Ephedrine
STIMULANTAlso known as: Ephedra, Ma Huang, Ephedra sinica alkaloid
What is Ephedrine?
Ephedrine is a sympathomimetic alkaloid that was widely used in weight loss and energy supplements until banned in 2004 after causing 155 deaths. This landmark case established modern FDA supplement oversight.
Why is Ephedrine Banned?
Unacceptable cardiovascular risk. Risk-benefit analysis showed benefits do not justify mortality risk. 155 deaths documented before ban.
Health Risks & Side Effects
Health Risk Level
This substance has a high risk of overdose and moderate addiction potential.
warningCommon Side Effects
- arrow_rightHeart attack
- arrow_rightStroke
- arrow_rightArrhythmia
- arrow_rightHypertensive crisis
- arrow_rightSeizures
- arrow_rightMyocardial infarction
blockContraindications
- arrow_rightHeart disease
- arrow_rightHigh blood pressure
- arrow_rightDiabetes
- arrow_rightThyroid disease
- arrow_rightMAO inhibitor use
How Does Ephedrine Work?
Alpha and beta-adrenergic agonist. Stimulates heart rate, blood pressure, and thermogenesis. Similar to adrenaline in effects.
History
Used in traditional Chinese medicine for thousands of years. Became popular in US supplements in the 1990s. FDA banned after documenting 155 deaths. This case drove development of modern supplement regulations.
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Research articles and educational resources
Overview
Ephedrine
Ephedrine is a central nervous system (CNS) stimulant and sympathomimetic agent that is often used to prevent low blood pressure during anesthesia. It has also been used for asthma, narcolepsy, and obesity but is not the preferred treatment. It is of unclear benefit in nasal congestion. It can be taken by mouth or by injection into a muscle, vein, or just under the skin. Onset with intravenous use is fast, while injection into a muscle can take 20 minutes, and by mouth can take an hour for effect. When given by injection, it lasts about an hour, and when taken by mouth, it can last up to four hours.
Scientific Research
From PubMed • 3 peer-reviewed studies
[The Adverse Effects of Ephedra Herb and the Safety of Ephedrine Alkaloids-free Ephedra Herb Extract (EFE)].
Ephedra Herb is defined in the 17th edition of the Japanese Pharmacopoeia (JP) as the terrestrial stem of Ephedra sinica Stapf., Ephedra intermedia Schrenk et C.A. Meyer, or Ephedra equisetina Bunge (Ephedraceae). The stems of Ephedra Herb contain greater than 0.7% ephedrine alkaloids (ephedrine and pseudoephedrine). Despite its high effectiveness, Ephedra Herb exert several adverse effects, including palpitation, excitation, insomnia, and dysuria. Both the primary and adverse effects of Ephedra Herb have been traditionally believed to be mediated by these ephedrine alkaloids. However, our study found that several pharmacological actions of Ephedra Herb were not associated with ephedrine alkaloids. We prepared an ephedrine alkaloid-free Ephedra Herb extract (EFE) by eliminating ephedrine alkaloids from Ephedra Herb extract (EHE) using ion-exchange column chromatography. EFE exerted analgesic, anti-influenza, and anticancer activities in the same manner as EHE. Moreover, EFE did not induce adverse effects due to ephedrine alkaloids, such as excitation, insomnia, and arrhythmias, and showed no toxicity. Furthermore, we evaluated the safety of EFE in healthy volunteers. The number of adverse event cases was higher in the EHE-treated group than in the EFE-treated group, although the difference was not significant. Our evidence suggested that EFE was safer than EHE.
Salbutamol.
Effects of Chronic Ephedrine Toxicity on Functional Connections, Cell Apoptosis, and CREB-Related Proteins in the Prefrontal Cortex of Rhesus Monkeys.
Ephedrine abuse has spread in many parts of the world, severely threatening human health. The mechanism of ephedrine toxicity is still unclear. To explore the possible neural mechanisms of ephedrine toxicity, this study established a non-human primate model of ephedrine exposure, analyzed the functional connectivity changes in its prefrontal cortex through resting state BOLD-fMRI, and then inspected the pathophysiological changes as well as the expression of the cyclic adenosine monophosphate response element-binding protein (CREB), phosphorylated CREB (P-CREB), and CREB target proteins (c-fos and fosB) in the prefrontal cortex. After ephedrine toxicity, we found that the prefrontal cortex of monkeys strengthened its functional connectivity with the brain regions that perform motivation, drive, reward, and learning and memory functions and weakened its functional connectivity with the brain regions that perform cognitive control. These results suggest that ephedrine toxicity causes abnormal neural circuits that lead to the amplification and enhancement of drug-related cues and the weakening and damage of cognitive control function. Histology showed that the neurocytotoxicity of ephedrine can cause neuronal degeneration and apoptosis. Real-time PCR and Western blot showed increased expression of CREB mRNA and CREB/P-CREB/c-fos/fosB protein in the prefrontal cortex after ephedrine toxicity. Collectively, the present study indicates that the enhancement of drug-related cues and the weakening of cognitive control caused by abnormal neural circuits after drug exposure may be a major mechanism of brain function changes caused by ephedrine. These histological and molecular changes may be the pathophysiological basis of brain function changes caused by ephedrine.