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Cachexia is frequently observed in a number of different chronic illnesses. Although a final common pathway has not yet been established, a number of features have been recognised irrespective of underlying aetiology. These aspects of the disease include activation of the immune system, muscle wasting through the ubiquitin-proteasome pathway and endothelial dysfunction. Targeting these aspects of cachexia involves downstream signalling of proinflammatory cytokines, proteasome inhibition and possibly the use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins). Apart from their cholesterollowering features, the latter class of drugs has recently been shown to improve endothelial dysfunction, to induce endothelial progenitor cells, and to have anti-inflammatory properties. These features have recently b een termed p leiotropic effects of statins. It is therefore tempting to speculate that cachectic patients will benefit from treatment with statins, and possibly also from immunosuppression per se. [ABSTRACT FROM AUTHOR]

Numerous studies have shown that weight loss is associated with an increase in mortality [1] [4]. Treating weight loss in the elderly can ameliorate many medical conditions. For example, rehabilitation time following post-hip fractures has been shown to decrease with nutritional supplementation [5]. In hospitalised geriatric patients, nutritional supplementation resulted in improvement in serum protein, nutritional status, and decreased mortality [6]. In a subset of geriatric inpatients, low serum albumin with weight loss predicts those patients at highest risk for dying during the subsequent 2 years [7]. Riquelme and Torres et al. [8] carried out a multivariate analysis of risk and prognostic factors in community-acquired pneumonia in the elderly and found that age by itself was not a significant factor related to prognosis. Among the significant risk factors, only nutritional status is amenable to medical intervention. In the cachectic elderly, medical, cognitive, and psychiatric disorders may diminish self-sufficiency in activities of daily living (ADL), thus reducing the quality of life and increasing the frequency of secondary procedures, hospitalisations, and need for skilled care [2, 9]. [ABSTRACT FROM AUTHOR]

Cancer-related anorexia-cachexia syndrome (CACS) is a complex syndrome characterised by progressive weight loss with depletion of host reserves of skeletal muscle and, to a lesser extent, adipose tissue, anorexia, reduced food intake, poor performance status and quality of life that often precedes death [1]. At the time of diagnosis, 80% of patients with upper gastrointestinal cancers and 60% with lung cancer have already experienced substantial weight loss [2]. The prevalence of cachexia increases from 50 to > 80% before death and in > 20% cachexia is the main cause of death [2]. CACS results from the interaction of the host and the tumour. However, its nature is incompletely understood [3] [6], including the dynamics of host response (activation of systemic inflammatory response, metabolic, immune and neuroendocrine changes) and those tumour characteristics or tumour-derived products that influence expression of the syndrome (e.g. proteolysis-inducing factor, PIF). [ABSTRACT FROM AUTHOR]

The causes of significant weight loss in older persons are: (1) anorexia/starvation, (2) sarcopenia, (3) cachexia, and (4) dehydration. Thus, the first step in management of weight loss is to make the diagnosis. Depression, which is the most common cause of weight loss in older persons [1, 2], can be treated with antidepressants, which can also reverse weight loss, but monoamine oxidase inhibitors and mirtazapine (Remeron) appear to have specific orexigenic effects. The management of cachexia in older persons is extraordinarily complex, and involves both treatment of the underlying disease and specific nutritional therapy. Similarly, severe anorexia, often due to cytokine excess,must be treated. [ABSTRACT FROM AUTHOR]

Cachexia is defined as physical wasting with loss of muscle mass and weight that is caused by disease [1]. It is common for elderly individuals who have disease to exhibit cachexia.Additionally,muscle mass loss is characteristic of the conditions of frailty and sarcopenia. Sarcopenia is the age-related loss of muscle mass [2]. Physical frailty has been characterised by Fried et al. [3] as a condition that results from reduced strength, reduced gait velocity, reduced physical activity, weight loss, and exhaustion. Clearly, sarcopenia and frailty could be classified as cachectic conditions because they are associated with muscle mass loss. This chapter will describe the causes of sarcopenia, treatment of sarcopenia, causes of cachexia in elderly individuals, and treatment of cachexia in elderly individuals. [ABSTRACT FROM AUTHOR]

