Xanax (Alprazolam) is a medication [of the benzodiazepine classification] commonly prescribed as a treatment for neuropsychiatric conditions such as: panic disorder, generalized anxiety disorder, and social anxiety disorder. On occasion, Xanax is also prescribed off-label for the management of nausea due to chemotherapy. Furthermore, Xanax is frequently pursued illicitly for the sake of recreational intoxication.
In 2010, alprazolam (the generic name for Xanax) was documented as being the most prescribed and the most misused benzodiazepine in the United States. When ingested, Xanax modulates activation of GABAA receptor subunits which opens chloride ion channels to hyperpolarize neurons. As a result of neuronal hyperpolarization, the firing rates of neurons decrease, CNS activity ends up downregulated, and Xanax users may experience a combination of: anxiolytic, amnesic, anticonvulsant, hypnotic, myorelaxant, and/or sedative effects.
In other words, Xanax might induce a combination of mental relaxation, physical relaxation, drowsiness, and brain fog (or cognitive impairment). If you received a Xanax prescription from a medical doctor for the management of a panic or an anxiety disorder, you’re probably curious as to how long it’ll take for the medication to “kick in” (and alleviate anxious symptoms) following its administration. Knowing how long it takes for Xanax to facilitate a therapeutic effect may help with optimization of administration timing.
How long does it take for Xanax to “kick in” or take effect?
It varies among Xanax users. Due to interindividual differences, is understood that not all Xanax users will notice the medication “kicking in” (i.e. taking effect) at the same rate. Certain individuals may administer Xanax and report noticing its effect within 15 minutes, whereas others may require additional time (e.g. up to 60 minutes) to notice that they’re under its influence.
The general consensus among researchers is that the onset of Xanax’s action falls within a range of 15 to 60 minutes. Evidence suggests that approximately 90% of the peak effect derived from Xanax should be attained [by most users] within the first hour of its administration. Moreover, on average, the maximal peak effect of Xanax will be attained within 0.7 and 1.8 hours after its administration; the compressed tablet (CT) usually kicks in slightly quicker than the extended-release (XR) formula.
The reason Xanax exhibits a rapid onset of action is due to the fact that, when ingested, alprazolam is efficiently absorbed, metabolized, distributed throughout bodily tissue, and uptaken within the brain. In a matter of minutes following its ingestion, alprazolam and its metabolites begin modulating neurochemical receptors throughout the central nervous system (CNS), chiefly: GABAA receptors (via the Alpha-1 subunit).
Assuming Xanax is administered as medically directed by a healthy individual, the medication should always begin working in less than 60 minutes. Despite the fact that Xanax should always take effect within an hour of administration, not all users will be cognizant of its action. Persons who aren’t consciously aware that they’re under the influence of Xanax within 1-2 hours of administration may wonder whether the drug is actually working.
Among those who don’t notice the effect of Xanax within 1 hour of ingestion, the two most likely culprits include: using too low of a dose and/or having a high preexisting tolerance. A person with a high preexisting tolerance to GABAergic modulators (e.g. alcohol, benzodiazepines, etc.) and/or an individual taking a small dose of Xanax might be unable to detect its effect following administration.
Conversely, persons devoid of tolerance to similarly-acting GABAergics and/or users of high Xanax doses will be very likely to notice the medication’s rapid onset of action. Nevertheless, even if you’re unable to consciously detect that you’re under the influence of Xanax (following its administration), this does not negate the fact that Xanax will have likely taken effect (via altering neurophysiology).
In rare cases, factors like concurrent substance use and/or preexisting medical conditions could interfere with the absorption and/or effect of Xanax – and ultimately explain why it never “kicked in” or began working. It’s also reasonable to suggest that certain individuals may not notice Xanax working (or working at full capacity) in the early stages of treatment due to: the need for dosage titration and/or lack of medication-induced neurophysiologic changes that only occur from a longer period of administration.
Note: It is necessary to note that not all Xanax users will find the medication to be of therapeutic value. A subset of Xanax users may find the medication to be ineffective in treating their medical condition(s) such as panic disorder. While Xanax is not guaranteed to alleviate medial symptoms, it always “kicks in” and alters neurophysiology of the user – regardless of whether they consciously notice this effect and/or find it beneficial.
