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Is Soma a benzo or barbiturate? Unpacking the drug's true identity

5 min read

First approved in 1959, the muscle relaxant Soma (carisoprodol) is commonly mistaken for a benzodiazepine or barbiturate due to its sedative effects. However, Soma is in a class of its own, a carbamate, though its pharmacology is closely linked to these other controlled substances. This article clarifies Soma's classification, mechanism of action, and why its effects blur the lines with more widely known sedative drug classes.

Quick Summary

Soma, or carisoprodol, is a carbamate muscle relaxant, not a benzodiazepine or a barbiturate. Its sedative effects and potential for abuse are due to its active metabolite, meprobamate, which has pharmacological actions similar to barbiturates, leading to its Schedule IV classification.

Key Points

  • Not a Benzo or Barbiturate: Soma (carisoprodol) is chemically classified as a carbamate muscle relaxant, not a benzodiazepine or barbiturate.

  • Meprobamate Metabolite: Soma is metabolized into meprobamate, a substance that has pharmacological actions similar to barbiturates, explaining its sedative and abuse potential.

  • GABA System Modulation: Its metabolite affects the brain's GABA system, a mechanism of action shared with both benzodiazepines and barbiturates, though with key differences.

  • Schedule IV Controlled Substance: Due to its potential for abuse and dependence, the DEA reclassified Soma as a Schedule IV controlled substance in 2012.

  • Risks of CNS Depression: Like other CNS depressants, Soma causes drowsiness and carries a high risk of overdose, especially when combined with alcohol, opioids, or benzodiazepines.

  • Short-Term Use Only: The FDA recommends that Soma be used for no longer than two to three weeks, as there is insufficient evidence for long-term efficacy and the risk of dependence increases.

In This Article

What Is Soma (Carisoprodol)?

Soma is the brand name for the generic drug carisoprodol, a centrally acting muscle relaxant prescribed for the short-term relief of discomfort associated with acute, painful musculoskeletal conditions. It is typically used as part of a treatment plan that includes rest and physical therapy. The drug works by blocking pain sensations between the nerves and the brain, which in turn leads to a sedative effect that helps relax the muscles.

Unlike direct-acting muscle relaxants that target the muscle tissue, Soma's effects on skeletal muscle relaxation are related to its central nervous system (CNS) depressant properties. However, its mechanism of action is often confused with benzodiazepines and barbiturates because it shares some key pharmacological characteristics, particularly through its active metabolite.

The Active Metabolite: Meprobamate

One of the primary reasons for the confusion surrounding Soma's classification is its metabolism in the body. When a person takes carisoprodol, it is broken down in the liver into several metabolites, with the major one being meprobamate. Meprobamate is a historically significant sedative and anxiolytic medication that was once widely prescribed but has since fallen out of favor due to its significant potential for abuse.

Meprobamate's pharmacological actions are similar to those of barbiturates, which exert a central nervous system depressant effect. This means that when a person takes Soma, they are essentially introducing a compound (carisoprodol) that is converted into a barbiturate-like substance (meprobamate). This metabolic pathway is responsible for many of Soma's sedative and habit-forming properties, bridging its effects with those of more established sedative classes.

Mechanism of Action

The calming and muscle-relaxing effects of Soma are a result of its interaction with the brain's GABA (gamma-aminobutyric acid) system. GABA is the primary inhibitory neurotransmitter in the CNS, and when its activity is enhanced, it results in sedation, muscle relaxation, and a reduction in anxiety.

  • Carisoprodol's Role: While the exact mechanism of the parent drug carisoprodol is not fully understood, it is believed to block interneuronal activity in the spinal cord and brain stem, leading to its muscle-relaxant effect.
  • Meprobamate's Role: Its metabolite, meprobamate, exerts barbiturate-like effects by acting as a positive allosteric modulator of GABA-A receptors. This means it increases the inhibitory effect of GABA, which is a mechanism shared with both benzodiazepines and barbiturates, though with important differences.

Benzodiazepines vs. Barbiturates: The Distinction

Benzodiazepines (like Xanax and Valium) and barbiturates (like phenobarbital) both work on the GABA-A receptor but in different ways, which accounts for their different safety profiles.

  • Benzodiazepines (Benzos): These drugs increase the frequency of chloride channel opening triggered by GABA. They are generally considered safer than barbiturates because they have a higher therapeutic index, meaning a larger dose is needed to cause a fatal outcome.
  • Barbiturates: These drugs increase the duration of chloride channel opening. At high doses, they can directly activate the GABA-A receptor even without GABA present, leading to profound CNS depression, respiratory failure, and a high risk of lethal overdose.

