Valerian is the common term used to refer to the plant valeriana officinalis, which has traditionally had its roots brewed as a tea or directly consumed for relaxation and sedation purposes as well as being an anti-insomniac. The herb is one of the more popular sedative options currently available despite the current body of evidence for it.
When looking at valerian and aspects of sleep, we find that empirical measurements of sleep are mostly unaffected. When assessing sleep quality by standardized and reliable surveys (such as the PSQI) there are no major changes noted, and movement measurements via wrist actinography also fail to turn up benefits with valerian relative to placebo; despite the aforementioned, limited studies with EEG do not some effect and it seems that when asking subjects how they feel ("Did you have a restful sleep") their subjective reportings seem to be better than placebo.
It is possible that valerian, like L-theanine, has properties associated with relaxation but it is wholly independent of any actual improvements in sleep quality. Unlike the aforementioned L-theanine however, high doses of valerian have been noted to have mild sedative properties.
Most other literature on valerian seems to be based around the sedative properties of valerian and is similarly either highly unreliable or simply not well researched enough to come to conclusions. It may hold promise in menstrual pain, however, due to it being a spasmolytic.
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Valerian supplementation tends to use the root, and supplements are standardized to contain 0.8-1% valerenic acid.
On the assumption that the product contains this amount of valerenic acid, standard dosing of valerian is 450mg taken an hour before sleep. If one chooses to take valerian during the day, multiple (2-3) doses are taken at approximately 300mg with meals.
The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Valerian has in your body, and how strong these effects are.
|Grade||Level of Evidence|
|A||Robust research conducted with repeated double blind clinical trials|
|B||Multiple studies where at least two are double-blind and placebo controlled|
|C||Single double blind study or multiple cohort studies|
|D||Uncontrolled or observational studies only|
|Level of Evidence ||Effect||Change||Magnitude of Effect Size ||Scientific Consensus||Comments|
At least according to an overall meta-analysis on the topic, valerian does not appear to be much greater than placebo for aiding sleep in otherwise healthy persons. This... show
There are isolated cases of minor reductions in the time taken to fall asleep (improvements in sleep latency), but the majority of the evidence and the only meta-analysis... show
|C||Symptoms of Menopause|
|C||Symptoms of PMS|
|C||Symptoms of OCD|
|C||Symptoms of Restless Leg Syndrome|
Valerian is the common name for the plant valeriana officinalis, which is a species of plant in the Valeriana genus (of the Valerianaceae family); its traditional uses are as a nightly sedative and as an anxiolytic tea. It is a particularly popular option for insomnia, with historical reports of this herb being used in Greece up to 2,000 years ago.
Valerian is a folk medicine for aiding sleep and preventing insomnia.
There is a plant known as 'Indian Valerian' (Valeriana wallichii) which seems to have similar properties to both valerian officinalis and Patchouli and should be considered a different supplement than valerian officinalis.
Valerian, for common supplemental purposes, refers only to the officinalis species as others may have widely different phytochemical compositions.
Valerian (root unless otherwise specified) tends to contain:
The essential oil of valerian (0.2%–2.8% dry weight) includes:
The major bioactives are the sequesterpenes known as valerenic acid and its related structures, which are at highest levels the root (specifically, in the essential oil of the root). There are a variety of other lignans and flavonoids that, while they may be inherently bioactive, their role in supplementation of valerian is not known, as they are present in very low concentrations.
Valerenic acid, the main bioactive in valerian, will degrade a small amount when stored at room temperature (20% over 500 days). Acetoxyvalerenic acid also degrades at room temperature; its degredation product, along with valernic acid's, is hydroxyvalerenic acid, which increases 5-fold while total sequesterpen levels drop by 30%.
