Feeling Sick

2020 ◽  
pp. 63-78
Author(s):  
Pamela K. Keel

Eating is fundamental to our survival and subject to numerous biological regulators that influence when, what, and how much we eat. This makes biological factors central to any answer for why someone develops purging disorder. Genetic factors impact body weight and temperament and may even influence a person’s susceptibility to nausea and vomiting. Yet data from family and twin studies suggest that genes may play a slightly smaller role in risk for purging disorder compared to other eating disorders. Instead, biological responses to food intake may explain the unique configuration of purging after consuming normal amounts of food in purging disorder. Compared to those with bulimia, individuals with purging disorder have greater release of hormones that trigger the brain to stop eating. Compared to those with bulimia and those without an eating disorder, individuals with purging disorder release excessive amounts of a hormone that triggers feelings of nausea and stomachache.

Author(s):  
Helen Loth

This chapter gives an overview of approaches, theoretical ideas, and techniques which music therapists have developed to work with adults and older teenagers who have eating disorders. Eating disorders are complex psychological disorders; the restriction of food intake and control of body weight serve to meet a psychological or emotional need. Music therapy can help people to explore and understand the psychological issues that may have led them to using eating as a way of controlling their feelings and emotions. Methods such as free and structured improvisation, songwriting and listening to pre-composed music can be used to help clients to address specific aspects of eating disorder pathology, such as being able to recognise and tolerate their feelings, connect with others, and make links between thoughts, feelings, and the body. Music therapy can have a significant role within the overall treatment of a person with an eating disorder.


Author(s):  
Pamela Keel

The epidemiology of eating disorders holds important clues for understanding factors that may contribute to their etiology. In addition, epidemiological findings speak to the public health significance of these deleterious syndromes. Information on course and outcome are important for clinicians to understand the prognosis associated with different disorders of eating and for treatment planning. This chapter reviews information on the epidemiology and course of anorexia nervosa, bulimia nervosa, and two forms of eating disorder not otherwise specified, binge eating disorder and purging disorder.


1993 ◽  
Vol 38 (7) ◽  
pp. 469-471 ◽  
Author(s):  
Clifford W. Sharp

A woman aged 58 who has been blind since the age of nine months presented with major depression and a 40 year history of an eating disorder characterized by a restriction of food intake and body disparagement. The case is additional evidence that a specifically visual body image is not essential for the development of anorexia nervosa and supports the view that the concept of body image is unnecessary and unproductive in eating disorders. Greater emphasis should be placed on attitudes and feelings toward the body, and the possibility of an eating disorder should be considered in cases of older women with an atypical presentation.


CNS Spectrums ◽  
2004 ◽  
Vol 9 (7) ◽  
pp. 523-529 ◽  
Author(s):  
Palmiero Monteleone ◽  
Antonio DiLieto ◽  
Eloisa Castaldo ◽  
Mario Maj

AbstractLeptin is an adipocyte-derived hormone, which is involved predominantly in the long-term regulation of body weight and energy balance by acting as a hunger suppressant signal to the brain. Leptin is also involved in the modulation of reproduction, immune function, physical activity, and some endogenous endocrine axes. Since anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by abnormal eating behaviors, dysregulation of endogenous endocrine axes, alterations of reproductive and immune functions, and increased physical activity, extensive research has been carried out in the last decade in order to ascertain a role of this hormone in the pathophysiology of these syndromes. In this article, we review the available data on leptin physiology in patients with eating disorders. These data support the idea that leptin is not directly involved in the etiology of AN or BN. However, malnutrition-induced alterations in its physiology may contribute to the genesis and/or the maintenance of some clinical manifestations of AN and BN and may have an impact on the prognosis of AN.


Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2441-2452 ◽  
Author(s):  
Tomokazu Hata ◽  
Noriyuki Miyata ◽  
Shu Takakura ◽  
Kazufumi Yoshihara ◽  
Yasunari Asano ◽  
...  

Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.


Author(s):  
David J. Nutt ◽  
Liam J. Nestor

Many of the same behavioural and brain disturbances observed in addiction are also seen in obesity and binge-eating disorder. This suggests that there are shared neural substrates between substance addiction and compulsive food consumption. Food intake and appetite are regulated by numerous appetite hormones that exert their effects through brain systems involved in reward sensitivity, stress, impulsivity, and compulsivity. There is now emerging evidence that appetite hormones (e.g. ghrelin, glucagon-like peptide-1, orexin) can modulate addictive behaviours (e.g. craving) and the intake of alcohol and drugs. Therefore, there is an emerging shift into a new field of testing drugs that affect appetite hormones and their receptors in the brain, and their use in regulating the brain mechanisms that lead to relapse in addiction disorders.


2020 ◽  
Vol 11 ◽  
Author(s):  
Do-Hyun Kim ◽  
Joong Sun Kim ◽  
Jeongsang Kim ◽  
Jong-Kil Jeong ◽  
Hong-Seok Son ◽  
...  

