Nervine settled everybody's nerves by sedating everyone

Nov 24 2012 Published by under Uncategorized

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Out-of-control libido or drug habit?  Take Nervine.  Nervous, excitable, wakeful, or restless?  Take Nervine.  Over-the-counter Nervine wasn't a wonder drug, just a cocktail of the oldest class of sedatives - inorganic bromides.

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Nervine contained the most commonly used bromides - sodium bromide (NaBr), potassium bromide (KBr), and ammonium bromide (NH4Br).  These particular bromides were once so popular that only aspirin sold better.  The use of bromides to treat "nerves" was so prevalent that 'bromide' entered the lexicon of common speech.  Instead of "calm down", people were instructed to "take a bromide".  Instead of calling someone a 'bore', the term 'bromide' was a used to denote "a commonplace or tiresome person".

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Bromides may owe their sedative effect to a family connection.  The element bromine is in the same chemical family as the element chlorine – the halogens.  Being a chemical family, chlorine and bromine have similar properties.  Both form single, negatively charged ions (monovalent anions) via oxidation-reduction reactions - chloride (Cl-) and bromide (Br-).

Chloride is found in nearly all of our cells, having its own set cell membrane-crossing highways (chlorine channel).  The regulated flow of chloride (as hydrated chloride) across neuron membranes is key to communication between neurons.  Being family and all, bromide (as hydrated bromide) can travel along chloride's highways.  But hydrated bromide is a teeny bit smaller than hydrated chloride, allowing hydrated bromide to get into cells faster than hydrated chloride.  A flood of anions, such as bromide or chloride, into a neuron makes it more negative than it would be at rest, a state called 'hyperpolarization'.  It's hard for other neutrons to stimulate - talk to - hyperpolarized neurons.  Less neuron stimulation can translate to a feeling of calm.

A temporary calm that came with a price beyond the one listed on the price tag.  Turns out, the level of bromide needed to sedate was pretty close to bromine's toxicity level.  Plus, people were using products like Nervine a too regularly to "settle their nerves".   When bromides were the most popular, bromine toxicity ("bromism") cases were at a high.

The classic symptoms of bromism include alteration in central nervous system functioning with headache, irritability, fatigue, slurred speech, ataxia, emotional instability, tremor and hallucinations all being reported.

[Horowitz, B. (1997)]

There were even reports of bromide-induced coma, dubbed 'The Bromide Sleep'.  Taking advantage of the swapability of chloride and bromide, bromism was often treated by loading a person with saline (sodium chloride solution).

Bromism, along with the development of safer sedatives, lead to the disappearance of  Nervine and similar products from American shelves by 1975.

If seems too outlandish that bromides were available at local shops, just remember that cocaine and heroin were once too.

 

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Image 1 is from Retronaut.

Image 2 is from Britannica Blog

Image 3 is from Polite Dissent

Image 4 is a screen capture of  Eli Lilly & Company's 1920 Handbook of pharmacy and therapeutics

 

Note 1: The depressant ethanol pre-dates bromides, but ethanol wasn't designed to be a sedative.

Note 2: Bromides were also commonly used to treat epilepsy and a great deal of what is known about bromide's biochemistry is due to epilepsy research.

Note 3: The action of neurons and the various parts of neurons was simplified.

 

References

Akabas, MH (2005) Chloride Channels. eLS. John Wiley & Sons Ltd, Chichester.

Brandenberger, H. (1997) Hypnotics and Sedatives Not Belonging to the Classes of Barbiturates and Benzodiazepines. Brandenberger, H. and Maes, R. (Ed.) Analytical Toxicology: For Clinical, Forensic, and Pharmaceutical Chemists (339-422). Berlin: Walter de Gruyter

Horowitz, B. (1997) Bromism from excessive cola consumptionJ Toxicol Clin Toxicol, 35(3):315-20.

Lee, S. and Rasaiah, J. (1996) Molecular Dynamics Simulation of Ion Mobility. 2. Alkali Metal and Halide Ions Using the SPC/E Model for Water at 25 °C J. Phys. Chem., 100, 1420-1425

Macleod, N. (1900) The Bromide Sleep: A New Departure in the Treatment of Acute Mania.  Br Med J., 1(2038): 134–136.

Macleod, N. (1899) Cure of Morphine, Chloral, and Cocaine Habits by Sodium Bromide.  Br Med J., 1(1998): 896–898.

Sangster, B., et al. (1983) The influence of sodium bromide in man: a study in human volunteers with special emphasis on the endocrine and the central nervous system. Food Chem Toxicol, 21(4):409-19

Sarapuk, J., et al. (1998) The role of counterions in the interaction of bifunctional surface active compounds with model membranes. Biochem Mol Biol Int., 44(6): 1105-10.

Schwarcz, J. Once Upon A Time. Schwarcz, J. The Fly in the Ointment: 70 Fascinating Commentaries on the Science of Everyday Life (203-256). Toronto:ECW Press

Scott, Medical Time Capsule: Bromide. Retrieved November 23, 2012 from http://www.politedissent.com/

Sourkes, T. (1991) Early clinical neurochemistry of CNS-active drugs. Bromides. Mol Chem Neuropathol., 14(2):131-42.

Suzuki, S., et al. (1994) Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res., 19(2):89-97.

van Geldetern, et al. (1993) The no-effect level of sodium bromide in healthy volunteersHum Exp Toxicol, 12(1):9-14.

van Leeuwen, F. and Sangster, B. (1987) The toxicology of bromide ionCrit Rev Toxicol, 8(3):189-213.

Wild, C., Dr. Mile's Nervine.  Retrieved November 21, 2012 from http://www.retronaut.com

Zwicky, A. Dr. Mile's Nervine. Retrieved November 21, 2012 from http://arnoldzwicky.wordpress.com/

 

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