Valerenic acid is mostly stable during storage, although minor degradation may occur over a prolonged period of time
The extracts of valerian used as a dietary supplement are highly aromatic
The standard extract of valerian tends to be an aqueous:ethanolic extract (30:70) of the roots, which usually has a concentration in the range of 4-7:1 (four to seven-fold concentrated) and is standardized for an 0.8% valerenic acid content. The recommended dosage is in the 400-900mg range assuming the aformentioned standardization, with some studies using up to 1,600mg over the course of the day and lower doses (400-600mg) being used as a one-time dosage taken an hour before sleep, since some trials comparing 450mg to 900mg for sleep failed to note any significant benefit with the higher dose.
The standard supplement of valerian is a 70% ethanolic extract standardized at 0.8% valerenic acid. It is usually taken in doses of 450mg. The dose is most commonly taken an hour before sleep, although sometimes the dose is increased when it is taken multiple times a day.
There is a fixed combination of valerian and hops (humulus lupulus) known as Ze91019, which is used as a sleep aid in Europe; supplementation of Ze91019 is supplementation of 250mg of a methanolic root extract of valerian and 60mg of the hops extract (also methanolic).
This combination appears to be a methanolic extract with a drug:extract ratio of 4–6:1 for valerian (4-6 times concentrated) and 5–7:1 for the hops, and has around 0.388% total valerenic acids (0.173% valerenic acid and 0.215% acetovalerenic acid) with no valepotriates, which are normally in the essential oil. The hops contained 0.479% total flavonoids expressed as rutin equivalents (REs).
Ze91019 is a standardized mixture of valerian and hops.
NSF-3 is another formulation where 450mg of each serving contains valerian (300mg at 0.8% valerinic acid) and hops (30mg standardized to 0.35% rutin), but also with the addition of true passionflower (passiflora incarnate) at 80mg (4% isovitexin); NSF-3 (450mg) appears to be comparable as 10mg zolpidem in improving sleep quality.
NSF-3 is another formulation combining valerian with hops, but also appears to include passionflower, and has been shown to be comparable to zolpidem in improving sleep quality in one study.
Another combination formula classified as Ze185 and with the brand name Relaxane® which consists of 90mg butterbur (7-14:1 concentration from 90% ethanolic extract), 90mg valerian (5-8:1 concentration from a 55% methanolic extract), 90mg passionflower (3-6:1 concentration from 50% ethanol), and 60mg lemon balm (3.5-5.5:1 concentration from 20% ethanol).
Ze185 (Relaxane®) is a combination of valerian with passionflower, lemon balm, and butterbur.
Valerian in the range of 18.75-1875µg/mL does not appear to induce the activity of CYP1A2 and the influence on CYP2E1 appears to be inhibitory in nature but due to it being less than 20% inhibition at even 1875µg/mL (lesser inhibition at lower concentrations) it is not thought to be relevant. Both CYP1A2 and CYP2E1 have shown no appreciable alterations in humans with 125mg taken thrice daily.
CYP2D6 activity appears to be increased by 20-40% of control in the presence of 18.75-1875µg/mL, a potency comparable in vitro to 50µM rifampicin. Another study found that the influence on CYP2C19 was to a slightly larger degree (57%) in the 18.75-187.5µg/mL range with no appreciable induction at 1875µg/mL. Despite the aforementioned, oral ingestion of 125mg valerian root thrice daily has failed to influence human kinetics of CYP2D6 while 1,000mg of valerian (1% valerenic acid) nightly for two weeks caused a mild inhibitory effect on CYP2D6.
When investigating CYP3A4 valerian extracts showed weak inhibition as the IC50 value was only 9.56% of its full potency suggesting weak inhibition, although there appeared to be a large variation (variation between 3.09%-70.49%). Elsewhere, CYP3A4 activity was found to be minorly increased with valerian in the concentration range of 187.5-1875µg/mL with no significant influence at 18.75µg/mL, but CYP3A4 activity in humans given 125mg of valerian thrice daily for 28 days has failed to find any induction and no inhibitory nor inductive actions were noted with two weeks nightly ingestion of 1,000mg valerian (1% valerenic acid).
