Before the mid-20th century, the understanding and treatment of depression were in a primitive state. The first dedicated pharmacological antidepressants, monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs), would not be discovered until the 1950s. In the decades prior, particularly the 1930s, medical professionals experimented with various substances and radical physical interventions. Among the most prevalent drug-based approaches was the widespread use of amphetamines, a class of stimulant drugs that offered a temporary, but ultimately problematic, solution for mood disorders.
The Early Use of Amphetamines for Depression
Amphetamine, originally introduced in the 1930s as a remedy for nasal congestion and narcolepsy, was soon recognized for its mood-elevating properties. Marketed as Benzedrine in an inhaler form, its use quickly expanded into psychiatry. Clinicians noted that the stimulant effect of amphetamines seemed to counteract the low energy and anhedonia (inability to feel pleasure) characteristic of depression.
- AMA Approval: In 1937, the American Medical Association (AMA) Council on Pharmacy officially approved amphetamine for mood elevation in depression.
- Widespread Acceptance: By the mid-1940s, millions of amphetamine tablets were consumed daily in the United States, prescribed not only for mood elevation but also for weight loss and other conditions.
- Mechanism of Action: Amphetamines work by increasing the activity of neurotransmitters like dopamine and norepinephrine in the brain, which produce a fast-acting but short-lived mood lift and energy boost.
While this appeared to be a breakthrough, the effectiveness of amphetamines was minimal for treating persistent, long-term depression. The euphoria was transient, and tolerance developed quickly, often leading to dose escalation and dependence.
The Limits and Dangers of 1930s Drug Therapy
The amphetamine-based approach to depression was far from a cure and came with significant risks. The short-term mood lift was often followed by a crash, and chronic use led to a number of dangerous side effects.
Side Effects and Abuse Potential of Amphetamines
- Addiction and Dependence: The potential for misuse and addiction was extremely high. Users often escalated their dosage to chase the initial euphoria, leading to severe dependence and withdrawal symptoms similar to major depression.
- Psychosis: Chronic abuse could lead to amphetamine psychosis, characterized by hallucinations, paranoia, and bizarre behavior.
- Withdrawal: Stopping amphetamines could trigger a crash with intense fatigue, irritability, and depression, which further complicated treatment.
Amphetamines were ultimately abandoned for treating depression following the introduction of more targeted and safer antidepressants in the 1950s. Laws in the 1970s further restricted their medical use.
Other Drug and Substance Use
Besides amphetamines, other substances with psychoactive effects were sometimes used. These included older remedies that had been used for centuries, though with limited efficacy for clinical depression:
- Opioids: Often used for their mood-enhancing properties, opioids were a historical treatment for melancholy and had a high potential for addiction.
- Cocaine: Also possessing stimulant and antidepressant properties, cocaine was sometimes used, though its dangers were becoming increasingly clear.
- Barbiturates and Sedatives: These were used to manage agitation or anxiety, though they did nothing to treat the underlying depression and carried a high risk of dependence and overdose.
Non-Pharmacological Treatments of the Era
The 1930s also saw the development and use of several physical and non-medication-based treatments, many of which were radical and lacked modern safety protocols. These included:
- Electroconvulsive Therapy (ECT): Pioneered in the late 1930s, ECT involved inducing a seizure with an electrical current. It was a more controlled method than earlier chemical shock therapies but was administered without the muscle relaxants and anesthesia used today, leading to risks of broken bones and memory loss.
- Insulin Coma Therapy: Based on observations that seizures could calm some psychiatric patients, this treatment induced a hypoglycemic coma by administering large doses of insulin.
- Psychosurgery: The prefrontal lobotomy, which was developed in the 1930s, involved surgically severing connections in the brain's prefrontal cortex. It gained popularity but often resulted in severe personality changes and death.
- Hydrotherapy: Patients were submerged in warm or cold water for extended periods to induce a calming effect. While less invasive than other methods, it was often used in the harsh institutional settings of the time.
The Shift to Modern Antidepressants
The mid-1950s marked a true revolution in psychiatric treatment with the accidental discovery of the first modern antidepressants. Researchers noted that an antituberculosis drug, iproniazid, had unexpected mood-boosting effects, leading to the development of the MAOI class of antidepressants. Around the same time, imipramine, initially trialed for schizophrenia, was found to be effective for depression, pioneering the tricyclic antidepressant (TCA) class.
These discoveries led to more focused, if still imperfect, treatments. MAOIs and TCAs had significant side effects and a high risk of toxicity in overdose. However, they paved the way for more targeted and safer medications like Selective Serotonin Reuptake Inhibitors (SSRIs), which emerged in the late 1980s. The introduction of SSRIs, such as Prozac, marked a new era in psychopharmacology, offering a better-tolerated alternative with a lower risk profile compared to older treatments.
Comparison of 1930s vs. Modern Depression Treatment
| Aspect | 1930s Treatment (Amphetamines/Early Methods) | Modern Treatment (e.g., SSRIs/SNRIs) |
|---|---|---|
| Primary Drug Class | Amphetamines (Stimulants) | Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs), etc. |
| Mechanism of Action | Broad stimulation of the central nervous system; indirectly boosting neurotransmitters | Specific modulation of neurotransmitters (e.g., blocking serotonin reuptake) |
| Efficacy | Short-lived mood lift; tolerance and ineffectiveness for persistent depression | Slower onset (weeks), but more sustained and proven efficacy for a wider range of depressive symptoms |
| Safety and Side Effects | High risk of addiction, psychosis, severe side effects; high overdose potential with other substances | Fewer, often manageable side effects; significantly safer in overdose situations |
| Non-Drug Interventions | Harsh physical therapies like ECT, insulin coma therapy, lobotomies | Modern, safer ECT; Psychotherapy (CBT, IPT); lifestyle interventions |
| Medical Context | Primitive psychopharmacology; institutionalization common; focus on symptom management | Advanced psychopharmacology; outpatient care; integrated mental health services |
A Glimpse into Early Mental Health Institutions
Many of the treatments of the 1930s, both pharmacological and physical, were administered within the confines of large, often overcrowded, state-run asylums. These institutions, which were the norm for serious mental illness, were a far cry from modern psychiatric facilities. Patient accounts describe a terrifying atmosphere where experimental treatments were carried out without clear protocols or regard for patient dignity. The heroic therapies, including the crude early versions of ECT, were conducted with limited anesthesia and restraint, leaving lasting psychological and physical trauma on many individuals.
Even non-invasive treatments like hydrotherapy were frequently used in these institutional settings to manage rather than cure symptoms. The limitations of these settings and the harshness of the treatments underscore the dramatic shift in understanding and approach to mental illness that would occur in the following decades with the advent of more targeted pharmacology.
Conclusion
To answer the question, what drug was widely used to treat depression in the 1930s, the primary agent was amphetamine, marketed under brand names such as Benzedrine. This practice reflects a time when psychopharmacology was in its infancy and a deeper understanding of mental illness and its neurochemical basis was still decades away. Amphetamines offered a temporary mood lift and energy boost but were fundamentally different from today's antidepressants, with significant risks of addiction and limited long-term efficacy. The shift from these primitive, often dangerous, drug and physical therapies to the development of the first true antidepressants in the 1950s marked a pivotal turning point in mental health treatment, setting the stage for the safer, more targeted medications we use today.