Comparison: Soma vs. Benzos and Barbiturates

To understand why Soma is distinct yet shares properties with other central nervous system (CNS) depressants, consider the comparison below:

Feature Soma (Carisoprodol) Benzodiazepines Barbiturates
Drug Class Carbamate Benzodiazepine Barbiturate
Mechanism Metabolized to meprobamate, which potentiates GABA-A receptors (barbiturate-like effects) Enhance GABA effects by increasing channel opening frequency Enhance GABA effects by increasing channel opening duration; direct GABA activation at high doses
Primary Use Short-term treatment of muscle spasms Anxiety, insomnia, seizures, muscle spasms Anesthesia, seizures (historically used for anxiety and insomnia)
Abuse Potential High potential for abuse and dependence, classified as Schedule IV High potential for abuse and dependence, classified as Schedule IV High potential for abuse and dependence, high risk of overdose
Overdose Risk Significant risk, especially when combined with other CNS depressants Significant risk, lower than barbiturates, but increased by combination with other depressants Extremely high risk due to respiratory depression

The Risks and Dangers of Soma

Because of its sedative effects and the activity of its meprobamate metabolite, Soma carries significant risks, which is why it is only recommended for short-term use (typically 2 to 3 weeks) and is a controlled substance.

  • Central Nervous System Depression: The most common side effects include drowsiness, dizziness, and headache, which can impair a person's ability to operate machinery or drive safely.
  • Synergistic Effects: When combined with other CNS depressants, such as alcohol, opioids, or benzodiazepines, the sedative effects are compounded. This combination, sometimes called the “Holy Trinity” of abuse, can lead to severe respiratory depression, overdose, and death.
  • Dependence and Withdrawal: Prolonged use can lead to physical dependence, and abrupt cessation can result in withdrawal symptoms similar to those experienced with barbiturate or alcohol withdrawal. Symptoms can include anxiety, tremors, insomnia, and hallucinations.
  • Abuse Potential: The pleasurable sedative and euphoric effects produced by Soma attract recreational users, particularly those with a history of substance abuse. Its potential for misuse led to its reclassification.

Regulation and Controlled Substance Status

For many years, Soma's abuse potential was underestimated, and it was not a scheduled controlled substance. However, a growing number of addiction cases, including its use in polydrug abuse, prompted a review by the Drug Enforcement Administration (DEA).

Effective January 11, 2012, the DEA classified carisoprodol as a Schedule IV controlled substance. This status indicates that the drug has a currently accepted medical use but also has a potential for abuse and physical dependence. The reclassification was a critical step in recognizing the drug's dangers and implementing stricter controls on its prescribing and dispensing.

Conclusion

In summary, Soma is neither a benzodiazepine nor a barbiturate by chemical classification. It belongs to a separate class of drugs known as carbamates. However, the reason for the frequent comparison is that its active metabolite, meprobamate, exerts barbiturate-like and benzodiazepine-like effects by enhancing the inhibitory neurotransmitter GABA in the brain. The key takeaway is that due to this mechanism and its potential for abuse and dependence, Soma is a controlled substance with risks similar to other CNS depressants, and it should only be used exactly as prescribed for short-term periods.

For additional information, the U.S. Drug Enforcement Administration provides important details on the scheduling of controlled substances, including Soma.

Frequently Asked Questions

A carbamate like Soma is a chemically distinct class from benzodiazepines (e.g., Xanax, Valium). While both can have sedative effects by influencing the GABA neurotransmitter system, benzodiazepines directly enhance the effect of GABA, whereas Soma's effects come primarily from its metabolite, meprobamate, which has more potent barbiturate-like effects.

Soma was classified as a Schedule IV controlled substance by the DEA in 2012 due to its potential for abuse and physical dependence. The risk of addiction, particularly when misused or taken for prolonged periods, is significant and led to the reclassification.

No, combining Soma with benzodiazepines is extremely dangerous and not recommended. Both are central nervous system depressants, and their combined effects can lead to severe sedation, respiratory depression, and even fatal overdose.

Common side effects of Soma include drowsiness, dizziness, and headache. Other side effects can include nausea, upset stomach, and irritability. These effects can be more pronounced with misuse or high doses.

Abruptly stopping Soma, especially after prolonged use, can trigger withdrawal symptoms. These symptoms can include insomnia, anxiety, tremors, hallucinations, and muscle twitching. A tapering schedule, as directed by a healthcare provider, is necessary to minimize withdrawal risks.

Soma is only approved and recommended for short-term use, typically no longer than two to three weeks. This is because most musculoskeletal injuries are acute and short-lived, and the risks of dependence and abuse increase with prolonged use.

Yes, many healthcare providers now prefer safer muscle relaxants that are not controlled substances due to Soma's abuse potential. Examples include cyclobenzaprine (Flexeril), metaxalone (Skelaxin), and methocarbamol (Robaxin).

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.