There appear to be a multitude of weak interactions between phase I enzymes and valerian when tested in vitro, but at this moment in time there is no appreciable induction noted with oral studies in humans suggesting no significant interactions with valerian and pharmaceuticals (at least at the level of phase I enzymes)
A 70% ethanolic extract of valerian roots (greater than 0.1% valerenic acids) appears to have weak inhibitory activity on UGT1A4 (IC50 of 406.5+/-35.3µM) with no detectable inhibitory activity on either UGT1A6 or UGT1A9 under 1mg/mL.
Valerian appears to have weak inhibitory actions on some enzymes in sulfation, and the practical significance of this pathway for oral supplementation is not certain (although doubtful)
The methanolic extracts of valerian root have failed to show any glutaminergic activity (assessed by neuronal activity) at concentrations up to 50µg/mL, a concentration which shows serotonergic effects and a concentration where valerian (water extract) is known to interact with receptors and modify glutamate binding (due to valerenic acid and isoborneol).
When looking at valerenic acid alone, it appears that 800ng/mL can increase glutamate binding in the presence of quinic acid by up to 49% while isoborneol suppresses it at this concentration by 14% yet increased glutamate binding of L-AP4 (mGluR III agonist), and it appears that the metabotropic glutamate receptors (mGluR I and mGluR II) may mediate some of the anxiolytic properties of valerian and isolated valerenic acid in zebrafish as glutamate signalling (specifically the II and II mGluRs) may be anxiolytic when activated.
There may be interactions with metabotropic glutamate receptors with compounds in valerian, although isoborneal and valerenic acid show opposing actions. These interactions may be related to anxiolytic properties of valerian, although the exact manner of interaction (either direct of via modifying the actions of other ligands) is not yet known
Valerian appears to be a positive modulator of the GABAA receptors acting in a concentration dependent manner independent of the GABA binding site on the GABAA receptors and enhancing GABAA neurotransmission, which is thought to underlie most of valerian's effects. This particular effect can be traced back to valerenic acid in particular binding to the β3 subunit of the GABAA receptor (mutating this subset out of mice blocks interactions with valerenic acid), and depleting valerian of the valerenic acid content seems to be associated with no detectable GABAergic signalling.
Derivatives of valerenic acid, notably acetoxyvalerenic acid, can also bind to this receptor without appreciable potentiation of the receptor and may block the actions of valerenic acid whereas hydroxyvalerenic acid also binds to this site without any per se influence yet can displace valerenic acid from its binding site. Hydroxyvalerenic acid seems to be less inhibitory than acetoxyvalerenic acid, since transforming the latter into the former elevates the overall actions of valerenic acid on the receptor.
Valerian extracts, in general, appear to enhance GABAergic signalling when tested in vitro. This is traced back to the valerenic acid content, and the other valerenic acids (hydroxy- and acetoxy-) seem to negatively influence the actions of valerenic acid on this receptor
When measuring the 50-100% methanolic extracts, there was no determinable binding to the GABAA receptor and all lignans appear inactive directly, but one lignan (pinoresinol-4,4'-di-β-d-glucoside) enhanced GABAA signalling by 23% at 10µM. 6-Methylapigenin, found in valerian, is also known to increase GABAA signalling in the presence of agonists such as Hesperidin (found in valerian in low levels, and an agonist with a 2-4mg/kg injection) or linarin (also sedative with injections). It is not known the role these play in valerian extracts, since depleting the extracts of valerenic acid seems sufficient to ablate GABAergic signalling in vitro.
The lignans and flavonoids in valerian appear to enhance GABA signalling either at concentrations which may be higher than expected with oral supplementation or via injections of the flavonoids into rodents. Practical significance of this information to human oral consumption is not known, and they seem to be much less relevant to GABAergic signalling than valerenic acid is
It is unsure whether or not the GABAergic system is relevant to oral supplementation of valerian, as it has been noted that valerian has failed to augment the effects of Alcohol which should have occurred with anything that potentiates GABAergic signalling (such as Ashwagandha).
