Stimulants are a group of chemicals called alkaloids derived from plants. These chemicals are capable of producing amphetamine-like effects. These plant-derived alkaloids are in absinthe, caffeine, khat(miraa), and ephedra.
Khat (qat) has been used in the Sub-Saharan Africa for more than 1000 years. Its use is now common in many parts of Africa and, until quite recently, legal in the United Kingdom, although there is an increasing movement to ban the plant. Its use is increasingly prohibited in Europe, not so much because chewing khat is associated with toxicity, but because distribution has fallen into the hands of organized crime. The other bad thing with khat is that it promotes laziness as users can chew for a whole day. Khat is illegal in the United States because it contains restricted drugs (mostly cathenone which is similar to amphetamine.)
Xanthine derivatives, especially caffeine, are the world’s most widely consumed natural stimulants. It’s found in fizzled drinks.
The other important naturally occurring stimulant is ephedrine. It’s derived from the plant Ephedra sinica A ruling by the U.S. Food and Drug Administration (FDA) caused it to be withdrawn from the herbal supplement market in 2004 (Thompson, 2004). The ruling was appealed and overturned, but now the FDA has won its appeal, and ephedra-containing products can no longer be sold (although ephedrine, its active ingredient, is still a legal drug used daily, on a large scale, by hospital anesthesiologists). Pharmaceutical grade ephedrine still remains, arguably (Lee et al., 2004), one of the preferred drugs for the treatment of anesthetic-related hypotension, especially in cardiac and obstetric surgery, where its use seems rarely to cause complications. Ephedra is found in cough medicines as ephedrine.
Absinthe is extracted from wormwood (Artemisia absinthiumand Artemisia pontica), a perennial herb related to sage (Salvia officinalis). The Egyptians used wormwood for medical purposes. Absinthewas mostly used in alcohol in 1870’s.
Manufacture of Absinthe
Absinthe is prepared either as a distillate of aromatic herbs or as a solution made by steeping the herbs in alcohol, so the physical characteristics of any particular sample will depend on the production techniques used by the manufacturer. It will also vary from batch to batch, particularly if the absinthe is home brewed or if the liqueur is made with components purchased from a “head shop.” A fairly high concentration of alcohol is required to keep the various essential oils in solution.
Below is a method of extraction
1. Combine 2.5 kg wormwood + 5 kg, anise 5 kg, and 5 kg fennel with 91 L of 85% ethanol.
2. Allow mixture to sit for 12 h (the process is called maceration).
3. Add 45 L of water.
4. Distill to 95 L of colorless distillate.
5. Add coloration consisting of 1 kg Roman wormwood + 1 kg hyssop + 500 gm lemon balm.
6. Add water to a final volume of 100 L, yielding 74 proof absinthe.
Absinthe is taken by mouth.
The active compounds in absinthe are hujones (αand β), camphor, and pinenes. Hujone act by blocking GABA gated chloride channels in the brain and causing the stimulation and euphoria. This mechanism is also responsible for the convulsions caused by absinthe.
Caffeine is present in many different plants and goes by many different names depending on the plant source. It is sometimes called guaranine when extracted from the guarana plant, mateine when found in yerba mate, and theine when found in tea. The main sources of caffeine in consumed beverages are the beans of the coffee plant and the leaves of the tea and yerba plants. Because of their high caffeine content, guarana berries are the main sources of caffeine in commercial food products. Cocoa contains little caffeine. Teas made from the leaves of Camellia sinensis also contain caffeine.
The stimulatory effects of caffeine are a result of its ability to block adenosine type 2A receptors. Blockade of these receptors activates adenyl cyclase, increases concentrations of cyclic AMP, and causes the closing of K+ channels that indirectly increase calcium concentration within cells. In the brain, this leads to stimulation of GABAergic neurons that inhibit the dopaminergic reward system. Basically high levels of cAMP causes the stimulation felt when one takes caffeine. Caffeine also has a diuretic effect through unknown mechanisms.
Effects of caffeine
The worst effects of caffeine is low fetal intrauterine growth. Caffeine causes hypertension probably by increasing blood levels of cAMP. Caffeine also causes insomnia.
Caffeine has also been shown to increase alertness and endurance in athletes.
Ephedrine is extracted from Ephedra sinica plants (primarily grown in Pakistani and China), or it can be synthesized, although most of the drug for sale is made from natural products. In recent years, Chinese production of ephedra extract powder (6%, 8%, 10% strengths) has been increasing.
Ephedrine can be taken orally or injected.
Ephedrine mainly stimulates β1 and β3 receptors. The net result of β1 stimulation is a modest, somewhat unpredictable increase in pulse and blood pressure. The degree of increase is somewhat unpredictable because of concomitant, but variable, increases in peripheral resistance—the phenomenon is known as diastolic runoff(Webb and Shipton, 1998). In some situations, administration of ephedrine may result in decreased systemic blood pressure, simply because β-induced vasodilation occurs concurrently in the extremities.
Toxic effects of ephedrine
Ephedrine-induced psychosis has been reported with some regularity (Herridge and a’Brook, 1968; Roxanas and Spalding, 1977; Whitehouse and Duncan, 1987; Ishigooka et al., 1991; Capwell, 1995; Doyle and Kargin, 1996; Jacobs and Hirsch, 2000; Boerth and Caley, 2003; Kim and LeBourgeois, 2004; Miller, 2005). Ephedrine psychosis closely resembles amphetamine psychosis: paranoia with delusions of persecution and auditory and visual hallucinations, but consciousness remains unclouded. Typically, patients with ephedrine psychosis will have to ingest more than 1000 mg/day. Recovery is rapid after the drug is withdrawn. The results of neurochemical studies suggest that the basis for ephedrine-induced behavioral changes may be altered dopamine metabolism.
Reference: Karch's Pathology of Drug Abuse – 5th Edition (2015).