Why Xanax usually kicks in rapidly (Reasons)
Most individuals who use Xanax will notice that it takes effect within 1 hour of administration. Assuming a clinically relevant dose is administered (i.e. a quantity that falls within the therapeutic range for the management of a particular medical condition), the medication will “kick in” rapidly on the first day of use. That said, although Xanax will begin working on the first day of use, some individuals with generalized anxiety disorder may require a full week of consistent Xanax administration to derive maximal symptomatic relief.
Included below is a list of reasons as to why Xanax is a generally considered fast-acting. Reasons as to why Xanax exhibits a rapid onset of action include: its pharmacokinetics (absorption, metabolism, distribution, etc.); its pharmacodynamics (interaction with neurochemical targets); and ability to simultaneously modulate numerous facets of brain activation (cerebral blood flow, neural connectivity, neuroelectrical frequencies, etc.).
Xanax is efficiently absorbed and distributed
Once ingested, Xanax is efficiently absorbed in the gastrointestinal tract wherein it is bound to plasma proteins (mostly albumin) and peak plasma concentrations are attained within 1 to 2 hours. Research suggests that the absolute bioavailability of orally-administered Xanax ranges between 80% and 100%. Within minutes of absorption, Xanax is distributed throughout the brain and central nervous system wherein it modulates aspects of the user’s neurophysiology.
Xanax rapidly modulates CNS activity
After Xanax crosses the blood-brain-barrier (BBB), it binds primarily to alpha-1 subunits positioned upon GABAA receptors. The binding of Xanax to alpha-1 subunits of GABAA receptors facilitates the opening of chloride ion channels, allowing for a greater influx of chloride ions.
An influx of chloride ions causes neurons to become hyperpolarized and exhibit negative membrane potentials. Negative membrane potentials indicate that neurons are less likely to fire or release excitatory neurotransmitters within the brain. Decreased neuronal firing results in downregulated CNS activation and predictable effects such as: reduced anxiety; drowsiness; muscle relaxation; memory impairment; and/or sleepiness.
Furthermore, rapid modulation of GABAA receptors by Xanax leads to a downstream shift in the activity of inhibitory interneurons within the ventral tegmental area (VTA) of the brain. The specific activation shift among inhibitory interneurons (as a result of Xanax) yields increased firing of dopamine-secreting neurons throughout the ventral tegmental area. As a result of this downstream effect, Xanax users end up with increased dopamine concentrations within the extracellular space – and heightened dopamine signaling.
This dopaminergic effect is what causes some individuals to experience a psychologically rewarding effect (i.e. pleasure) while under the influence of Xanax. In any regard, the rapid binding of Xanax to GABAA receptor subunits and downstream impact of this binding throughout the brain is what explains its relatively quick onset of action.
Xanax also alters PNS activity
Although Xanax acts primarily upon GABAA receptors within the central nervous system (CNS), it also indirectly modulates activity throughout the peripheral nervous system (PNS). Specifically, Xanax shifts activity of the autonomic nervous system (ANS) by simultaneously decreasing activation of the sympathetic branch and increasing activation of the parasympathetic branch.
Decreasing activation of the sympathetic nervous system while concurrently increasing activation of the parasympathetic nervous system – counteracts “fight-or-flight” reactions associated with intense anxiety and panic attacks. The rapid impact of Xanax throughout the peripheral nervous system may induce a combination of observable effects including: muscle relaxation (or reduced muscle tension); pupil constriction; arterial blood vessel dilation; reduced blood pressure; and slowed heart rate.
Though you might not notice Xanax immediately working or “kicking in” to alleviate symptoms of the medical condition for which it was prescribed (e.g. an anxiety disorder), you’ll probably be able to detect the medication working based on its rapid peripheral effect. If you notice things like heightened muscle relaxation, lower blood pressure, and slower heart rate – these are signs that Xanax has “kicked in.”
Xanax can quickly shift cerebral blood flow, regional activity, and neuroelectrical activity
Another reason that Xanax may take effect faster than most users expect is related to its nearly-instantaneous modulation of: cerebral blood flow, regional activation, and neuroelectrical activity. For example, research by Roy-Byrne, Fleishaker, Arnett, et al. (1993) reported that a single dose of Xanax reduced whole-brain cerebral blood flow by 25% to 30%.
