient with near-normal LH response to estrogen was considered fully recovered by the Psychiatric Unit. Several alterations in the hypothalamic-pituitary-adrenal axis has been reported in anorexia nervosa. Seven anorectic patients and 7 aged-matched women were challenged by ACTH 17–24, 250 μg (i.v.) and the ratio of increments in adrenal steroid products to precursors monitored. ACTH-induced increments in cortisol with respect to increments in 17-OH-progesterone was similar in anorectics and controls. On the contrary, the ratio of increments of androstenedione with respect to increments in 17-OH-progesterone were greater in anorexia nervosa than controls. These results suggest that in anorexia nervosa the 11-beta-21-alpha-hydroxilase system is normal but a deficient 17–20 desmolase system is present. Finally, the altered pattern of GH secretion in anorexia was studied using GHRH (1 μg/kg) as stimulus of pituitary GH secretion. The GH response to GHRH was similar in anorexia nervosa patients to that in controls, suggesting that the altered response observed in these patients under different stimuli could be located at hypothalamic level. In conclusion, for the different endocrinological abnormalities tested in anorexia nervosa patients the primary disturbance seems to exist at the hypothalamic level or above, and the peripheral disturbances are secondary to the central one.

Discordant patterns of hyperprolactinaemia and galactorrhoea in secondary amenorrhoea.

ABSTRACT Hyperprolactinaemia occurred in 40 of 123 unselected patients (33%) with functional secondary amenorrhoea. Galactorrhoea was present only in 15 of these patients (38 %). On the other hand, galactorrhoea was found in 10 of 83 euprolactinaemic patients (12%). The frequency and severity of hyperprolactinaemia and galactorrhoea dissociated in various forms of amenorrhoea. Anorexia nervosa was characterized by euprolactinaemia and the absence of galactorrhoea. Self-induced weight loss resulted in amenorrhoea with a moderate degree of hyperprolactinaemia in 23 % of the cases. Yet, galactorrhoea was uncommon (1.6 %). Amenorrhoea following stress was also associated with moderate hyperprolactinaemia in 31 % of patients and a low frequency of galactorrhoea. By contrast, both hyperprolactinaemia and galactorrhoea occurred more frequently (36 %) and were more severe in patients who had post-pill amenorrhoea, but still 50 % of hyperprolactinaemic patients had no galactorrhoea and 28 % of euprolactinaemic patients had galactorrhoea. This discordance was accentuated in those patients who had been pregnant even if pregnancy did not immediately precede amenorrhoea. Galactorrhoea (63 %) and hyperprolactinaemia (36 %) were common in these patients and very high serum prolactin values were sometimes seen. Our results point to different mechanisms involved in the regulation of hypothalamic pituitary function and breast secretion in various forms of secondary amenorrhoea, and they may help select patients in whom the prolactin assay is likely to identify indication for specific treatment.