Cyclo-oxygenase-2 (COX-2) is an enzyme catalysing the synthesis of prostaglandins (PGs) from arachidonic acid. Cells contain genes coding for two isoforms of COX (COX-1 and COX-2). COX-1 is expressed constitutively in most tissues and appears to be responsible for the production of PGs that mediate normal physiological functions, such as maintenance of the integrity of the gastric mucosa and regulation of renal blood flow. In contrast, COX-2 is undetectable in most normal tissues: it is induced by cytokines, growth factors, oncogenes and tumour promoters, and it contributes to the synthesis of PGs in inflamed and neoplastic tissues [1]. COX-2 is induced in many human tumours and is associated with aberrant angiogenesis in a number of pathological settings, especially those involving inflammation. It has been well demonstrated that dysregulation of COX-2 expression correlates with development of gastrointestinal cancers. [ABSTRACT FROM AUTHOR]

Cachexia is characterised by accelerated loss of adipose tissue and skeletal muscle in the context of a chronic inflammatory response [1] [3]. It is a common complication of advanced cancer [4]. About half of all cancer patients suffer from this syndrome, which is among the most debilitating and life-threatening complications [5]. The key feature of this syndrome is weight loss, but other symptoms, such as anorexia, fatigue, vomiting and anaemia, and accelerated malnutrition with depletion of whole-body lipid and protein stores are frequently observed. Cancer cachexia contributes to immobility, a propensity to infection, shortened duration of survival, and overall decreased quality of life [6]. [ABSTRACT FROM AUTHOR]

Over the past few years, many authors have approached the problem of the treatment of cancer cachexia focusing on either the knowledge of the main pathogenetic events, or the outcomes of the treatment in terms of symptoms or improvement in quality of life [1] [8]. The relevance of clinical investigations of cancer anorexia-cachexia has epidemiological and clinical roots, considering that it is very frequent in advanced and terminal disease (up to 40% of patients with advanced disease, and more than 80% of terminal patients), and that its clinical manifestations often represent a source of great concern for both patients and relatives [1] [5]. The clinical approach to cancer anorexia-cachexia has been directed towards different targets, and it can be aetiological, pathogenetic or symptomatic according to the attention paid to tumour growth, the main pathogenetic events, or the clinical behaviour of the syndrome. However, it is mandatory to define both the biological and clinical rationale of the different therapeutic options, and the outcomes of every therapeutic approach, using an evidence-based model. [ABSTRACT FROM AUTHOR]

A large fraction of patients with advanced cancer develop cachexia [1], a wasting syndrome characterised by anorexia, asthenia, and profound losses of adipose tissue and skeletal muscle mass. The association of cachexia syndrome with poor prognosis, loss of functional status and poor quality of life has motivated researchers to develop therapeutic strategies for this problem [2]. [ABSTRACT FROM AUTHOR]

Cachexia is pervasive among patients suffering from chronic diseases, including cancer, liver cirrhosis and chronic renal failure. The development of cachexia dramatically impacts on the clinical course of the underlying disease, by increasing morbidity and mortality, and impinging on patients' quality of life. Also, weight loss influences outcome by increasing drug-induced toxicity and impeding completion of the therapeutic schedule. Particularly in cancer patients, weight loss is a reliable predictor for toxicity from treatment and shorter survival [1]. [ABSTRACT FROM AUTHOR]

For a long time the use of testosterone-derivative drugs (nandrolone decanoate and others) has been indicated for patients with cancer anorexiacachexia syndrome (CACS) on the basis of a truly protein anabolic effect [1], but the above drugs have a limited use because of some severe sideeffects (liver damage, endocrine effects). [ABSTRACT FROM AUTHOR]

Cancer cachexia is a major symptom burden for patients with cancer.Cachexia occurs in up to one half of all patients diagnosed with cancer [1] and is more frequent in patients with lung and upper-gastrointestinal cancer.Cancer cachexia results from the interaction of the host and the tumour. However, the nature of this interaction is incompletely understood [2] [5], including the dynamics of the host response (activation of the systemic inflammatory response, metabolic, immune and neuroendocrine changes) and those tumour characteristics or tumour-derived products that influence expression of the syndrome (e.g. proteolysis-inducing factor [PIF]). The relative importance of individual mediators and pathways in different patients or tumour types is unclear, as is the reason why individuals with apparently similar tumours should show considerable variation in their tendency to develop cachexia.As ability to discriminate the relative importance in vivo of different mediators improves, so too should the ability to develop appropriately targeted therapy. [ABSTRACT FROM AUTHOR]