This initial reduction in cerebral blood flow was associated with simultaneous memory impairment, decreased plasma epinephrine, and lower self-awareness. What’s more, a study by Wolf, Pinkham, Satterhwaite, et al. (2013) documented that acute administration of Xanax quickly modified activity in various brain regions, including the: nucleus accumbens, amygdala, thalamus, and hypothalamic-pituitary-adrenal axis.
Specifically, Xanax has been shown to markedly increase blood flow and activity in the nucleus accumbens, possibly generating effects such as: euphoria, disinhibition, impulsivity, risk-taking, and addiction. On the other hand, Xanax is also suggested to markedly reduce blood flow and activity in the amygdala, thalamus, and hypothalamic-pituitary-adrenal (HPA) axis, possibly generating effects such as: sedation, poor coordination, and delayed reaction time.
In addition to quickly modifying cerebral blood flow and regional activation, Xanax may rapidly alter neuroelectrical activity (i.e. brain waves). A study by van Lier, Drinkenburg, van Eeten, et al. (2004) discovered that benzodiazepines like Xanax appear to increase beta waves and gamma waves via GABAA receptor modulation.
Though one might expect benzodiazepines like Xanax to increase slow-wave neuroelectrical activity (e.g. alpha and theta waves), they counterintuitively increase fast-wave neuroelectrical activity as a compensatory response to the CNS inhibition. Perhaps a combination of changes in cerebral blood flow, regional activation, and/or neuroelectrical activation contribute to the rapid onset of action associated with Xanax.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/8471128
- Source: https://www.ncbi.nlm.nih.gov/pubmed/23070072
- Source: https://www.ncbi.nlm.nih.gov/pubmed/15223295
Placebo-like effect from Xanax (?)
Even though Xanax commonly facilitates a clear effect within 20 to 60 minutes of its ingestion, it’s reasonable to hypothesize that this initial effect could be augmented by and/or partially explained by preexisting expectation from the user. Preexisting expectation among a Xanax user that the medication will “kick in” rapidly could generate a placebo-like effect.
It is understood that strong expectation or belief [that a medication like Xanax will work] can alter substantially alter neurophysiology of the person who expects it. If you strongly expect Xanax to work well and/or rapidly, there’s a chance that your standalone expectation might alter your neurophysiology to induce noticeable therapeutic effects within minutes of administration; some may consider this a placebo-like effect.
For certain Xanax users, it’s possible that a placebo-like effect (as a result of expectation that the medication will work quickly) could synergize with the actual effect provided by the medication to explain the rapid onset of the medication’s action. For example, someone might expect that Xanax will work within 15 minutes of administration – and this expectation may alter neurophysiology to provide an effect within this expected timeframe (possibly before the medication “kicks in”).
Whether a placebo-like effect actually explains rapid onset of Xanax’s action is subject to debate. Nevertheless, while a placebo-like effect might have zero impact on Xanax’s onset of action (even in rapid responders), we cannot discount the possibility that it may augment the actual neurophysiologic effect of Xanax to explain rapid response times in select users.
Why Xanax might not “kick in” right away (Reasons)
If you take Xanax once and don’t notice any effect from its administration, there are some potential explanations for the lack of initial effect. Some reasons that Xanax might not “kick in” on the first day of treatment include: insufficient dosing; impaired absorption; concurrent substance use (especially of medications that counteract its effect); and lack of neurophysiologic adaptation to the medication.
For example, if you’re using an extremely small (i.e. subtherapeutic) Xanax dose, you may not notice any substantial effect from the medication due to the small quantity administered. Another individual may not consciously notice any effect from Xanax due to a combination of low dosing, high tolerance to benzodiazepines, and/or simultaneous administration of a substance with pharmacodynamics in opposition to those of Xanax.
Low Xanax dose
Because Xanax is associated with rapid induction of tolerance, it is generally a smart idea to initiate treatment with a very low dose – and titrate up to a minimal effective dose. As a result, some individuals may initiate treatment with a Xanax dose so low, that they don’t derive any therapeutic benefit – or notice the medication exerting an effect.
If your starting dose doesn’t facilitate any noticeable effect, a medical doctor may will likely instruct you to gradually increase your dose to a quantity that facilitates a noticeable therapeutic effect. Among adults with anxiety disorders, Xanax is typically administered on an “as needed” basis at dosages from 0.25 mg and 0.5 mg (t.i.d.) – whereas among adults with panic disorders, Xanax may be administered at dosages up to 10 mg per day.
