Many studies were carried out in the 1950s and 1960s aiming at investigating special aspects of metabolic malfunction and changes in body composition secondary to chronic diseases. The evidence emerging from these studies made it apparent that multiple mechanisms act in combination, forming a complex web of metabolic imbalance with catabolism dominating the anabolic drive, resulting in weight loss. A first attempt at a comprehensive overview of the complex pathophysiology of cachexia with special emphasis on cardiac cachexia was made by Pittman and Cohen in 1965 [45,46] (Fig. 2). Their review of related studies addressed three main pathophysiolog-ical mechanisms of cardiac cachexia:
1. Dietary factors
2. Loss of potential nutrients
The findings of Pittman and Cohen may be summarised as follows: dietary factors, i.e. reduced supply of nutrients to the body, as discussed before, are generally accepted as a factor of primary importance in the genesis of cachexia. Many reasons for a reduced food intake in the setting of chronic disease have been discussed. Patients frequently complain of gastrointestinal problems and many reasons were identified: reduced gastric
motility, delayed gastric emptying, a reduced capacity due to hepatomegaly, ascitis, meteorism and pain due to distension or splanchnic angina. Psychological factors may also account for reduced eating, such as depression and fear of increased discomfort after a meal. In this context, a change in the pattern of eating was also shown. Instead of eating a full meal three times per day, patients start to eat small portions of food irregularly throughout the day. This 'nibbling' instead of'gorging' has been suggested to affect the intermediate metabolism and make the calorie uptake less efficient [47, 48]. An excessive loss of potential nutrients due to impaired absorption or excessive excretion has been shown for fat as well as for protein and vitamins .
At the same time, an increased metabolic rate due to increased energetic demands of specific tissues and general calorie-consuming factors such as increased body temperature may further contribute to an unfavourable balance of the body energy metabolism. As a result, the catabolic drive may chronically dominate the anabolic pathways. The constant drain of the body's energy reserves may eventually lead to a pathological tissue degradation.
More than a century of studying the specific phenomenon of cachexia in patients with chronic heart failure has passed. The nineteenth century brought the medical term and the clinical recogni-
tion of cardiac cachexia; the twentieth century focussed on more sophisticated pathophysiological studies of this subject. With regard to therapeutic options, however, cachexia in chronic heart failure, as in many other diseases, is still a mostly unknown and unconquered territory. In 1964, Pittman and Cohen concluded: 'Besides the avoidance of ... potentially harmful forms of therapy, the only known treatment of cardiac cachexia requires improvement in cardiac function' . This may be extended reespectively to cachexia in general that occurs secondary to chronic diseases. We believe that the twenty-first century will see major improvements towards the development of therapy strategies aiming at reducing or even reversing cachexia in chronic diseases.
I thank the staff of the libraries of the National Heart & Lung Institute, the Hammersmith Hospital, St Marie's Hospital, and the Imperial College South Kensington Campus for their support in the extensive literature search. Klaus Wojciechowski assisted substantially in the research of literature sources.
W.D. was supported by the 'Verein der Freunde und Förderer der Berliner Charité', Germany and the National Heart & Lung Institute, London, UK.
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