Experienced oncologists acknowledge that the cancer anorexia/weight loss syndrome predicts a shorter survival for patients with advanced, incurable disease. Several powerful, well-conducted studies have borne out this clinical impression. DeWys et al. focused on weight loss in a multiinstitutional, retrospective review of 3047 cancer patients and observed that loss of more than 5% of premorbid weight predicted an early demise [1]. This prognostic effect occurred independently of tumour stage, tumour histology and patient performance status. Weight loss was also associated with a trend towards lower chemotherapy response rates. [ABSTRACT FROM AUTHOR]

Cancer cachexia is a multifactorial, multifaceted problem for which there is no uniform pathophysiological or clinical definition [1]. It is generally accepted as a complex syndrome with several cardinal features, including anorexia, early satiety, severe weight loss, muscle wasting, ischaemia, anaemia and oedema [2]. The essential characteristic that distinguishes cachexia from simple starvation is that the features of cachexia cannot be readily reversed by nutritional support alone [3]. [ABSTRACT FROM AUTHOR]

The focus of palliative care is illness-oriented, with the main aim being to relieve suffering. In contrast, the disease-oriented approach aims to improve the natural course of a disease and the length of life. Caring for nutritional issues of patients with advancing, progressive and terminal illness improves when the nutritional interventions focus on the effects of the illness on patients and relatives, and do not target curative or diseaseoriented endpoints (such as weight, oral intake). This brief chapter highlights the concept of palliative care, issues of palliative nutritional endpoints and decision making, the potential importance of treatment of symptoms and syndromes such as constipation as causes for secondary anorexia/ cachexia, issues of palliative symptom and syndrome management, and terminal care. [ABSTRACT FROM AUTHOR]

The anorexia/cachexia syndrome is one of the most common causes of death among patients with cancer and is present in 80% at death [1]. The term ‘cachexia' derives from the Greek kakòs, which means ‘bad', and hexis, meaning ‘condition'. The characteristic clinical picture of anorexia, tissue wasting, loss of body weight accompanied by a decrease in muscle mass and adipose tissue, and poor performance status that often precedes death has been named cancer-related anorexia/cachexia (CAC) [2] [5]. Since the 1980s, the previous concepts explaining CAC were replaced by a more complex insight, which stresses the interaction between metabolically active molecules produced by the tumour itself and the host immune response. One of the main features of the cachectic syndrome is anorexia, which may be so significant that spontaneous nutrition is totally inhibited. The pathogenesis of anorexia is most certainly multifactorial but not yet well understood. [ABSTRACT FROM AUTHOR]

A number of novel pathways and mediators controlling food intake, body weight, and energy expenditure have been identified using molecular and genetic techniques [1, 2]. It is now accepted that body weight is regulated by a feedback loop, in which peripheral signals from the gut, liver, and fat provide nutritional information via hormones and afferent vagal input to integrated centres in the brainstem and the hypothalamus. At these sites, monoaminergic and peptidergic neurons interact to integrate and transduce the incoming signals, thereby modulating food intake [2]. In this type of regulation, orexigenic and anorexigenic neuromediators are in a constant balance to maintain homeostasis. In several clinical diseases, ranging from inflammatory conditions such as obesity to cancer, an imbalance among these neuromediators occurs, leading, respectively, to either hyperphagia, with an increase in food intake, or to anorexia, with a decrease in food intake [3, 4]. [ABSTRACT FROM AUTHOR]

Involuntary weight loss and its end-stage manifestation, the anorexia and cachexia syndrome, is a frequent complication of cancer. The incidence of weight loss varies both with the primary site of the malignancy and its stage. At presentation, 15-48% of cancer patients report weight loss, while more than 80% of those with advanced disease note involuntary weight loss [1]. A weight loss of as little as 5% from premorbid weight predicts a poor prognosis, particularly among patients with lymphoma, lung, breast or gastrointestinal malignancies. Weight loss of less than 5% adversely impacts survival, with the greatest effect seen in those patients with good performance status [1]. Involuntary weight loss adversely affects quality of life as well [2] [4]. [ABSTRACT FROM AUTHOR]

