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抑郁与糖尿病之间的关联:寻找共同的发病机制。

The link between depression and diabetes: the search for shared mechanisms.

机构信息

Department of Psychological Medicine, Institute of Psychiatry, King's College London, London, UK.

Diabetes and Nutritional Sciences Division, King's College London, London, UK.

出版信息

Lancet Diabetes Endocrinol. 2015 Jun;3(6):461-471. doi: 10.1016/S2213-8587(15)00134-5. Epub 2015 May 17.

DOI:10.1016/S2213-8587(15)00134-5
PMID:25995124
Abstract

Depression is twice as common in people with type 1 or type 2 diabetes as in the general population, and is associated with poor outcomes. Evidence is growing that depression and type 2 diabetes share biological origins, particularly overactivation of innate immunity leading to a cytokine-mediated inflammatory response, and potentially through dysregulation of the hypothalamic-pituitary-adrenal axis. Throughout the life course, these pathways can lead to insulin resistance, cardiovascular disease, depression, increased risk of type 2 diabetes, and increased mortality. Proinflammatory cytokines might directly affect the brain, causing depressive symptoms. In type 1 diabetes, mediators of depression are not well studied, with research hindered by inconsistent definitions of depression and scarcity of observational, mechanistic, and interventional research along the life course. Despite few studies, evidence suggests that familial relationships and burden of a lifelong disorder with an onset early in personality development might contribute to increased vulnerability to depression. Overall, longitudinal research is needed to identify risk factors and mechanisms for depression in patients with diabetes, particularly early in the life course. Ultimately, improved understanding of shared origins of depression and diabetes could provide the potential to treat and improve outcomes of both disorders simultaneously. These shared origins are targets for primary prevention of type 2 diabetes.

摘要

抑郁症在 1 型或 2 型糖尿病患者中的发病率是普通人群的两倍,并且与不良结局相关。越来越多的证据表明,抑郁症和 2 型糖尿病具有共同的生物学起源,特别是先天免疫过度激活导致细胞因子介导的炎症反应,并且可能通过下丘脑-垂体-肾上腺轴的失调。在整个生命周期中,这些途径可能导致胰岛素抵抗、心血管疾病、抑郁症、2 型糖尿病风险增加和死亡率增加。促炎细胞因子可能直接影响大脑,导致抑郁症状。在 1 型糖尿病中,抑郁症的介质尚未得到很好的研究,由于抑郁症的定义不一致以及沿生命周期的观察性、机制性和干预性研究稀缺,研究受到阻碍。尽管研究较少,但有证据表明,家族关系和终生疾病的负担,以及在个性发展早期发病,可能导致对抑郁症的易感性增加。总的来说,需要进行纵向研究来确定糖尿病患者抑郁症的风险因素和机制,特别是在生命周期的早期。最终,对抑郁症和糖尿病共同起源的深入了解可能为同时治疗和改善这两种疾病的预后提供潜力。这些共同的起源是预防 2 型糖尿病的主要目标。

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