In the event that you don’t notice any effect from low dose Xanax on the first day of treatment, it’s likely that you’ll notice an inhibitory effect (characterized by reduced anxiety and/or drowsiness) as you increase the dose. Individuals with high tolerance to similar-acting GABAergic substances and/or persons with low self-awareness may have the most difficult time noticing an effect from low dose Xanax at the beginning of treatment.
Delayed CNS adaptation to Xanax
Although properly-dosed Xanax generally reduces anxiety on the first day of treatment, not all users will derive maximal benefit from the medication on Day 1. A subset of users may notice Xanax “working” on the first day of administration, but they may not experience a therapeutically-relevant effect. That said, with ongoing treatment and possibly dosage adjustments, the medication should eventually “kick in” and provide noticeable symptomatic relief.
Though suboptimal dosing may explain why Xanax doesn’t work well in the first few days of treatment, it’s also possible that a subset of users may need to undergo neurophysiologic adaptation to the medication in order for it to fully “kick in.” Because neurophysiologic adaptation to Xanax may require up to a full week of treatment, this might explain delays in the onset of Xanax’s action for a subset of individuals.
While the specific CNS adaptations that might be required for Xanax to begin facilitating a maximal therapeutic effect remain unknown, it’s fair to speculate that alterations in: neural connectivity; regional activation; gene expression; and enzyme activation – might be implicated. If these adaptations are delayed or require time (e.g. up to 7 days) to emerge, this could explain why Xanax remains ineffective (or suboptimally effective) until it’s been used consistently for 3 to 7 days.
Variables that influence Xanax’s onset of action
There are many variables that could influence the rate at which Xanax takes effect – or the ability of a person to notice it working. Such influential variables could influence: Xanax dosage; level of tolerance; user genetics; concurrent substance use; and medical diagnoses. Other variables such as: the way in which Xanax is administered, the specific Xanax format (immediate vs. extended-release), and self-awareness of the user might determine how quickly the medication “kicks in.”
The initial dosage of Xanax that’s initially prescribed may influence the rate at which it takes effect. It is understood that larger doses of Xanax reach higher peak plasma concentrations and exert a more pronounced neurophysiologic effect than smaller doses. Though large and small doses of Xanax should reach the brain in the same amount of time, smaller doses deliver a smaller quantity of the drug – and don’t modulate neurophysiology as much as larger doses.
For this reason, it should be much easier to consciously notice the effect of a large Xanax dose than a smaller one. Moreover, if a person receives a very low Xanax dose at the beginning of treatment, it’s possible that the dose might be too low to induce a noticeable effect – or for the user to experience therapeutic benefit. For example, if you start taking Xanax at a dose of 0.125 mg or 0.0625 mg – you may not notice the medication working (due to the extremely low dose).
On the other hand, if you initiate Xanax treatment with a larger dose such as 0.5 mg or 1 mg – the medication should induce a noticeable effect due to substantial neurophysiologic modulation being facilitated by the high dose. In other words, a 1 mg dose of Xanax will modify activation of GABAA receptors significantly more than a 0.0625 mg dose. In brief, it should be easier to notice Xanax kicking in after administering a high dose – compared to a low dose.
Tolerance to GABA receptor modulators
Tolerance to medications that modulate GABA receptors (in a similar manner to Xanax) may influence the significance of Xanax’s effect – and/or how quickly users are able to detect its effect. If you have a history of ingesting substances that interact with GABA receptors to facilitate an inhibitory effect, you may have developed cross-tolerance – or resistance to the effects of a substance that acts similarly to Xanax.
For example, if you’ve been drinking alcohol regularly or using other benzodiazepine medications, you may find it difficult to detect the moment at which Xanax “kicks in” – and you might not feel much different when the medication finally takes effect. Assuming you have developed a preexisting tolerance to GABA receptor modulators (that act similarly to Xanax), the extent of your tolerance relative to your Xanax dose will likely determine the medication’s efficacy – and possibly the rate at which it “kicks in.”
Additionally, it should be noted that if you’re a long-term Xanax user, you might end up developing tolerance to a specific dose of Xanax – such that the medication stops working unless the dosage is increased. Tolerance is caused by compensatory responses throughout the central nervous system such as: increase or decrease in neurochemical receptor counts; shifts in neurotransmitter production; and altered gene expression to counterbalance for the ongoing effect of Xanax.
