Insulin Coma Therapy of Schizophrenia: Some Critical Remarks on Dr. Sakel's Report

1951 ◽  
Vol 97 (406) ◽  
pp. 132-135 ◽  
Author(s):  
W. Mayer-Gross
Keyword(s):  
Insulin Therapy ◽  
Insulin Treatment ◽  
Insulin Coma ◽  
Insulin Coma Therapy

From Dr. Sakel's address there emerge two questions regarding the indications for insulin treatment in the psychoses which are worth discussing on this occasion:(1) General indications for the treatment: Should every case of schizophrenia undergo insulin therapy, i.e., be admitted to a hospital as soon as the illness has been diagnosed ?(2) Special indications and procedure: What is the role of convulsions in insulin therapy ? What proof is there of the presumed antagonism between coma and convulsion ? Are there any facts supporting the idea that insulin fixes the results of convulsion therapy ?

scholarly journals ‘A landmark in psychiatric progress’? The role of evidence in the rise and fall of insulin coma therapy

2021 ◽  
pp. 0957154X2110625
Author(s):  
Robert Freudenthal ◽  
Joanna Moncrieff
Keyword(s):  
Randomized Trials ◽  
Insulin Treatment ◽  
Considerable Debate ◽  
Insulin Coma ◽  
The 1950S ◽  
Psychiatric Profession ◽  
Insulin Coma Therapy

This paper examines the evidence behind the use and decline of insulin coma therapy as a treatment for schizophrenia and how this was viewed by the psychiatric profession. The paper demonstrates that, from the time of its introduction, there was considerable debate regarding the evidence for insulin treatment, and scepticism about its purported benefits. The randomized trials conducted in the 1950s were the result, rather than the origins, of this debate. Although insulin treatment was subsequently abandoned, it was still regarded as a historic moment in the modernization of psychiatry. Then, as now, evidence does not speak for itself, and insulin continued to be incorporated into the story of psychiatric progress even after it was shown to be ineffective.

Cortisone in the Treatment of Schizophrenia

1952 ◽  
Vol 98 (412) ◽  
pp. 401-403 ◽  
Author(s):  
Linford Rees ◽  
G. M. King
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Therapeutic Value ◽  
Consultant Physician ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Secretory Products ◽  
Insulin Coma Therapy ◽  
Normal Controls

Recent research has given rise to the hope that the secretory products of the adrenal cortex might be useful in the treatment of schizophrenia.Two main lines of research have stimulated renewed interest in the role of the adrenal cortex in the pathophysiology of schizophrenia. A number of investigations have produced evidence that the responsivity of the adrenal cortex of schizophrenic patients to stress is lower than that of normal controls (Freeman et al., 1944; Hoagland et al., 1946; Pincus and Elmadjian, 1946; Pincus et al., 1949).Another series of investigations has shown that adrenocortical activity is stimulated by insulin coma therapy, electronarcosis and electroconvulsive therapy (Hemphill and Reiss, 1942; Mikkelsen and Hutchins, 1948; Rees (1949a); Parson et al., 1949).Cranswick and Hall (1950) reported that desoxycortone acetate and ascorbic acid appeared to be therapeutically valuable in schizophrenia. Rees and King (1951) carried out a controlled investigation on the treatment of schizophrenia with desoxycortone acetate and ascorbic acid, and found no evidence that the method was of any therapeutic value. It was pointed out that the investigation did not preclude the possibility that other products of the adrenal cortex might be therapeutically useful in schizophrenia.The present paper describes a controlled investigation in the therapeutic value of cortisone administration in schizophrenia.We are indebted to Dr. Ernest Evans, Consultant Physician, East Glamorgan Hospital, for making available a supply of cortisone for the investigation.

Role of topical insulin therapy as an adjunct in the management of pressure ulcer

2020 ◽  
Vol 2 (3) ◽  
pp. 01-03
Author(s):  
Ravi Chittoria
Keyword(s):  
Wound Healing ◽  
Insulin Therapy ◽  
Pressure Ulcer ◽  
Healing Rate ◽  
Pressure Sore ◽  
Pressure Sores ◽  
Established Method ◽  
Wound Bed Preparation ◽  
Wound Healing Rate

Pressure ulcer or pressure sore is one of the complications seen in bedridden patients. Management of these ulcers is often challenging. But there is no well-established method that accelerates the wound healing rate. Various adjunctive methods are used for wound bed preparation before definitive reconstruction plan is made. Here we describe our experience in the role of insulin therapy as an adjunct in the management of pressure sores.

scholarly journals Insulin coma therapy: let's be factual

2014 ◽  
Vol 38 (6) ◽  
pp. 308-308
Author(s):  
Harold Bourne
Keyword(s):  
Insulin Coma ◽  
Insulin Coma Therapy

14-3-3 Facilitates Insulin-Stimulated Intracellular Trafficking of Insulin Receptor Substrate 1

2002 ◽  
Vol 16 (3) ◽  
pp. 552-562 ◽  
Author(s):  
Xiaoqin Xiang ◽  
Mingsheng Yuan ◽  
Ying Song ◽  
Neil Ruderman ◽  
Rong Wen ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Intracellular Trafficking ◽  
High Speed ◽  
Insulin Treatment ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Integral Role ◽  
Endogenous Proteins

Abstract The appearance of a complex between tyrosine-phosphorylated insulin receptor substrate 1 (IRS-1) and PI3K in a high-speed pellet fraction (HSP) is thought to be a key event in insulin action. Conversely, the disappearance of the IRS-1/PI3K complex from this fraction has been linked to insulin desensitization. The present study examines the role of 14-3-3, a specific phospho-serine binding protein, in mediating the disappearance of IRS-1 from the HSP after insulin treatment. An in vitro pull-down assay using recombinant 14-3-3 revealed that insulin enhances the association of 14-3-3 with IRS-1 in cultured adipocytes and that this is completely inhibited by wortmannin. An association of IRS-1 and 14-3-3 was also observed and was maximal after stimulation by insulin, when endogenous proteins were immunoprecipitated. Epidermal growth factor (EGF), 12-O-tetradecanoylphorbol-13-acetate, and okadaic acid, other agents that cause serine/threonine phosphorylation of IRS-1, also stimulated IRS binding to 14-3-3. The enhancement of IRS-1 binding to 14-3-3 by insulin was accompanied by movement of IRS-1 and the p85 subunit of PI3K from the HSP to the cytosol. In keeping with a key role of 14-3-3 in mediating this redistribution of IRS-1, the complexes of IRS-1 and 14-3-3 were found in the cytosol but not in the HSP of insulin-treated cells. In addition, colocalization of IRS-1 and 14-3-3 was observed in the cytoplasm after insulin treatment by confocal microscopy. Finally, the addition of a phosphorylated 14-3-3 binding peptide to an adipocyte homogenate (to remove 14-3-3 from IRS-1) increased the abundance of IRS-1/PI3K complexes in the HSP and decreased their abundance in the cytosol. These findings strongly suggest that 14-3-3 participates in the intracellular trafficking of IRS-1 by promoting the displacement of serine-phosphorylated IRS-1 from particular structures. They also suggest that 14-3-3 proteins could play an integral role in the process of insulin desensitization.

The Role of Insulin Therapy in Critically Ill Patients

2005 ◽  
Vol 4 (6) ◽  
pp. 353-360 ◽  
Author(s):  
Lies Langouche ◽  
Ilse Vanhorebeek ◽  
Greet Van den Berghe
Keyword(s):  
Insulin Therapy ◽  
Critically Ill ◽  
Critically Ill Patients
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