Benzodiazepines May Harm the Brain
Anxiety disorders have been on the rise in recent years, and along with them prescriptions for benzodiazepines such as Zanax® and Valium® have also been climbing. For the past 2-3 years, the number of prescriptions has been sitting at around 1.3M per year in the US1 – and while this is only about half the prescribing rate for opiates, it is cause for concern given that these medications are both addictive and pose the risk of overdose. According to the Centers for Disease Control, in 2019 and 2020, benzodiazepines were involved in 17% of reported overdose deaths, with deaths from legal use climbing 22% and from illegal use 520%.2
A new study now indicates that there may be a mechanism for benzodiazepines to contribute to cognitive decline. The study, conducted at Ludwig Maximilian University Of Munich (LMU), used a rodent model to look at the mechanism by which one drug, diazepam, may cause damage leading to conditions like dementia.3 The researchers found that diazepam binds to and activates a receptor (TSPO) on immune cells in the brain called microglia. This activation, in turn, caused the microglia to break down the connections between neurons (synapses).
Given the collective risks of benzodiazepines - and the rising need – new, safer treatment options are needed to address anxiety disorders, sleep disorders, and seizure disorders so that doctors and patients alike can be less reliant on this drug class.
- de Dios C, Fernandes BS, Whalen K, et al. Prescription fill patterns for benzodiazepine and opioid drugs during the COVID-19 pandemic in the United States. Drug Alcohol Depend. 2021;229:109176. doi:10.1016/j.drugalcdep.2021.109176
- CDC. A Day to Remember: International Overdose Awareness Day. Centers for Disease Control and Prevention. Published August 20, 2021. Accessed May 23, 2022. https://www.cdc.gov/drugoverdose/featured-topics/ioad-benzo-overdose.html
- Shi Y, Cui M, Ochs K, et al. Long-term diazepam treatment enhances microglial spine engulfment and impairs cognitive performance via the mitochondrial 18 kDa translocator protein (TSPO). Nat Neurosci. 2022;25(3):317-329. doi:10.1038/s41593-022-01013-9