Significance and potency of GABAergic signalling following oral ingestion in humans has not yet been demonstrated, despite it potentially underlying the main two claims of valerian (sleep enhancment and anxiolysis)
Valerian methanolic extract (35%) has been noted to displace LSD (ligand to some serotonin receptors) from the 5-HT6 receptor by by 12-13% at 10-100µg/mL, and the higher tested concentration (100µg/mL) is able to displace LSD from binding to the 5-HT7 receptor by 11% and the 5-HT4E receptor by 31%. That being said, reliable IC50 values (concentration required to displace 50%) were not seen in vitro up to 1000µg/mL, and elsewhere the interaction with the 5-HT6 and 5-HT7 receptors have failed to be replicated with the 50-100% methanolic extracts.
No known interaction occurs with 5-HT1A, 5-HT1B, 5-HT2C, or 5-HT3 receptor subsets with the basic extract and all lignans have failed to influence 5-HT1A signalling; there appears to be weak binding affinity to the 5-HT2B receptor, with 51% binding at 50µg/mL.
The 5-HT5A receptor appears to have affinity for the methanolic extracts and valerenic acid, with the former having agonistic properties on this receptor with 80% binding at 50µg/mL and the latter appears to have partial agonist properties with an IC50 of 17.2µM (Ki of 10.7µM).
Appears to associate with some serotonin receptors at moderate to high concentrations, but due to the molecule(s) mediating these interactions not being isolated it is uncertain what role valerian would play in regards to serotonin signalling
One study in vitro noted binding affinity to the serotonin transporter, with 53% binding affinity at 50µg/mL.
Affinity for the serotonin receptor has been noted at moderate concentrations, but an inhibitory or inductive role was not elucidated and the significance of this for oral supplementation not known
Valerian methanolic extracts do not appear to have any affinity for dopamine receptors (D1, D2, D3, D4.4, and D5) nor the dopamine transporter up to 100µg/mL.
No significant interactions have been noted with dopamine signalling with valerian extract
A valerian methanolic extract at 100µg/mL appears to have affinity for the ML2 receptor by displacing the ligand (iodomelatonin) by 56%, although 10µg/mL was ineffective and there were no associations with the ML1 receptor nor th melanin concentrating hormone (MCH) receptor, the latter also linked to sleep disorders. The IC50 in regards to displacing the ligand on ML2 was determined to be 74µg/mL, while interactions with ML1 required 450µg/mL to reach the IC50 value and both being less than the reference compound of Melatonin (122nM and 170pM for ML2 and ML1, respectively).
Interactions with the melatonin receptors have failed to occur elsewhere with up to 50µg/mL of the 50-100% methanolic extracts, or with petroleum or dichloromethane extracts.
Interactions with melatonin signalling have been noted with valerian in vitro, but relative to melatonin itself these interactions are very weak and probably not relevant to oral supplementation
The olivil lignan in valerian known as 4'-O-β-d-glucosyl-9-O-(6"-deoxysaccharosyl)olivil appears to be an A1 receptor ligand, and exerts 80+/-5% affinity at 100μM and initially showing a Ki of 5.28+/-0.68μM; when investigating further, it appears that this lignan had a Ki of 23.6-31μM for the low affinity state (26nM for high affinity without GTP), and due to having an EC50 value of 3.98+/-0.42μM it was deemed a partial agonist. This affinity has been replicated elsewhere in the range of 150-190µM (EC50 in activating the receptor between 850-900µM) which was comparable to hops (130µM) while the compound formulation of the two (Ze91019) did not appear to be synergistic and incubation of neurons with valerian extracts appears to suppress A1 siganlling in a concentration dependent manner up to 10mg/mL.
The water extract of valerian appears to be able to signal through A1 receptors, and a lignan from the roots has been confirmed to being a partial A1 agonist. The concentrations at which these act appreciably appear to be pretty high, and due to the content of these lignans in valerian being low it is thought that adenosine signalling is not practically relevant to oral supplementation of valerian
It appears that the anti-epileptic properties of the valerian water extract (roots at 200-800mg/kg injections) in amygdala-kindled rats is partially aborgated by A1 receptor antagonism, suggesting signalling through this receptor.
