Is DHEA Replacement Therapy Beneficial?

我们对预防身体虚弱和丧失独立性的研究的主要重点一直是 对运动的适应。然而，由于大多数美国人没有锻炼的动力，我们已经开始评估 保持健康和预防虚弱的其他方法。在这些人中，最强大的似乎是DHEA 替代疗法。在这种背景下，这项研究的总体目标是确定长期 脱氢表雄酮(DHEA)替代疗法具有有益的效果，可以(A)延缓虚弱的发展 和残疾，(B)预防2型糖尿病和冠心病，(C)提高生活质量， 以及d)获得关于脱氢表雄酮作用机制的信息。脱氢表雄酮和脱氢表雄酮硫酸盐(DHEAS)血浆浓度 在-20岁时达到峰值，25岁后迅速明显下降。DHEA是PPARa激活剂。PPARA发挥着重要作用 在调节脂代谢和控制炎症方面的作用。脱氢表雄酮似乎也对肌肉有合成代谢作用。 还有骨头。这项研究是一项随机、双盲、安慰剂对照的脱氢表雄酮替代试验。它是 旨在确定在65-75岁的老年女性和男性中，12个月的脱氢表雄酮替代对(A)躯干和 内脏脂肪，(B)胰岛素抵抗和血清甘油三酯，(C)肌肉质量和力量，(D)骨密度，(E) 慢性炎症，(F)动脉内皮依赖性血管扩张，和(G)幸福感。的具体目标 本研究旨在验证服用脱氢表雄酮12个月后将(A)导致躯干显著减少的假设。 通过将代谢转变为脂肪氧化和增加能量浪费来减少内脏脂肪；(B)减少胰岛素抵抗 和降低血清甘油三酯；(C)增加肌肉质量和力量，通过减少分解代谢刺激和增加 合成代谢刺激；(D)通过增加合成代谢刺激和减少分解代谢刺激增加骨密度；(E) 减轻慢性炎症，减少外周血单核细胞产生促炎细胞因子； (F)改善动脉内皮依赖性血管扩张；及(G)改善一般幸福感。一个主要重点 这项研究的重点是DHEA替代的生物学效应的机制。

The major emphasis of our research on the prevention of physical frailty and loss of independence has been on the adaptations to exercise. However, because most Americans are not motivated to exercise, we have started to evaluate other approaches to maintenance of health and prevention of frailty. Of these, the most powerful appears to be DHEA replacement therapy. In this context, the overall goals of this study are to determine whether long term dehydroepiandrosterone (DHEA) replacement therapyhas beneficial effectsthat could (a) delay the development of frailty and disability, (b) protect against development of type 2 diabetes and coronary artery disease, (c) improve quality of life, and d) obtain information on the mechanisms of DHEAaction. DHEAand DHEA sulfate (DHEAS) plasma concentrations peak at -20 yr of age and decline rapidly and markedly after age 25 yr. DHEAis a PPARa activator. PPARa plays major roles in regulating lipid metabolism and controlling inflammation. DHEA also appears to have anabolic effects on muscle and bone. The study proposed here is a randomized, double blind, placebo-controlled trial of DHEA replacement. It is designed to determine the effects of 12 mo of DHEA replacement in 65-75 yr old women and men on (a) truncal and visceral fat, (b) insulin resistance and serum triglycerides, (c) muscle mass and strength, (d) bone mineral density, (e) chronic inflammation, (f) arterial-endothelium-dependent vasodilation, and (g) sense of well being. The specific aims of this study are to test the hypotheses that 12 mo of DHEA replacement will (a) Result in significant decreases in truncal and visceral fat by shifting metabolism to fat oxidation and increasing energy wastage; (b) Decrease insulin resistance and decrease serum triglycerides; (c) Increase muscle mass and strength, by decreasing catabolic stimuli and increasing anabolic stimuli; (d) Increase bone mineral density by increasing anabolic stimuli and decreasing catabolic stimuli; (e) Reduce chronic inflammation and decrease pro-inflammatory cytokine production by peripheral blood mononuclear cells; (f) Improve arterial endothelium dependent vasodilation; and (g) improve general sense of well being. A major emphasis of this research is on the mechanisms responsible for the biological effectsof DHEAreplacement.