In conclusion, if you have high tolerance to GABAergics like Xanax (or Xanax itself) relative to the impact of your dose, you might not notice the medication working – even if it has taken effect. That said, if you have zero tolerance to GABAergic substances, you should have an easier time noticing the effect of Xanax within the first 20 to 60 minutes of ingestion.
Concurrent medication use with Xanax
If you’re using another substance with Xanax (or multiple substances), including: prescription medications, over-the-counter drugs, dietary supplements, or illicit drugs – the concurrent use of these agents may influence the amount of time it takes for Xanax to “kick in” – as well as the significance of its effect. Certain substances administered with Xanax may affect its: pharmacokinetics (absorption, metabolism, elimination) and/or its pharmacodynamics (its effect upon neurochemical targets within the CNS).
Because Xanax interacts with CYP3A4 hepatic enzymes in metabolism, any concurrently-administered agent that induces or inhibits CYP3A4 function – might influence the rate at which Xanax takes effect and/or how quickly it is eliminated from the body. For example, CYP3A4 inhibitors like Cimetidine, Erythromycin, Itraconazole, and Ketoconazole may increase systemic exposure to Xanax – possibly enhancing its peak effect or duration of effect.
Oppositely, CYP3A4 inducers like Carbamezepine, Glucocorticoids, and Phenytoin may reduce systemic exposure to Xanax – possibly minimizing its peak effect or duration of effect. Interestingly, smoking cigarettes may impact the onset of action associated with Xanax, as well as the significance of its effect. Studies report 15% to 30% reductions in plasma concentrations of Xanax in smokers compared to nonsmokers.
Moreover, concurrently-administered substances could potentially augment OR counteract the neurochemical effects facilitated by Xanax – such that they influence its onset of action and degree of therapeutic efficacy. For example, co-administration of a CNS depressant with Xanax (e.g. alcohol) will augment the GABAergic modulation facilitated by Xanax, possibly leading to faster onset of action and/or a more potent effect. (Read more: “Mixing Xanax and Alcohol“).
Conversely, the administration of an agent that counteracts the pharmacodynamics of Xanax and/or its CNS suppression – may reduce its efficacy or delay its onset of action. For example, co-administration of a psychostimulant with Xanax (e.g. Adderall) should counteract some of its CNS suppression, possibly leading to a less potent and/or noticeable effect.
In summary, if you’re using any substance with Xanax – realize that this might affect the rate at which Xanax takes effect. Certain substances might make Xanax “kick in” quickly – whereas others might delay its onset of action. Additionally, the significance of Xanax’s effect may increase or decrease depending on the substance(s) used with it – making it easier or more difficult to notice when Xanax “kicks in.”
Xanax user genetics (CYP3A4/5)
The genetics of a particular Xanax user might determine its onset of action and/or how quickly it takes effect after administration. Research by Fukasawa, Suzuki, and Otani (2007) reports that genetically-mediated CYP3A5 enzyme expression could influence the pharmacokinetics of Xanax – or how efficiently it is absorbed, metabolized, and eliminated.
Furthermore, because Xanax undergoes metabolism via the CYP3A4 enzyme, it is thought that genetically-mediated CYP3A4 expression might also impact Xanax pharmacokinetics. This considered, if you happen to exhibit atypical expression(s) of CYP3A5 and/or CYP3A4 – there’s a chance that Xanax might be absorbed, metabolized, and/or eliminated at a different rate compared to the general population.
Persons with atypical CYP3A5 and/or CYP3A4 expression (as is mediated by their genes) may find that Xanax “kicks in” quicker or slower than it does for others. Additionally, atypical gene expression of CYP3A5 and/or CYP3A4 might increase or decrease the potency of Xanax’s effect – and possibly the total duration of its effect.
In most cases, poor metabolizers will exhibit increased systemic exposure to Xanax and higher plasma concentrations (compared to normative metabolizers) due to less efficient metabolism, whereas rapid metabolizers will exhibit decreased systemic exposure to Xanax and lower plasma concentrations (compared to normative metabolizers) due to more efficient metabolism. Additionally, the amount of time Xanax stays in your system may be slightly influenced by genes implicated in metabolism.
