Xanax (Alprazolam)

Xanax (Alprazolam)


Effects Classification:
Anxiolytic; Sedative; Benzodiazepine
Common Names: Xanax; Niravam; Alprazolam
Chemical Name: 8-chloro-1-methyl-6-phenyl-4H-[1,2,4]-triazolo[4,3-a] [1,4]benzodiazepine
Description: Alprazolam is a benzodiazepine anxiolytic commonly prescribed as a sleep aid and for the treatment of anxiety disorders. It is considered to be one of the shorter duration benzodiazepines.

Basics / General Info

Alprazolam’s exact mechanism of action is unknown. However, it is presumed to work by enhancing the effects of the body’s GABA (Gamma-Amino Butyric Acid). GABA is the nervous system’s primary inhibitory neurotransmitter, found in the brain and spinal cord. GABA tells the neurons that it contacts to slow down or stop firing, and this has a general calming and quieting effect on the brain. Alprazolam and other benzodiazepines enhance the activity of already existing GABA. Contrary to popular belief, they do not increase the nervous system’s biological synthesis of GABA. (Erowid)


Primary effects include euphoria, drowsiness, sedation, a decrease in social inhibitions, and intense relaxation.

Onset – Effects are generally felt 20-40 minutes after oral ingestion (faster via sublingual), although it can take up to an hour to feel the full effects.

Duration – Alprazolam is considered a “short-acting” benzodiazepine. Users report that the effects of the drug last from 2 to 6 hours with lingering after-effects of several more hours.


Side effects may include drowsiness, dizziness, clumsiness, loss of muscle coordination, amnesia, dry mouth, headache, vivid dreams, and changes in libido. Serious, adverse reactions to alprazolam are very rare, but they do occur. Users who experience any of the following reactions after administration should seek immediate emergency medical attention: yellowing of the skin or eyes, hallucinations, a rash, or an allergic reaction (difficulty breathing, closing of the throat, swelling of lips, face, etc.). Contraindications # Combining alprazolam with alcohol or other CNS depressants can lead to a dangerous and in some cases fatal slowing of the central nervous system and respiratory system. Other contraindications include: * Liver or kidney disease * Depression * History of drug or alcohol abuse * Acute narrow angle glaucoma * Co-administration of ketoconazole, an anti-fungal medication, or any other anti-fungal medications (due to alprazolam’s interaction with drugs that inhibit metabolism via cytochrome P450 3A) Addiction Potential # Alprazolam is both physically and psychologically addicting. Even for those who take it for medical reasons, it may become habit-forming, especially if used on a daily basis. Suddenly stopping daily use of alprazolam could be extremely dangerous, especially if the user has been taking 4 mg or more daily for 6 months or more. In rare cases, suddenly stopping this medication can cause tremors, seizures, and in very rare cases, coma and even death. Medical experts recommend gradually tapering off of alprazolam, rather than abruptly stopping it.

According to Peter Breggin, an Ithaca-based psychiatrist and author of “Toxic Psychiatry,” long-term use of Xanax and other benzodiazepines can result in cognitive impairment. Breggin makes reference to a letter to the editor in the July 1989 issue of “Archives of General Psychiatry,” where Isaac Marks and colleagues cite studies showing that long-term use of small doses of Xanax can lead to an enlargement of the cerebral ventricular, which is a sign of a brain atrophy.

Read more: http://www.livestrong.com/article/177450-the-long-term-side-effects-of-xanax/#ixzz18EMr4jnX


Alprazolam was first released by Upjohn (now a part of Pfizer). It is covered under U.S. Patent 3,987,052, which was filed on October 29, 1969, granted on October 19, 1976 and expired in September 1993. Alprazolam was released in 1981. The first approved indication was panic disorder. Upjohn took this direction at the behest of a young psychiatrist David Sheehan. Sheehan’s suggestion was to use the new distinction the DSM-III created in the classification of anxiety disorders between generalized anxiety disorder (GAD) and panic disorder in order to market alprazolam specifically for the latter. Panic disorder was, at that point, perceived to be rare and treatable only with tricyclic antidepressants; benzodiazepines were thought to be ineffective. However, from his clinical experience, Sheehan knew panic disorder to be both widespread among the populace and responsive to benzodiazepines. He suggested to Upjohn that marketing alprazolam for panic disorder would both cover new diagnostic territory and emphasize the unique potency of this drug. Sheehan describes that the first group of patients treated by alprazolam was so impressed by its action that the company knew outright that the drug was going to be a hit. A few of those patients actually pooled their money and purchased stock in Upjohn. Several months later, when alprazolam was approved by the United States Food and Drug Administration, they sold out and made a profit. Alprazolam has an exceptional history insofar as soon after its introduction a number of case reports were published in the medical literature of severe withdrawal symptom-related case reports of psychoses, seizures, and intense rebound anxiety upon discontinuation of alprazolam. Several studies found that initial treatment of panic disorder with alprazolam was significantly superior but after 8 weeks of use alprazolam lost its effectiveness and was no more effective than placebo. It was found that behavioural therapy and the drug imipramine however, proved superior to both placebo and alprazolam. It has been argued that placebo is superior than alprazolam after 8 weeks of use due to lack of rebound withdrawal effects and side effects. Controversy exists in that there are allegations that the drug manufacturer suppressed these negative findings regarding lack of sustained efficacy. (taken from Wikipedia)


The acute and late CNS glutamine response to benzodiazepine challenge: A pilot pharmacokinetic study using proton magnetic resonance spectroscopy. Psychiatry Res. 2010 Dec 30; 184(3): 171-6 Henry ME, Jensen JE, Licata SC, Ravichandran C, Butman ML, Shanahan M, Lauriat TL, Renshaw PF Benzodiazepines (BZs), which are typically used as anxiolytics, act by modulating inhibitory signaling through gamma-aminobutyric acid A (GABA)(A) receptors. Functionally, the inhibitory effects of GABA may be counterbalanced by the excitatory effects of glutamate (Glu) as the two neurotransmitter systems are metabolically linked through their synthetic intermediate glutamine (Gln). The primary aim of this study was to determine whether the effects of different BZs on the GABA and Glu/Gln systems would vary according to the pharmacokinetics of the different drugs. Proton magnetic resonance spectroscopy ((1)H MRS) was used to measure GABA, Glu, and Gln levels in six healthy adult volunteers 1h and 10h following immediate release alprazolam, extended release alprazolam, clonazepam, or placebo. Although there were no differences between 1 and 10h when the drugs were examined individually, there was a trend level difference between the 1- and 10-h effects of BZs on Gln when the BZs were combined. In post-hoc comparisons, the difference in the Gln to creatine (Cr) ratio was 0.04 for the BZs versus placebo at 1h and 0.01 at 10h following the administration of drug (t(11)=2.49, P=0.03 1h; t(10)=0.65, P=0.53 10h; no correction for multiple comparisons). An increase in Gln/Cr at 1 h post-BZ is consistent with a functionally synergistic relationship between Glu/Gln and GABA in the brain. It also suggests that MRS may have sufficient sensitivity to detect acute drug effects.