According to the World Health Organization physical inactivity causes 10-16% of deaths for breast and colorectal cancers. However, in Italy, approximately 41% of the population still remains sedentary. Moreover, physical activity is correlated with a lower risk of development and death for many common kinds of cancer. Moderate and regular exercise reduces metabolic syndrome, obesity, fat mass, and in particular visceral fat, which is active in the carcinogenesis as well as reduces testosterone and estrogens availability. "High activity" occupations are a protective factor against tumor development. Another important factor is timing, that is the life period when physical activity is performed. Physical exercise has a strong effect on breast and colorectal cancer risk reduction. Exercise may be a critical adjuvant therapy in the management of many cancers and it may enhance the therapeutic effects of traditional treatments. After cancer diagnosis, exercise prescription can have very positive effects. There is a strong evidence that regular post-diagnosis exercise could increase survivorship by 50-60% with the strongest evidence currently for breast and colorectal cancers. Many questions, about how, how long and when physical activity should be practiced in order to reduce cancer incidence and mortality and improve life quality, are still unsolved.

Diabetic subjects have a higher infective risk than healthy people, with more frequent and severe infections. This predisposition to infections is determined by hyperglycemia, microangiopathy and altered immune system. In particular, there is a polymorphonuclear leukocytes disfunction including chemotaxis, phagocytosis, bacterial killing and cellular activation by infective stimulus. These alterations are due to abnormal properties of polymorphonuclear leukocytes (PMN) in diabetic patients. Several parameters like phagocytosis of bacterial cells, chemiluminescence during oxidative burst and cell membrane deformability are related to glycaemia and glycated hemoglobin. Recent acquisitions show an altered integrin pattern on diabetics PMN, at baseline and after in vitro stimulation with soluble stimulus like fMLP or PMA. This could influence the interactions between PMN and endothelial cells and the diapedesis. Receptorial alterations on PMN surface may be ascribed to the abnormalities of the cytoscheleton, of the endocytosis and of the transduction mechanism, due to hyperglycemia.

Recently the definition, the pathophysiology and even the clinical utility of metabolic syndrome (MS) have been discussed. The risk induced by each component of the metabolic syndrome is higher than the risk induced by MS alone. MS alone is, in fact, a weaker predictor of cardiovascular disease than diabetes. New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. IGF/IGFBP system could be a link between insulin resistance and cardiovascular disease. RBP-4 can attenuate insulin signalling in skeletal muscle and induce hepatic gluconeogenesis. The belief that insulin-resistance is the main cause of MS could change in favour of the adipose tissue dysfunction. The most common cause of a reduced capacity of the adipose tissue to store fats is the increased dietary intake, also present in lipodistrophy, type 1 diabetes mellitus and polycystic ovarian syndrome. The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. The comprehension of adipose tissue dysfunction mechanisms offers new possibilities of prevention and therapy.

New evidence about diabetic microangiopathy has enabled us to identify an integrated pathogenesis of diabetic complications, including classic metabolic pathways induced by hyperglycaemia, insulin-resistance, hyperinsulinaemia, hormonal alterations and growth factors. Oxidative stress is the most important cause of endothelial damage inducing leukocyte adhesion, altered coagulation and inflammation. Adhesion molecules are a marker of endothelial damage and a potential therapeutic target. Changes in the extracellular matrix induced by TGFbeta1 and lower levels of eparan-sulfate, increased thickness of basement membranes and loss of pericytes are early events of diabetic retinopathy and diabetic nephropathy. Capillary rarefaction produced by genetic factors or by fetal undernourishment contributes to the beginning of insulin-resistance and hypertension. Psychophysical tests, electroretinogram and evoked potentials show retinal functional alterations; fundoscopy and retinal fluorescein angiography show retinal anatomic alterations. The diagnosis of diabetic neuropathy is based not only on traditional neurological examination and electroneurograms, but also on neurothesiometry for sensory testing. Medical treatment of diabetic microangiopathy is based on control of glycaemia, lipemia and blood pressure using glytazones, ACE-inhibitors, angiotensin II receptor antagonists and statins. New knowledgeabout microangiopathy pathogenesis suggests potential drugs for its therapy (ruboxistaurin, AGE-inhibitors, angiopoietin-1 and anti-VEGF, etc.), not yet on sale.