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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism of critical illness is characterised by a combination of starvation and stress. There is increased production of cortisol, catecholamines, glucagon and growth hormone and increased insulin-like growth factor-binding protein-1. Phagocytic, epithelial and endothelial cells elaborate reactive oxygen and nitrogen species, chemokines, pro-inflammatory cytokines and lipid mediators, and antioxidant depletion ensues. There is hyperglycaemia, hyperinsulinaemia, hyperlactataemia, increased gluconeogenesis and decreased glycogen production. Insulin resistance, particularly in relation to the liver, is marked. The purpose of nutritional support is primarily to save life and secondarily to speed recovery by reducing neuropathy and maintaining muscle mass and function. There is debate about the optimal timing of nutritional support for the patient in the intensive care unit. It is generally agreed that the enteral route is preferable if possible, but the dangers of the parenteral route, a route of feeding that remains important in the context of critical illness, may have been over-emphasised. Control of hyperglycaemia is beneficial, and avoidance of overfeeding is emphasised. Growth hormone is harmful. The refeeding syndrome needs to be considered, although it has been little studied in the context of critical illness. Achieving energy balance may not be necessary in the early stages of critical illness, particularly in patients who are overweight or obese. Protein turnover is increased and N balance is often negative in the face of normal nutrient intake; optimal N intakes are the subject of some debate. Supplementation of particular amino acids able to support or regulate the immune response, such as glutamine, may have a role not only for their potential metabolic effect but also for their potential antioxidant role. Doubt remains in relation to arginine supplementation. High-dose mineral and vitamin antioxidant therapy may have a place.
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PMID:Nutritional interventions in critical illness. 1734 68

Although it appeared relatively suddenly, the current obesity epidemic - largely manifest in industrialized societies but now spreading to the rest of the world - is the result of interaction between human biology and human culture over the long period of human evolution. As mammals and primates, humans have the capacity to store body fat when opportunities to consume excess energy arise. But during the millions of years of human evolution such opportunities were rare and transient. More commonly ancestral hominins and modern humans were confronted with food scarcity and had to engage in high levels of physical activity. In tandem with encephalization, humans evolved elaborate and complex genetic and physiological systems to protect against starvation and defend stored body fat. They also devised technological aids for increasing energy consumption and reducing physical effort. In the last century, industrialization provided access to great quantities of mass-produced, high-calorie foods and many labour-saving and transportation devices, virtually abolishing starvation and heavy manual work. In the modern obesogenic environment, individuals possessing the appropriate combination of ancestral energy-conserving genes are at greater risk for overweight and obesity and associated chronic diseases.
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PMID:Evolutionary origins of obesity. 1825 54

Anorexia nervosa and Bulimia nervosa are the main types of eating disorders described in the International Classification of Diseases ICD-10. The main features are eating patterns such as refusal to eat enough food or loss of control, followed by counter-regulatory measures. In addition, preoccupation with body shape and weight and with food is an important feature of eating disorders. Severe medical conditions may occur as a result to starvation, malnutrition and purging. Binge eating disorder has been included as an additional variant of disturbed eating in the American classification system of mental disorders (DSM-IV). The main characteristic of the binge eating disorder is binge eating, but without counter-regulatory measures. Patients with anorexia nervosa are foremost underweight (BMI < 17.5 kg/m2), those with a bulimia nervosa are usually in the normal weight range. On the other hand, patients with the binge eating disorder are overweight or obese. Etiological models are multifaceted and include predisposing and sustaining factors as well as triggers for the onset of the disorder. The course is variable and marked by changes between remission and clinically relevant symptoms. Psychotherapy is the treatment of choice.
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PMID:[Eating disorders--diagnosis and treatment]. 1843 6

The dramatic increase in the number of obese and overweight persons has spurred interest in control of appetite, body weight, and adiposity. Leptin is the humoral component of a negative feedback loop between adipose tissue and brain. Leptin is secreted from fat in proportion to the degree of adiposity, is transported across the blood-brain barrier (BBB), and acts in the brain to decrease appetite and increase thermogenesis, actions that ultimately decrease adiposity. However, leptin fails as an adipostat because leptin resistance arises in obesity. The BBB transporter is the first part of the feedback loop to fail, producing the so called "peripheral resistance" to leptin. In this sense, obesity is a disease of the BBB. Failure of leptin as an adipostat raises the question of what its primary role is as does its effects on reproduction, bone, immunity, breathing, cognition, and neurogenesis. Kinetics analysis shows that the BBB transporter performs most efficiently at low serum levels of leptin, suggesting that the feedback loop evolved to operate at lower leptin levels than those seen in ideal body weight. We suggest that low levels of serum leptin inform the brain that adipose reserves are adequate to expend calories on functions other than feeding, such as reproduction and the immune system. This feedback loop is short-circuited when an animal enters starvation. Hallmarks of starvation include decreased secretion of leptin by adipose tissue and hypertriglyceridemia. Triglycerides inhibit the transport of leptin across the BBB, thus attenuating the leptin signal across the BBB and providing a mechanism for peripheral leptin resistance. Triglycerides are elevated in both starvation and obesity. We postulate that hypertriglyceridemia evolved as a starvation signal to the brain that acts in part to inhibit the transport of the leptin across the BBB. The hypertriglyceridemia of obesity invokes this aspect of the starvation response, inducing leptin resistance at the BBB. Thus, the BBB plays important roles in both obesity and starvation.
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PMID:The blood-brain barrier as a cause of obesity. 1867 2

