Ephedrine, originally isolated from plants of the Ephedra plant, occurs as the naturally-occurring isomers 1-ephedrine and d-pseudoephedrine, and other pharmacologically active isomers include d-ephedrine and 1-pseudoephedrine. Ephedrine and associated alkaloids are structurally similar to the amphetamines and, by stimulating adrenergic receptors, can increase arterial blood pressure through both peripheral vasoconstriction and cardiac stimulation. Ephedrine compounds are adrenergic sympathomimetic agents and have antihistamine activity; 1-ephedrine is widely used as a bronchodilator, while d-pseudoephedrine is widely used as a decongestant. Compounds of these groups are present in a very wide range of prescription and over-the-counter pharmaceutical formulations. Ephedrine is a typical indirect-acting sympathicomimetic agent. This substance may also be referred to as agonists, where the name agonist is qualified by a descriptor of the receptor stimulated, for example, a beta-agonist. Acting indirectly, the main action of ephedrine is to elicit release of noradrenaline (norepinephrine) from presynaptic sites. This in turn activates both alpha- and beta-adrenoceptors.

It has even been reported that ephedrine may be an example of a trace substance that belongs in the human diet, and that it provides an opportunity to attack obesity at a level that is close to causative. Ephedrine was originally thought to suppress the hunger center in the human brain. However, research has shown that ephedrine acts mainly by stimulating thermogenesis. Namely, it increases the metabolic rate and stimulates lipolysis (fat breakdown). Though it has some central stimulant effect, and thus mediates suppression of hunger, ephedrine’s main mode of action appears to be peripheral and, in part, causative since it offsets the decline in metabolic rate that normally occurs on caloric restriction. The effect of ephedrine on the peripheral metabolic rate is derived from actions on energy-generating tissues combined with stimulation of the release of fat from stored fat depots (adipose tissue). This effect not only increases the generation of energy but also adds the availability of substrates to be utilized for this energy generation. A valuable consequence of these two actions is the sparing of body protein, which, depending on the composition of the diet, may even result in a gain of body protein (anabolic effect). Ephedrine and associated alkaloids are structurally similar to the amphetamines which act on the brain by stimulating the release of norepinephrine and dopamine at the nerve synapses, by stimulating adrenergic receptors, can increase arterial blood pressure through both peripheral vasoconstriction and cardiac stimulation.

Ephedrine stimulates the production of catecholamines such as norepinephrine. Norepinephrine or noradrenaline is thought to start the thermogenic process by stimulating metabolism in fat cells via the neurocrine axis that involves beta-adrenergic receptors. This in turn results in lipolysis, or the liberation of fat in fat cells via an increase in the basal metabolic rate. This pharmacological action results in weight loss effect in obese people. The thermogenic action which results from ephedrine’s effects on metabolic rate and lipolysis persists throughout its use period, and may intensify as use continues. The effects of ephedrine can often be intensified by concomitant use of methylxanthines such as caffeine. Ephedrine products have been often advertised as weight-loss promoters, energy enhancers, and alternatives to illegal psychoactives and have been sold for years without labeling indicating the potential adverse effects, contraindications, or dosage recommendations. Side effects from ephedrine can be variable, and do not always depend on the dose consumed. In addition, ephedrine is dangerous to people with hypertension, heart disease, or diabetes.