Melatonin (N-acetyl-5-methoxytriptamine) is the best-known among the indoles produced by the pineal gland (also called the epiphysis) according to a circadian rhythm. The pineal gland is the regulator of photic and nonphotic effects of the sun; indeed, it is the anatomical structure that coordinates the body's functions with the most important environmental rhythm, that is the light/dark rhythm. This fact may help us in understanding the history of the pineal gland: ancient myths and philosophic systems all over the world assigned a significant role to this gland, with respect to the health of the body and the spirit. Indeed, Cartesius (Reneé Descartes) described the pineal gland as the site of the soul. The Greek name given by Vesalius to the pineal gland, epiphysis (επι = above; φυσισ = nature), implies that it is the counterpart of the hypophysis (υπο = below φυσισ = nature), whereas effectively the physiological activity of the pineal gland counterbalances that of the hypothalamic-pituitary-adrenal (HPA) axis. [ABSTRACT FROM AUTHOR]

Patients with cancer often suffer from progressive involuntary weight loss, which is called cancer wasting. Clinical features of this syndrome include anorexia, early satiety, depletion of lean and fat body mass, muscle weakness, fatigue and impaired immune function. It occurs in 30-90% of cancer patients depending on location, stage, type, grade, spread and anticancer treatment [1]. Patients with cancer of lung, pancreas, head-and-neck area and upper gastrointestinal tract often suffer from wasting [2] [5]. [ABSTRACT FROM AUTHOR]

The management of cancer in the older person is an increasingly common problem, as 60% of all neoplasms occur in individuals age 65 and older [1]. Aging is associated with a progressive decline in life-expectancy, functional reserve, and social resources, and an increased prevalence of comorbidity [2]. This process is highly individualised and poorly reflected in chronologic age. The diversity of the older population affects both clinical practice and clinical research, and underlies the main challenges of geriatric oncology. These include the formulation of individual treatment plans and of research protocols. [ABSTRACT FROM AUTHOR]

The mechanism of loss of weight (cachexia), appetite (anorexia), and strength (asthenia) of most patients with advanced, incurable cancer encompasses a complex combination of paraneoplastic primary anorexia-cachexia syndromes (ACS). In addition, there are often secondary ACS due to other complications of advanced cancer, such as severe symptoms, disrupted function of the gastrointestinal tract, and reduced physical ability [1]. [ABSTRACT FROM AUTHOR]

Weight loss is frequently seen in patients with advanced cancer and has long been recognised to be associated with decreased survival [1]. Cancer cachexia is a complex syndrome depending on cytokines, eicosanoids, and classical hormones, and characterised by progressive weight loss with depletion of host reserves of skeletal muscle and adipose tissue. It is the net result of profound metabolic changes that appear in patients with advanced stages of cancer, and is characterised by net breakdown of skeletal muscle and alterations in fat and carbohydrate metabolism. Cachexia is the most common paraneoplastic syndrome, and is also referred to as the cancer anorexia-cachexia syndrome, with features of anorexia, early satiety, weakness, and fatigue. [ABSTRACT FROM AUTHOR]

Approximately 80% of patients with advanced-stage cancer have cancer anorexia-cachexia syndrome (CACS), in which one of the main manifestations is malnutrition [1]. CACS is characterised by anorexia, decreased food intake, tissue wasting, and body weight loss. It is also associated with changes in lipid, protein, and carbohydrate metabolism, leading to a decrease in fat and muscle mass, which independently influence mortality in cancer patients [2] [5]. Anorexia and reduced food intake occur during growth of the tumour, thus compromising host defences which, in turn, detrimentally influences outcome [1]. Reduced food intake and malabsorption reduce energy intake, even though energy expenditure is increased [6] [8]. [ABSTRACT FROM AUTHOR]

Cancer cachexia (CC) is probably the most debilitating and life-threatening paraneoplastic syndrome. It is characterised by weight loss, anorexia, asthaenia, loss of skeletal muscle protein, depletion of lipid stores, and severe metabolic alterations. CC syndrome is present in about 50% of cancer patients, especially those with tumours of the gastrointestinal tract and lung, and less frequently in those with haematological malignancies and other solid neoplasms, such as breast and thyroid cancer. The majority of terminally ill cancer patients experiences CC, which accounts for about 20% of cancer deaths. This figure translates into approximately 2000000 deaths per year worldwide [1]. [ABSTRACT FROM AUTHOR]

Progressive atrophy of skeletal muscle in cancer cachexia leads to reduced power output and weakness (asthenia), resulting in reduced physical activity and a lower quality of life of the cancer patient. Eventually, loss of respiratory muscle becomes so extensive that function becomes significantly impaired, resulting in death through hypostatic pneumonia. Death normally occurs when patients have lost about 35% of their ideal body weight. [ABSTRACT FROM AUTHOR]

