Insulin Shock Therapy (IST), also known as Insulin Coma Therapy (ICT), was a psychiatric treatment method used primarily for schizophrenia during the mid-20th century. This practice involved intentionally lowering a patient’s blood sugar to dangerously low levels to induce a coma. Although initially embraced as a biological approach to severe mental illness, the therapy was ultimately discontinued. This abandonment was due to severe risks to patients and a lack of verifiable long-term benefit, as overwhelming evidence showed the harms greatly outweighed any perceived therapeutic outcomes.
The Procedure and Initial Rationale
The development of this treatment began with Polish-Austrian psychiatrist Manfred Sakel in the late 1920s. Sakel was using insulin to treat morphine addiction when an accidental overdose caused a patient to enter a coma. The patient emerged with a perceived improvement in their mental state, leading Sakel to hypothesize that a controlled metabolic shock could “reset” the brain and alleviate symptoms of psychosis, particularly in patients with schizophrenia.
The technique, often called “Sakel’s technique,” involved daily injections of increasingly large doses of insulin. These massive doses caused profound hypoglycemia, or low blood sugar, leading to stupor, convulsions, and finally, a deep coma lasting up to an hour. The coma was then terminated by administering an intravenous injection of glucose or via a naso-gastric tube.
This rigorous process was repeated up to six days a week, sometimes for 50 to 60 comas over several months or even years. The intensive nature of this treatment required specialized units and constant, round-the-clock nursing supervision. Proponents in the 1930s and 1940s reported high success rates, claiming improvement in up to 70% of early-stage schizophrenia cases.
Immediate Dangers and Patient Mortality Rates
The intentional induction of a deep hypoglycemic coma carried immediate, severe dangers that contributed to the therapy’s rejection. The primary threat was the risk of an irreversible coma, where the patient could not be revived, leading directly to death. Fatality rate estimates typically ranged from 1% to nearly 5% of treated patients.
Patients were also at high risk of developing permanent neurological damage due to prolonged oxygen deprivation to the brain. The lack of glucose, the brain’s main fuel source, caused cellular damage that resulted in lasting cognitive impairment. Patients frequently experienced severe seizures and convulsions during the transition into or out of the coma.
Complications also included aspiration pneumonia, a serious respiratory condition caused by inhaling stomach contents or saliva while comatose. The intensive nature of the treatment meant patients were liable to develop “after-shocks” and hypoglycemic episodes when not actively receiving treatment, necessitating continuous monitoring.
Failure to Prove Long-Term Effectiveness
As the therapy’s usage became widespread in the 1940s and 1950s, scientific scrutiny undermined its supposed therapeutic value. Early positive results were often based on anecdotal evidence or studies that lacked appropriate control groups, making genuine efficacy difficult to distinguish from other factors. Later controlled studies were unable to replicate the dramatic success rates claimed by initial proponents.
A significant controlled trial published in The Lancet in 1957 compared patients receiving insulin-induced coma with those receiving unconsciousness induced by barbiturates. The study found no difference in outcomes between the two groups. This suggested that the coma itself, rather than insulin as a specific agent, was the source of any temporary effect, challenging the therapy’s core biological premise.
Further randomized comparisons in the late 1950s failed to establish a long-term benefit. Researchers observed that temporary improvements were often short-lived, resulting in high readmission rates and little lasting influence on the long-term prognosis of schizophrenia. This lack of scientific validation confirmed the treatment was hazardous and therapeutically unreliable.
Professional Condemnation and Safer Alternatives
The combination of significant patient risks and evidence demonstrating poor efficacy led to the professional condemnation and rapid phase-out of Insulin Shock Therapy. By the mid-1950s, disillusionment with the procedure was widely discussed in psychiatric literature. The treatment was gradually abandoned in many institutions throughout the 1960s and was largely obsolete by the 1970s.
The obsolescence was accelerated by the introduction of the first generation of antipsychotic medications, such as chlorpromazine, in the mid-1950s. These neuroleptic drugs offered a substantially safer, more manageable, and effective means of controlling the symptoms of psychosis. A 1958 comparison showed that chlorpromazine was comparable in outcome to IST but was significantly safer and easier to administer, making the risky coma treatment medically unjustifiable.
The logistical demands of IST, which required intensive staffing and specialized units, also became untenable compared to the simplicity of pharmacotherapy. The rise of modern psychopharmacology provided a less invasive and scientifically grounded alternative, solidifying the professional decision to cease the use of Insulin Shock Therapy.