Abnormalities in nutritional status of peritoneal dialysis (PD) patients include too high body mass (overweight, obesity), too low body mass (underweight, starvation) or changes in body composition (malnutrition) without or with normal body weight. In vivo neutron activation analysis is considered the reference gold standard for the determination of protein malnourishment in end-stage renal disease patients, but body mass index (BMI) is the most frequently used parameter in nutritional assessment surveys. The association between BMI and outcome of PD patients is controversial, but so-called obesity paradox (the higher BMI the longer survival) remains frequently reported. The use of metabolic syndrome with high BMI as a crucial component is not more predictable in the prognosis of outcome in PD patients than using separately each risk factor of metabolic syndrome. Underweight/starvation is univocally underlined as associated with morbidity and mortality, but prevalence of severe undernutrition is decreasing over last decades, at least in well developed countries. PD patients may also present features of malnutrition without decreased body mass or even with increased body weight. It mainly concerns to deficiencies of vitamins, minerals and trace elements. Serum albumin concentration has serious limitations as a marker of nutritional status, because is influenced by volemic status and inflammation. Nutritional interventions in undernourished patients (oral, intestinal or intravenous feeding, amino acid peritoneal solution, supplementation of vitamins and trace elements) may correct deficiencies, but their influence on PD patients survival remains unclear.
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PMID:The role of nutritional status in the outcome of peritoneal dialysis patients. 1985 51

Brazil is going through problems with obesity as well as malnutrition and starvation--the nutritional transition. This is a cross sectional study with a sample of 1322 children under 10 years of age, residents in Ferros, Minas Gerais, Brazil, enrolled in SISVAN. Results showed that: 20.7% of children had nutritional disorder (10.1% nutritional risk, 3.8% malnourished and 6.7% overweight risk). Malnutrition risk factors were also identified: low birth-weight, RP = 3.57, IC 95% (1.96-6.52); stunting, RP = 19.36, IC 95% (11.53-32.52); no breastfeeding, RP = 2.23, IC 95% (1.19-4.18); family income below RS 95, RP = 2.39, IC 95% (1.10-5.16). Prevalence for overweight was higher than for malnutrition. While the rural population presented higher prevalence for nutritional risk and malnutrition, in the urban area there was higher prevalence of risk for overweight. These results show the need for specific nutritional interventions according to the specific issues identified.
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PMID:[Nutritional assessment in children under 10 in Ferros, Minas Gerais]. 2064 33

Positive caloric balance often causes pathologic adipocyte and adipose tissue anatomical and functional changes (termed adiposopathy or 'sick fat'), which may lead to pathogenic adipocyte and adipose tissue responses and metabolic disease. Fat weight loss may improve adiposopathy, and thus improve metabolic disease in overweight patients. Unfortunately, the efficacy of non-surgical weight loss therapies is often limited due to redundant physiological systems that help 'protect' against starvation and/or negative caloric balance. One strategy to overcome these limitations is to combine weight loss drug therapies having complementary mechanisms of action, thereby affecting more than one physiologic process influencing body fat accumulation. Phentermine is a noradrenergic sympathomimetic amine approved for short-term treatment of obesity. Topiramate is a sulfamate-substituted monosaccharide derivative of the naturally occurring sugar monosaccharide D-fructose approved as a treatment for migraine headaches and seizure disorders. Although known to facilitate weight loss since its approval, topiramate monotherapy does not have a regulatory indication as an anti-obesity agent. Phentermine HCl/topiramate controlled-release (PHEN/TPM CR) is a combination agent containing immediate-release phentermine and controlled-release topiramate. Clinical trials involving thousands of patients demonstrate PHEN/TPM CR to be effective in improving the weight of patients, and also effective in improving adiposopathy-associated metabolic diseases. This review examines the pathophysiology of adiposopathy as a contributor to metabolic disease, the data supporting phentermine monotherapy, topiramate monotherapy and their combination as anti-obesity and anti-adiposopathy agents, and the preliminary evidence supporting PHEN/TPM CR as a generally well-tolerated and effective agent to improve metabolic disease.
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PMID:Phentermine, topiramate and their combination for the treatment of adiposopathy ('sick fat') and metabolic disease. 2070 65