Cancer cachexia is one of the worst effects of malignancy, accounting for nearly a third of cancer deaths. It is a pathological state characterised by weight loss together with anorexia, weakness, anaemia, and asthaenia. The complications associated with the appearance of the cachectic syndrome affect both the physiological and biochemical balance of the patient and influence the efficiency of anticancer treatment, resulting in a considerably decreased survival time. At the metabolic level, cachexia is associated with loss of body lipid stores. Alterations in lipid metabolism are partially mediated by changes in circulating hormone concentrations (insulin, glucagon, and glucocorticoids, in particular) or in their effectiveness. However, a large number of observations point towards cytokines, polypeptides released mainly by immune cells, as the molecules responsible for the above-mentioned metabolic derangements. The role of humoral factors in fat metabolism in the cancer patient has been discussed; among cytokines, tumour necrosis factor-α (TNF-α) seems to have a key role in the lipid metabolic changes associated with cancer cachexia. [ABSTRACT FROM AUTHOR]

During disease, a formidable biological fight occurs between invading cells and the defending host.As a consequence, both sides use all the available weapons to succeed: invaders will try to shut off the host defence systems while the host will try to isolate and destroy the invaders. Metabolic perturbations inevitably develop and, if the challenge is prolonged over time, changes in body composition occur. Thus, cachexia could be considered as ‘collateral damage' in the fight between invading cells and the defending host. [ABSTRACT FROM AUTHOR]

Cancer-related anorexia-cachexia syndrome (CACS) may result from circulating factors produced by the tumour or by the host immune system in response to the tumour, such as cytokines released by lymphocytes and/or monocyte/ macrophages. A number of proinflammatory cytokines, including interleukin (IL)-1, IL-6, tumour necrosis factor (TNF)-α, interferon (IFN)α and IFN-γ, have been implicated in the pathogenesis of cachexia associated with human cancer. TNF-α was first identified by Rouzer and Cerami [1] as a specific circulating mediator of the wasting resulting from a chronic experimental infectious disease. It was named cachectin and was subsequently found to be identical to TNF-α. However, data from numerous clinical and laboratory studies suggest that the action of cytokines, although important, may not alone explain the complex mechanism of CACS [2] [5]. IL-1 and TNF-α have been proposed as mediators of the host's response to inflammation [6]. [ABSTRACT FROM AUTHOR]

Protein energy malnutrition (PEM) is, alone or associated with other diseases, the first step in the development of cachexia [1] [3]. An insufficient amount of food is the leading cause of malnutrition and infectious diseases are the second. In developing countries, 20% of the population — more than 800 million people — eats a quantity of food only sufficient to supply energy for a sedentary life, i.e. 1.2-1.4 times the resting energy expenditure (REE).More than 192 million children suffer from PEM and 2 billion people lack different micronutrients (vitamins, minerals, essential fatty and amino-acids) [4] [7]. Even in Western countries, where an enormous surplus of food is produced, many groups of people, especially the poor, the elderly, drug addicts, pregnant women, patients with liver, kidney and gastro-intestinal (GI)-tract diseases, cancer, AIDS, show nutritional defects. In general, 60% of the world's population (41% in developing countries) consumes less than 2600 Kcal/person/day, an amount of energy considered barely sufficient for limited activity. [ABSTRACT FROM AUTHOR]

The cachectic syndrome, characterised by marked weight loss, anorexia, asthaenia, and anaemia, is invariably associated with the presence and growth of the tumour and leads to a malnutrition status due to the induction of anorexia or decreased food intake. In addition, the competition for nutrients between the tumour and the host leads to an accelerated starvation state that promotes severe metabolic disturbances in the host, including hypermetabolism, which leads to decreased energetic efficiency. Although the search for the cachectic factor(s) started a long time ago, and although many scientific and economic efforts have been devoted to its discovery, we are still far from a complete understanding of cancer cachexia. The chapter discusses the different signalling pathways, particularly the role of transcriptional factors, involved in muscle wasting. The main aim is to summarise and evaluate the different molecular mechanisms and catabolic mediators (both humoral and tumoural) involved in cancer cachexia, since they may represent targets for promising future clinical investigations. [ABSTRACT FROM AUTHOR]

