Tattersall R B
Department of Diabetes University Hospital Nottingham, UK.
Diabet Med. 1994 Aug-Sep;11(7):618-35. doi: 10.1111/j.1464-5491.1994.tb00324.x.
One of the longest-running controversies in medicine concerns the aims of diabetes treatment. The question debated for 80 years has been whether the clinician should just relieve symptoms, or try to achieve the much more difficult objective of near-physiological normality as measured by an absence of glycosuria and/or normal blood sugar levels. At the beginning of World War One, most clinicians and physiologists thought the severity of diabetes was inversely proportional to the number of functioning islets of Langerhans. Hyperglycaemia, it was hypothesized, stressed the surviving islets and led to a downward spiral of increasing glandular fatigue and hyperglycaemia. The aim of undernutrition was to rest the damaged tissue in the hope of promoting a return of functional efficiency and possibly regeneration. Most experts stressed that rest of the islets could only be achieved by abolishing glycosuria and restoring normal blood sugar levels. The first clinical use of insulin in 1922 led to astonishing improvements in the health and strength of patients with diabetes and the concept of pancreatic rest seemed to be confirmed when some regained such carbohydrate tolerance that after weeks or months they could reduce the dose of insulin without developing glycosuria. Initially there were expectations that insulin would allow the islets of Langerhans to recover completely, so that diabetes was cured. Most physicians insisted that the best chance of preserving what pancreatic function remained was biochemical normality. It was also contended that patients who had normal blood sugar levels were more healthy than those without and had fewer 'complications'. The complications in question were mainly infective, since specific diabetic tissue damage was not recognized until the late 1930s. The toll of microvascular complications (retinopathy and nephropathy) in those whose lives had been saved by insulin did not become apparent until the late 1930s and early 1940s, when it generated an often acrimonious debate about whether they were due to the metabolic disorder or an associated phenomenon. Liberalization of diet in patients taking insulin began in 1926 and by 1930 it was clear that patients who were prescribed 200 g of carbohydrate per day felt better and more energetic than those on the old regimens of 50 g or less per day. Even these more liberal diets were measured but, in the early 1930s some paediatricians, feeling that a strict measured diet was psychologically damaging, experimented with 'free' or unmeasured diets.(ABSTRACT TRUNCATED AT 400 WORDS)
医学领域持续时间最长的争议之一涉及糖尿病治疗的目标。80年来一直争论的问题是,临床医生应该仅仅缓解症状,还是试图实现一个困难得多的目标,即通过无糖尿和/或正常血糖水平来衡量的接近生理正常状态。第一次世界大战开始时,大多数临床医生和生理学家认为糖尿病的严重程度与朗格汉斯胰岛的功能数量成反比。据推测,高血糖会给存活的胰岛带来压力,导致腺体疲劳和高血糖的恶性循环。营养不足的目的是让受损组织得到休息,以期促进功能效率的恢复,并可能实现再生。大多数专家强调,只有消除糖尿并恢复正常血糖水平,才能让胰岛得到休息。1922年胰岛素首次用于临床,使糖尿病患者的健康和体力有了惊人的改善,当一些患者恢复了碳水化合物耐受性,几周或几个月后可以减少胰岛素剂量而不出现糖尿时,胰腺休息的概念似乎得到了证实。最初,人们期望胰岛素能让朗格汉斯胰岛完全恢复,从而治愈糖尿病。大多数医生坚持认为,保持剩余胰腺功能的最佳机会是生化正常。也有人认为,血糖水平正常的患者比血糖不正常的患者更健康,“并发症”也更少。当时所说的并发症主要是感染性的,因为直到20世纪30年代末才认识到特定的糖尿病组织损伤。直到20世纪30年代末和40年代初,胰岛素挽救了生命的患者中微血管并发症(视网膜病变和肾病)的危害才显现出来,当时引发了一场激烈的争论,即这些并发症是由代谢紊乱还是相关现象引起的。1926年开始放宽接受胰岛素治疗患者的饮食,到1930年,每天摄入200克碳水化合物的患者比每天摄入50克或更少碳水化合物的旧饮食方案患者感觉更好、更有活力,这一点已经很明显。即使是这些更宽松的饮食也是经过计量的,但在20世纪30年代初,一些儿科医生认为严格的计量饮食对心理有损害,于是尝试了“自由”或不计量的饮食。(摘要截选至400字)