Sarcopenia and nutrition.

Preserving or restoring adequate nutritional status is a key factor to delay the onset of chronic diseases and to accelerate recovery from acute illnesses. In particular, consistent and robust data show the loss of muscle mass, that is, sarcopenia, is clinically relevant since it is closely related to increased morbidity and mortality in healthy individuals and patients. Sarcopenia is defined as the age-related loss of muscle mass and function. International study groups have recently proposed separate definitions and diagnostic criteria for sarcopenia. Unfortunately, the rate of agreement in assessing the prevalence of sarcopenia is just fair, which highlights the need for a common effort to harmonize definitions and diagnostic criteria. Sarcopenia should be distinct from myopenia, which is the disease-associated loss of muscle mass, although in clinical practice it may be impossible to separate them (i.e., in old cancer patients). The pathogenesis of sarcopenia is complex and multifactorial. Consequently, its treatment should target the different factors involved, including quantitatively and qualitatively inappropriate food intake and reduced physical activity.

Omega-3 fatty acids in cancer.

PURPOSE OF REVIEW: Significant achievements have been obtained in cancer treatment, but the clinical relevance of drug approach in daily practice remains questionable due to the high costs, limited efficacy, and negligible influence on quality of life. A new concept is emerging which is based on the early combination of chemotherapy and nutrition therapy. RECENT FINDINGS: Inflammation dictates tumour initiation, progression and growth. Omega-3 fatty acids exert anti-inflammatory effects, and therefore recent studies investigated their role in cancer prevention, in cancer cachexia treatment and in enhancement of antitumour therapies. Limited evidence suggests a role for omega-3 fatty acid supplementation in cancer prevention, but they have been shown to preserve muscle mass and function in cancer patients even during active treatment. During chemotherapy, omega-3 fatty acids may contribute to a reduced inflammatory response, but whether cancer treatment toxicity can be prevented remains to be assessed. Finally, small studies showed that omega-3 fatty acids increase response rate to chemotherapy. SUMMARY: Combination of chemotherapy and omega-3 supplementation appears an effective strategy to enhance the clinical outcome of cancer patients in their curative and palliative clinical trajectory.

Neuroinflammation: a contributing factor to the pathogenesis of cancer cachexia.

The clinical journey of cancer patients is frequently complicated by the development of a complex and multifaceted syndrome, the main features of which are reduced appetite, decreased food intake, progressive weight loss, and wasting of muscle mass and adipose tissue, which is not prevented by the provision of calories and proteins. This syndrome, termed Cachexia, is responsible for increased morbidity, reduced survival, and impinged quality of life of cancer patients. The pathogenesis is complex and involves deranged metabolism of peripheral tissues and profound alterations of brain neurochemistry. Recent studies indicate that brain neurochemistry is perturbed during tumor growth by cancer-induced increased intrahypothalamic expression of proinflammatory cytokines. The attending neurochemical chaos mediates the anorexigenic behavioral responses associated to cancer cachexia, but recent data seem to suggest that neuronal output also may be involved in the metabolic changes occurring at the peripheral level.

The growth hormone secretagogue receptor (Ghs-R).

The growth hormone secretagogue receptor (GHS-R) is a component of the ghrelin signaling pathway and is involved in mediating the pleiotropic effects of ghrelin. Two isoforms have been identified, but only GHS-R1a binds with acyl ghrelin and transduces its message. However, the inactive variant of GHS-R, GHS-R1b, appears to play a critical role in modulating the activity of GHS-R1a by forming heterodimeric complexes which attenuates trafficking of the active variant to the cell surface. The molecular mechanisms of signal transduction are complex and are specific of the tissues where GHS-R1a is expressed. The potent induction of GH secretion and the stimulation of appetite are the most intensively studied functions of GHS-R1a. However, the tissue distribution of GHS-R1a extends beyond the pituitary and the hypothalamus, and reflects the different biological functions of the ghrelin/GHS-R system. GHS-R1a is also expressed in other brain areas, in the pancreas, adipose tissue, immune cells and cardiovascular system, and modulates learning and memory, glucose and lipid metabolism, inflammatory response and cardiac performance. The pleiotropic effects of the ghrelin/GHS-R system suggest their exploitation to prevent and treat a number of clinical conditions. Among many other syndromes and diseases, cancer cachexia, aging related cognitive decline, obesity and diabetes may significantly benefit from the use of GHS-R1a agonists or antagonists.