Benzodiazepines are marketed (informally) as “psych meds” as if they primarily act on anxiety and stimulation circuits in the brain, but there is no such thing as a “psych med” because there are no targets that are only found in the brain and because there are no drugs that when taken orally primarily go to the brain.
They have the highest relative uptake into the adrenal gland and they have the highest absolute uptake into muscle and fat.
They probably act on GABA receptors found widely outside of the nervous system. While they are not active on the unique GABA receptors in the liver, they are probably active at GABA receptors on the lungs, kidneys, immune cells, reproductive organs, and pancreas.
GABA itself regulates mitochondrial metabolism indirectly, but benzodiazepines have two independent mitochondrial targets that lie directly in the mitochondrial membrane and are unrelated to their actions on GABA receptors.
There is no evidence that benzos are more powerful regulators of GABA metabolism than of mitochondrial metabolism. In fact, their solubility in fat and cell membranes might make them much more efficient at accessing their mitochondrial targets than at accessing GABA receptors.
Like SSRIs, benzos are whole-body mitochondrial drugs.
As with SSRIs, benzos are playing with mitochondrial fire.
These claims are supported by the evidence and arguments found in the first installment of this series:
Benzodiazepine Withdrawal Is Mitochondrial Dysfunction
Benzodiazepines (“benzos”) are drugs used to treat anxiety, insomnia, seizures, spasms, alcohol withdrawal, and related forms of overstimulation.
People who use benzos have 60% greater mortality per unit time than people who don’t, but people who quit them have 60% greater mortality per unit time than people who stay on them. We cannot say whether these trends represent causation. However, they raise the possibility that benzo use puts one between a rock and a hard place and emphasize that the safest position is gained by never using them in the first place if their use can be safely avoided.
This article covers alternatives to benzos following the hierarchy derived from The Five Laws of Mitochondrial Health.
This is not an article about how to treat anxiety, insomnia, seizures, spasms, alcohol withdrawal, and related forms of overstimulation without benzos. This is because each of these problems is far broader than activating GABA receptors.
This is, instead, an article on how to do what benzos do using food-first strategies that are do not pose the same tradeoffs and risks as drugs.
Strategies are included for one or both of two reasons: either they have clear evidence of increasing GABA or GABA activity and also have evidence of clinical benefit in humans; or they have head-to-head comparisons with benzodiazepines against some clinical endpoint suggesting comparability or non-inferiority.
These strategies can be a component to healthfully handling anxiety, insomnia, seizures, spasms, alcohol withdrawal, and related forms of overstimulation, but not the whole approach to any of them.
This is educational in nature and not medical or dietetic advice. See terms for additional and more complete disclaimers.
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