A decline in functional status is a profound predictor of morbidity and mortality [1]. The mortality rate increases from 15% in individuals with only one impairment in an instrumental activity of daily living (IADL) to 21% in persons with one or two IADL impairments. In subjects with five or six IADL impairments, the mortality rate reaches 37% [2]. Disabled older adults are four to six times more likely to die than the nondisabled [3]. Up to half of the geriatric patients admitted to a hospital have either loss of or a diminished performance in at least one ADL during admission. This decline in functional status occurs as early as the second day of hospital admission [4, 5]. [ABSTRACT FROM AUTHOR]

Anorexia-cachexia syndrome [1] and lipodystrophy [2] [6] are two conditions frequently associated with the course of HIV infection. Under many circumstances, they can be included as components of a single disease, multifactorial in origin, leading to alterations of energetic metabolism and to body fat tissue modifications. The risk for the clinician is of only partially considering the two diseases, for which, until recently, a true definition [3] was lacking. The approach to therapy, due to the multifactorial origin, must be multidisciplinary, involving experts in nutrition, infectious diseases, physiology, gastroenterology, etc. [ABSTRACT FROM AUTHOR]

The physiological decline in food intake that occurs with aging is an appropriate response to the reduced physical activity of this population. This physiological decline is termed the ‘anorexia of aging' [1]; however, cachexia in the elderly seems to be reaching epidemic levels, with 30-40% of men and women over age 75 being 10% underweight or more [2]. There is no agreed upon definition for cachexia, which means ‘poor condition' in Greek [3]. While it has traditionally been thought that chronic illness fully explains the pathogenesis of cachexia, this concept is proving inadequate [4]. In general, cachexia is characterised by weight loss due to loss of fat and skeletal muscle mass [5]. [ABSTRACT FROM AUTHOR]

The association between weight loss and severe chronic obstructive pulmonary disease (COPD) has long been recognised. Fowler and Godlee [1] first described the association of weight loss and emphysema in the late nineteenth century. Attempts to establish different COPD classifications led to the realisation that body weight might be an important disease determinant [2]. This led to the classical description of the pink puffer (emphysematous type) and the blue bloater (bronchitic type). The pink puffing patient is characteristically thin, breathless, and with marked hyperinflation of the chest. The blue and bloated patient may not be particularly breathless, at least when at rest, but has severe central cyanosis. In the 1960s, several studies reported that low body weight and weight loss are negatively associated with survival in COPD [3]. Nevertheless, therapeutic management of weight loss and muscle wasting in patients with COPD has become of interest only recently, since these features were generally considered as terminal progression in the disease process and therefore inevitable and irreversible. [ABSTRACT FROM AUTHOR]

The word cachexia is derived from the Greek words kakòs, meaning ‘bad,' and hexis, meaning ‘condition' [1]. From an epidemiological point of view, while patients with haematological malignancies and breast cancer seldom have this syndrome, most other solid tumours are associated with a high frequency of cachexia [2]. Indeed, its prevalence increases from 50% to more than 80% before death, and in more than 20% of patients cachexia is the main cause of death [3]. [ABSTRACT FROM AUTHOR]

Aging is associated with changes in body composition that have important consequences on health and physical function. Thus, studying body composition changes is of increasing interest in geriatric research, and measures are being developed to favourably influence body composition in old age, in addition to exercise and diet. [ABSTRACT FROM AUTHOR]

The pathophysiology, evaluation, and treatment of malnutrition have been extensively investigated in recent years, and knowledge has accumulated gradually. As a result, it is now well-known that several benign digestive diseases may cause malnutrition. This chapter reviews recent clinical aspects of malnutrition related to common digestive diseases, such as Crohn's disease, short bowel syndrome, chronic liver diseases, and chronic pancreatitis. In addition, recent progress in nutritional support in the treatment of these diseases is discussed. [ABSTRACT FROM AUTHOR]

Cachexia (body wasting) in patients with cardio-vascular illness usually develops when patients have chronic heart failure (CHF). As an increasing public health problem and a leading cause of morbidity and mortality worldwide, CHF is associated with a poor prognosis [1]. The onset of cachexia in CHF patients (cardiac cachexia) is a serious complication of their disease and even worsens the prognosis of the underlying disease [2]. This connection between advanced heart failure and significant weight loss has long been recognised. The earliest report dates back to the school of medicine of Hippocrates some 2300 years ago. The term ‘cachexia' is of Greek origin and derives from the words kakos (bad) and hexis (condition). The term ‘cardiac cachexia' was first used in 1860 by Mauriac [3]. [ABSTRACT FROM AUTHOR]