A patologização do sedentarismo

A identifica????o do sedentarismo como fator de risco para doen??as cr??nico-degenerativas influenciou significativamente nas recomenda????es de sa??de p??blica em defesa de estilos de vida fisicamente ativos. O artigo estuda o processo de patologiza????o do sedentarismo e seus desdobramentos para o campo da sa??de p??blica. Num primeiro momento, discutimos de que maneira o modelo biom??dico serve de base para a transposi????o de aspectos da conduta humana como ???fator de risco??? e, a seguir, como patologia, tal qual no caso espec??fico da ???S??ndrome da Morte Sedent??ria???, assim classificada por alguns autores. Em seguida, analisamos como essa vis??o vem sendo difundida no campo da sa??de, tomando por base um programa institucional que, ao mesmo tempo em que transforma o sedentarismo em doen??a, apresenta a atividade f??sica como um rem??dio cujos resultados podem se estender a todas as esferas da vida. Nessa linha de racioc??nio, em que os mal-estares de nossa civiliza????o s??o medicalizados e tornados mercadoria ao serem transformados em riscos e patologias, a atividade f??sica torna-se vacina para o corpo social.The identification of physical inactivity as a risk factor for chronic degenerative diseases has significantly influenced public health recommendations in support of physically active lifestyles. This study analyzes the pathologization of sedentariness and its implications in the public health field. First we discuss how the biomedical model serves as a basis to transform aspects of human behavior into ???risk factors??? and subsequently into pathologies such as the ???Sedentary Death Syndrome???, as some authors classify it. Second, we analyze how this view is being spread in the health field; our analysis is based on an institutional program which transforms sedentariness into illness while presents physical activity as a medicine whose results can reach all aspects of life. According to this rationale, in which the discomforts of our civilization are medicalized and made into commodities as they are transformed into risks and pathologies, physical activity becomes a vaccine to be applied to the social body

Tesaglitazar, a novel dual peroxisome proliferator-activated receptor alpha/gamma agonist, dose-dependently improves the metabolic abnormalities associated with insulin resistance in a non-diabetic population

Aims/hypothesis Insulin resistance is associated with abnormalities in lipid and glucose metabolism, which are major components of metabolic syndrome and risk factors for vascular disease. This study examined the effect of tesaglitazar (Galida), a novel, dual-acting peroxisome proliferator-activated receptor α/γ agonist, on lipid and glucose metabolism in patients with evidence of insulin resistance. Methods A 12 week, multicentre, randomised, double-blind, placebo-controlled, dose-finding study compared the efficacy and safety of oral tesaglitazar (0.1, 0.25, 0.5 and 1.0 mg/day) and placebo in 390 non-diabetic patients with hypertriglyceridaemia (plasma triglyceride concentration >1.7 mmol/l) and abdominal obesity (waist-to-hip ratio >0.90 for men and >0.85 for women). Results A 1.0-mg dose of tesaglitazar reduced fasting triglycerides (the primary endpoint) by 37% (95% CI: −43% to −30%; p<0.0001), non-HDL-cholesterol by 15% (95% CI: −20% to −10%; p<0.0001) and NEFA by 40% (95% CI: −51% to −27%; p<0.0001), and increased HDL-cholesterol by 16% (95% CI: 8 to −24%; p<0.0001). At the end of treatment there was a dose-dependent increase in patients with pattern A LDL particle diameter (40% at baseline vs 87% at 12 weeks for tesaglitazar 1.0 mg). Tesaglitazar produced significant reductions in fasting insulin concentration (−35%; p<0.0001) and plasma glucose concentration (−0.47 mmol/l; p<0.0001). Respiratory infection and gastrointestinal symptoms were the most common adverse events and were similarly frequent in all groups. Conclusions/interpretation Tesaglitazar was well tolerated and produced significant, dose-dependent improvements in lipid and glucose metabolism and insulin sensitivity. Tesaglitazar may have the potential to prevent vascular complications and delay progression to diabetes in these patients