RESUMEN
BACKGROUND: Current guidelines for prevention and treatment of cardiovascular disease (CVD) emphasise the importance of a healthy lifestyle. However, successful lifestyle intervention is proving to be a challenge for healthcare professionals. OBJECTIVES: Evaluation of the effect of lifestyle intervention on cardiovascular risk factors, on reaching treatment targets and on the estimated risk of cardiovascular morbidity and mortality. METHODS: The effect of a six-month multidisciplinary structured lifestyle intervention programme was assessed in 186 patients with and without a history of CVD. RESULTS: Multidisciplinary structured lifestyle intervention reduced the estimated ten-year risk of cardiovascular morbidity and mortality. The relative risk reduction was similar in patients with and without a history of CVD, the absolute risk reduction was higher in patients with a history of CVD. In both groups blood pressure and body weight decreased, and the maximal work rate and maximal oxygen uptake increased significantly. Blood levels of total cholesterol and cholesterol/HDL ratio decreased significantly in patients with a history of CVD. In addition, target levels for blood pressure and physical fitness were more frequently reached in both patient groups. CONCLUSION: Multidisciplinary structured lifestyle intervention had beneficial effects on cardiovascular risk factors. Relative risk reduction was similar in patients with and without evidence of cardiovascular disease. Follow-up is needed to see how well these effects can be maintained.
RESUMEN
GH release is increased by reducing circulating free fatty acids (FFAs). Aging is associated with decreased plasma GH concentrations. We evaluated GH releasing capacity in nine healthy elderly men after administration of GH-releasing peptide 2 (GHRP-2), with or without pretreatment with the antilipolytic drug acipimox, and compared the GHRP-2-induced GH release with the response to GHRH. The area under the curve (AUC) of the GH response after GHRP-2 alone was 4.8 times higher compared with GHRH alone (1834 +/- 255 vs. 382 +/- 78 microg/L.60 min, P: < 0.001). Acipimox, which reduced FFAs from 607 micromol/L to 180 micromol/L, increased the GH AUC to 1087 after GHRH and to 2956 microg/L.60 min after GHRP-2 (P: < 0.01). The AUC after acipimox/GHRP-2 were positively correlated with the AUC after GHRP-2 alone (r = 0.93, P: < 0.01); this was also observed between acipimox/GHRH and GHRH alone (r = 0.73, P: = 0.03). Significant negative correlations were observed between basal FFAs and AUC after GHRH or GHRP-2 after combining the data with and without acipimox (r = 0.58, P: = 0.01 and r = 0.48, P: = 0.04, respectively), and between basal FFAs and GH at t = 0 (r = -0.44, P: = 0.001). Interestingly, GHRP-2 administration was followed by a significant early rise in plasma FFAs by 60% (P = 0.01), indicating an acute lipolytic effect. In conclusion, reduction of circulating FFAs strongly enhances GHRP-2-stimulated GH release in elderly men. The data indicate that the decreased GH release associated with aging can be reversed by acipimox and that the pituitary GH secretory capacity in elderly men is still sufficient.