Other genes that affect the pharmacodynamics of Xanax by influencing the production of GABA, distribution of GABA receptors, and/or density of GABA receptors – may determine the potency of Xanax’s effect – and/or account for user-specific differences in the onset of Xanax’s action. The bottom line: If Xanax isn’t working as quickly as you expected – your genes may be to blame.
Preexisting medical conditions
Preexisting medical conditions can impact the rate at which Xanax takes effect and/or whether you are able to consciously detect when it “kicks in.” It is thought that individuals with neurodegenerative disorders and/or brain damage might not respond as well to Xanax (as persons without damage) and/or that these persons may have a difficult time noticing its effect [even if it’s working] due to preexisting perceptual deficits.
Oppositely, it’s also reasonable to hypothesize that individuals with neuropsychiatric disorders such as bipolar disorder may exhibit heightened sensitivity to the neurochemical action facilitated by Xanax such that it “kicks in” at a faster pace than usual. In addition, various medical conditions such as alcoholism, hepatic impairment, renal impairment, and obesity – have been shown to alter the pharmacokinetics of Xanax.
Altered pharmacokinetics of Xanax as a result of preexisting medical conditions could influence its onset of action and its therapeutic efficacy. If you don’t notice Xanax “kicking in” or taking effect in 20 to 1.8 hours after administration, understand that a preexisting medical condition may be culpable for its delayed onset of action.
There are a variety of user-specific variables that might impact the rate at which Xanax takes effect. The specific format of Xanax ingested, its mode of administration, and other administration details (e.g. timing, stomach fullness, etc.) – are all user-specific variables that could influence the rate at which Xanax takes effect. Moreover, the self-awareness of a Xanax user may impact how quickly he/she is able to detect the drug’s effect after ingestion.
Xanax format (IR vs. XR): The format of Xanax that you use could determine the rate at which Xanax begins working. Xanax is manufactured in 2 formats: standard compressed tablets, commonly referred to as “immediate release” (IR), and “extended-release” (XR) tablets. A study by Sheehan and Sheehan (2007) compared the speed of onset of action between each Xanax format (IR and XR) in outpatients with panic disorder.
It was reported that the magnitude of effect and amount of time needed to attain peak therapeutic benefit were similar between the formats; each facilitated 90% of its maximal effect within 1-hour of ingestion. Although average times to peak benefit were similar between the formats, the immediate-release (IR) format elicited peak benefit in ~1.5 hours, whereas the extended-release format elicited peak benefit in ~1.6 hours.
Based on this study, it’s fair to speculate that the shorter-acting (IR) format might “kick in” slightly faster (by about ~10 minutes) than the extended-release (XR) format. A report by Susman and Klee (2005) noted that extended-release (XR) Xanax at a dose of 6 mg reached peak plasma concentrations in 4 to 12 hours, whereas immediate-release Xanax administered at a dose of 1.5 mg (q.i.d.) reached peak plasma concentrations within 1 to 2 hours; this may imply that the immediate-release format would exhibit a faster onset of effect.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/17514187
- Source: https://www.ncbi.nlm.nih.gov/pubmed/15841187/
Mode of Xanax administration: The modality of Xanax administration can influence how quickly it takes effect. When used properly in accordance with instruction from a medical doctor, Xanax is generally administered orally. That said, some individuals may administer Xanax via alternative modalities, including: inhalation; intravenous injection; and/or sublingual ingestion.
According to research by Reissig, Harrison, Carter, et al. (2015), the onset of action following Xanax inhalation is extremely rapid – and significantly quicker than the onset of action associated with oral administration. It was noted that it took around ~2 minutes for most individuals to notice an effect following inhalation, whereas this same effect took ~49 minutes via oral administration.
A study by Smith, Kroboth, Vanderlugt, et al. (1984) compared the onset of action between oral and intravenous Xanax administration. The onset of effect was significantly quicker with intravenously-administered Xanax (IV) compared to orally-administered Xanax. Lastly, research documented that the onset of action associated with sublingual Xanax administration is relatively identical to that of oral administration.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/25199955
- Source: https://www.ncbi.nlm.nih.gov/pubmed/6152055
- Source: https://www.ncbi.nlm.nih.gov/pubmed/3680603
Administration details: Specific details associated with the way in which you administer Xanax could influence the rate at which it takes effect. Such details include: whether Xanax is administered with food versus on an empty stomach; the specific foods you eat with or before Xanax (if you take it with food); and the time of day at which you use Xanax.