Food restriction induces a loss of body mass that is often followed by rapid regaining of the lost weight when the restriction ends, consequently increasing a risk of development of obesity. To determine the physiological and behavioral mechanisms underlining the regaining, striped hamsters were restricted to 85% of initial food intake for 4 weeks and refed ad libitum for another 4 weeks. Changes in body mass, energy budget, activity, body composition and serum leptin level were measured. Body mass, body fat mass and serum leptin level significantly decreased in food-restricted hamsters, and increased when the restriction ended, showing a short "compensatory growth" rather than over-weight or obesity compared with ad libitum controls. During restriction, the time spent on activity increased significantly, which was opposite to the changes in serum leptin level. Food intake increased shortly during refeeding, which perhaps contributed to the rapid regaining of body mass. No correlation was observed between serum leptin and energy intake, while negative correlations were found in hamsters that were refed for 7 and 28 days. Exogenous leptin significantly decreased the time spent on activity during food restriction and attenuated the increase in food intake during refeeding. This suggests that low leptin in restricted animals may function as a starvation signal to induce an increase in activity behavior, and high leptin likely serves as a satiety signal to prevent activity during refeeding. Leptin may play a crucial role in controlling food intake when the restriction ends, and consequently preventing overweight.
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PMID:Energy budget, behavior and leptin in striped hamsters subjected to food restriction and refeeding. 2337 94

Functional imaging data in adult patients with anorexia nervosa (AN) support a dysfunctional signal in the ventral striatum as neural signature of AN. In the present study, development of this signal was investigated with the prediction that a characteristic pattern of ventral-striatal signalling will be shown in response to cues associated with food restriction that reflects the evolvement of starvation dependence over time. The signal was assessed in adolescent patients with AN, whose duration of illness was about five times shorter relative to the adult sample. During functional magnetic resonance imaging subjects were required to estimate weights of body images (underweight, normal weight, overweight) and to process each stimulus in a self-referring way. Relative to age-matched, young healthy controls, underweight stimuli were already associated with greater activity of the ventral striatum, and processing of normal-weight stimuli elicited already reduced signalling. Subjective preferences showed exactly the same pattern of results. Relative to adult AN, the present data reveal a developing dysfunctional signal that, if untreated, will essentially contribute to the maintenance of AN. We discuss putative mechanisms that may play a crucial role in the development of AN, and also deduce new hypotheses about the involvement of the midbrain dopamine system, of which illness-related alterations may contribute to the development of AN.
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PMID:Role of the ventral striatum in developing anorexia nervosa. 2415 Feb 24

Ghrelin regulates homeostatic food intake, hedonic eating, and is a mediator in the stress response. In addition, ghrelin has metabolic, cardiovascular, and anti-aging effects. This cross-sectional study examined associations between total plasma ghrelin, caloric intake based on 3day diet diaries, hedonic eating attitudes, stress-related and metabolic factors, and leukocyte telomere length in overweight (n=25) and obese women (n=22). We hypothesized associations between total plasma ghrelin and eating behaviors, stress, metabolic, cardiovascular, and cell aging factors among overweight women, but not among obese women due to lower circulating ghrelin levels and/or central resistance to ghrelin. Confirming previous studies demonstrating lowered plasma ghrelin in obesity, ghrelin levels were lower in the obese compared with overweight women. Among the overweight, ghrelin was positively correlated with caloric intake, giving in to cravings for highly palatable foods, and a flatter diurnal cortisol slope across 3days. These relationships were non-significant among the obese group. Among overweight women, ghrelin was negatively correlated with insulin resistance, systolic blood pressure, and heart rate, and positively correlated with telomere length. Among the obese subjects, plasma ghrelin concentrations were negatively correlated with insulin resistance, but were not significantly correlated with blood pressure, heart rate or telomere length. Total plasma ghrelin and its associations with food intake, hedonic eating, and stress are decreased in obesity, providing evidence consistent with the theory that central resistance to ghrelin develops in obesity and ghrelin's function in appetite regulation may have evolved to prevent starvation in food scarcity rather than cope with modern food excess. Furthermore, ghrelin is associated with metabolic and cardiovascular health, and may have anti-aging effects, but these effects may be attenuated in obesity.
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PMID:Associations of ghrelin with eating behaviors, stress, metabolic factors, and telomere length among overweight and obese women: preliminary evidence of attenuated ghrelin effects in obesity? 2446 87


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