Licorice and dried ginger decoction (Gancao-ganjiang-tang, LGD) is used for nausea and anorexia, accompanied by excessive sweating in Traditional Chinese Medicine. Herein, we investigated the therapeutic effects of LGD using the activity-based anorexia (ABA) in a mouse model. Six-week-old female BALB/c AnNCrl mice were orally administered LGD, water, licorice decoction, dried ginger decoction, or chronic olanzapine, and their survival, body weight, food intake, and wheel activity were compared in ABA. Additionally, dopamine concentration in brain tissues was evaluated. LGD significantly reduced the number of ABA mice reaching the drop-out criterion of fatal body weight loss. However, LGD showed no significant effects on food intake and wheel activity. We found that in the LGD group the rise of the light phase activity rate inhibited body weight loss. Licorice or dried ginger alone did not improve survival rates, they only showed longer survival periods than chronic olanzapine when combined. In addition, LGD increased the dopamine concentration in the brain. The results from the present study showed that LGD improves the survival of ABA mice and its mechanism of action might be related to the alteration of dopamine concentration in the brain.


1999 ◽  
Vol 276 (6) ◽  
pp. R1617-R1622 ◽  
Author(s):  
David Michaud ◽  
Hymie Anisman ◽  
Zul Merali

Bombesin (BN) suppresses food intake in rats whether given centrally or systemically. Although the brain BN-sensitive receptors are known to be essential for the anorexic effect of systemic BN, the mode of communication between the gut and the brain remains unclear. This study assessed whether the anorexic effect of systemic BN is mediated humorally or via neural circuits. Afferent neurons were lesioned using capsaicin (50 mg/kg sc) on postnatal day 2, and responses to BN were assessed during adulthood. Capsaicin treatment decreased body weight gain significantly from postnatal age 4–7 wk. Peripheral BN (4–16 μg/kg ip) dose dependently suppressed food intake in control animals. However, this effect was completely blocked in capsaicin-treated rats. In contrast to systemic effects, feeding-suppressant effects of centrally administered BN (0.01–0.5 μg icv) were not affected by capsaicin treatment. This research suggests that peripheral BN communicates with the brain via a neuronal system(s) whose afferent arm is constituted of capsaicin-sensitive C and/or Aδ-fibers, whereas the efferent arm of this satiety- and/or anorexia-mediating circuitry is capsaicin resistant.


2006 ◽  
Vol 361 (1471) ◽  
pp. 1219-1235 ◽  
Author(s):  
Stephen C Woods ◽  
Thomas A Lutz ◽  
Nori Geary ◽  
Wolfgang Langhans

The control of food intake and body weight by the brain relies upon the detection and integration of signals reflecting energy stores and fluxes, and their interaction with many different inputs related to food palatability and gastrointestinal handling as well as social, emotional, circadian, habitual and other situational factors. This review focuses upon the role of hormones secreted by the endocrine pancreas: hormones, which individually and collectively influence food intake, with an emphasis upon insulin, glucagon and amylin. Insulin and amylin are co-secreted by B-cells and provide a signal that reflects both circulating energy in the form of glucose and stored energy in the form of visceral adipose tissue. Insulin acts directly at the liver to suppress the synthesis and secretion of glucose, and some plasma insulin is transported into the brain and especially the mediobasal hypothalamus where it elicits a net catabolic response, particularly reduced food intake and loss of body weight. Amylin reduces meal size by stimulating neurons in the hindbrain, and there is evidence that amylin additionally functions as an adiposity signal controlling body weight as well as meal size. Glucagon is secreted from A-cells and increases glucose secretion from the liver. Glucagon acts in the liver to reduce meal size, the signal being relayed to the brain via the vagus nerves. To summarize, hormones of the endocrine pancreas are collectively at the crossroads of many aspects of energy homeostasis. Glucagon and amylin act in the short term to reduce meal size, and insulin sensitizes the brain to short-term meal-generated satiety signals; and insulin and perhaps amylin as well act over longer intervals to modulate the amount of fat maintained and defended by the brain. Hormones of the endocrine pancreas interact with receptors at many points along the gut–brain axis, from the liver to the sensory vagus nerve to the hindbrain to the hypothalamus; and their signals are conveyed both neurally and humorally. Finally, their actions include gastrointestinal and metabolic as well as behavioural effects.


2000 ◽  
Vol 71 (1) ◽  
pp. 39-47 ◽  
Author(s):  
W. M. Rauw ◽  
P. Luiting ◽  
M. W. A. Verstegen ◽  
O. Vangen ◽  
P. W. Knap

AbstractIn the accompanying paper, specific genetic factors for body weight and food intake were identified in non-reproductive male and female mice of a line selected for high litter size at birth (average of 22 born per litter) and a non-selected control line (average of 10 born per litter). The existence of these factors are indicated by variation in efficiency parameters such as growth efficiency and maintenance requirements. Residual food intake (RFI) and Parks’ estimates of growth efficiency (AB) and maintenance requirements (MEm) were used to quantify these factors. In the growing period, females had a higher RFI (are less efficient) than males. At maturity, selected mice had higher RFI than control mice and selected females had higher RFI than selected males. AB was higher in selected-line mice than in control-line mice, and higher in males than in females. MEm was higher in selected-line mice than in control-line mice, and higher in females than in males. The results indicate the existence of specific genetic factors for both growth efficiency and maintenance requirements. Selected females may increase RFI in the adult state to anticipate the metabolically stressful periods of pregnancy and lactation, to support a genetically highly increased litter size.


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