Research by Erdman, Stypinski, Combs, et al. (2007) reported that the absorption rate of Xanax (IR) decreases when administered with a standard, high-fat breakfast – compared to administration on an empty stomach. Average maximum plasma concentrations were reduced by ~25% and time to reach maximum concentrations was delayed ~1.5 hours as a result of food consumption prior to ingestion.
According to FDA Access Data, food increases the maximum plasma concentrations of Xanax XR tablets. Specifically, the consumption of a high-fat meal around 2 hours before Xanax XR ingestion will increase the average plasma concentrations by ~25%. This considered, taking Xanax IR on an empty stomach and XR ~2 hours after a high-fat meal may yield fastest onsets of action.
The time of day at which Xanax is administered can affect maximum plasma concentrations – and possibly how rapidly it takes effect. FDA Access Data suggests that Xanax XR tablets exhibit 30% greater peak plasma concentrations when administered at night – compared to morning. That said, time to reach peak plasma concentrations was delayed by an hour as a result of nighttime administration; suggesting a potentially quicker onset of effect in the morning.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/17655512
- Source: https://www.accessdata.fda.gov/drugsatfda_docs
Level of self-awareness: The level of a Xanax user’s self-awareness may determine how quickly he/she is able to notice the medication “kicking in.” Though Xanax should always take effect at a relatively standard rate in healthy users, persons with low self-awareness may have a difficult time detecting the specific time at which the medication begins working.
Individuals with low self-awareness may not notice the medication “working” until it reaches peak plasma concentrations. On the other hand, individuals with high self-awareness should notice the medication “working” very rapidly – well before it reaches peak plasma concentrations.
Know that although the level of your self-awareness won’t affect whether Xanax works, it might explain your ability (or lack thereof) to notice the earliest moment at which it “kicks in.” If you have high self-awareness, you’ll likely notice Xanax taking effect sooner than if you’re lacking in self-awareness.
My Experience: How long does it take for Xanax to work for me?
15 to 35 minutes. I have a history of regularly using both standard or immediate-release Xanax (IR) and the extended-release (XR) version. My experience is consistent with the medical literature such that I generally detected the “IR” version kicking in at slightly a faster rate than the “XR” version.
Nevertheless, the difference in onset of action rate between the two Xanax formats wasn’t anything substantial. I’d notice the IR format taking effect and reaching peak effect about 10 minutes before the XR format. The effect of the IR format lasted around 4 hours, whereas the effect of the XR version persisted for around 10 hours.
Within minutes of taking Xanax (regardless of the format), I would consciously notice: slowed thought speed, decreased anxiety, subtle drowsiness, cognitive impairment, foggy thinking, and modest coordination deficits. Because my cognition suffered while under the influence of Xanax, I preferred to use the “IR” version “as needed” for a shorter effect (and a shorter duration of cognitive impairment).
By using Xanax “as needed,” I never built up tolerance to its anxiolytic effect and was able to use relatively small doses (e.g. 0.0625 mg, 0.25 mg, or 0.5 mg) and derive substantial therapeutic benefit. Moreover, I’m highly medication sensitive, self-aware, and tend to have high anxiety – the combination of which makes it easy for me to detect Xanax taking effect within minutes of ingestion.
How long did it take for you to notice Xanax working?
If you have a history of using Xanax, leave a comment below and note how long it generally takes for you to notice Xanax “kicking in” or taking effect after administration. Additionally, mention whether you noticed Xanax facilitating an effect on the very first day of treatment – or if you required longer-term treatment and/or dosage adjustments to eventually notice the medication working.
To help other readers get an understanding of your Xanax use, share some details including: Xanax format (e.g. XR); your dose (e.g. 1.5 mg, q.i.d.); mode of administration (e.g. oral); and the cumulative duration over which you’ve used Xanax (e.g. 4 months). Furthermore, note whether: you’re using Xanax with other medications (or as a standalone agent); you’re taking it with food or on an empty stomach; and/or you have any medical conditions that may interfere with Xanax’s effect.
Assuming you have difficulty detecting the effect of Xanax – or have found it to be suboptimally effective, have you considered that: preexisting tolerance to GABAergics; concurrent substance use; medical conditions; and/or low self-awareness – might explain this? Everything considered, most individuals should notice the effect of Xanax within the first hour of administration – assuming the dosage is sufficient.