Adenosinergic signalling appears to be implicated following injections of valerian to rats, but the dose injected is very high
Valerian has been noted to have affinity for the neuropeptide 1 (NPY1) receptor by displacing the ligand by 11-13% in the concentration range of 10-100µg/mL, with no apparent associated with NPY2.
Has affinity for receptors involved in appetite regulation, although valerian in regards to appetite has not yet been studied
In amygdala-kindled rats (known to experience anticonvulsive effects from A1 but not A2A adenosine receptor activation) injections of the water extract of the roots of valerian at 500-800mg/kg (but not 200mg/kg) is able to exert anticonvulsive effects in a manner that is partially blocked with an A1 receptor antagonist. Oddly, the petroleum ether extract (50-100mg/kg) had proconvulsive effects.
Any possible anti-epileptic effects seem to be related to adenosinergic neurotranmission by mimicking adenosine signalling on the A1 receptor, although this may require large injections of valerian and not apply to oral supplementation
The root of valerian has traditionally been used to treat anxiety which is thought to be due to valerenic acid potentiating GABAA receptors, a property not shared with its derivaties hydroxyvalerenic acid and acetoxyvalerenic acid despite all three binding to the same site on GABAA receptors (β3).
It has been noted in a rat study that when given a controlled amount of total acids (0.5-2.0mg/kg), those with a higher valerenic acid content relative to acetoxyvalerenic acid (12:1) exerted anxiolytic benefits at the lower dose whereas a higher dose (2.0mg/kg) was required for the 1:1.5 ratio.
The ability of valerenic acid to bind to GABAA receptors and potentiate their signalling is thought to underlie anxiolytic properties
One human study in generalized anxiety disorder (GAD) using valerian valepotriates at 81.3mg daily for four weeks and assessing symptoms by HAM-A and STAI-Trait rating scales (as well as self report) failed to find a significant benefit with the valepotriates relative to placebo or the reference drug (diazepam).
Preliminary human evidence has failed to find any benefit associated with valerian in the treatment of anxiety
The first pilot studies of eight persons with valerian noted that it was able to improve sleep latency (time required to fall asleep) assessed by wrist activity measurement with 450mg of the extract performing similar to 900mg, but the larger dose being associated with drowsiness the following day and only the lower dose being associated with subjective reports of a better sleep latency. This study appeared to set the stage for the dosage (450mg) and studies on sleep latency in otherwise healthy persons, logically extending to persons with insomnia (the population that would benefit most from valerian interventions).
A meta-analysis on valerian and insomnia (albeit its inclusion criteria assessed all human studies) did an analysis of trials assessing sleep latency. Of the ten trials that qualified for the analysis due to assessing sleep latency (nine located online) the analysis found that the overall difference was a decrease in time to fall asleep by 0.7 minutes, failing to reach statistical significance; subgroup analysis based on study quality (Jadad rating) and excluding select studies from analysis failed to procure significant results, and the two studies showing the most magnitude in reducing sleep latency both crossed the zero point and were statistically insignificant.
A meta-analysis of sleep latency has failed to find significant benefits to sleep latency associated with valerian, and the nonsignificant trend was very minor in its magnitude (less than a minute reduction)
When looking at rodent research, flavonoids such as linarin appear to enhance phenobarbital induced sleep time when injected (7-14mg/kg) while valerenic acid and 6-methylapigenin are inhernetly inactive but in the presence of other flavonoids can enhance their activity. The combination of linarin (4mg/kg) and valerenic acid (5mg/kg) injected into rats appears to be most effective.
Isolated flavonoids form valerian may enhance sleep time when injected by either directly activating GABAergic signalling or enhancing the activity of other agents (endogenous or exogenous) that increase GABAergic signalling
Research reviews on the topic of valerian and sleep quality have initially reported a benefit associated with valerian in improving sleep quality (RR of 1.8 and 95% CI of 1.2-2.9) with other reviews being unable to find benefits based on the evidence at the time. The most recent meta-analysis to date assessing trials in the aforementioned reviews plus new trials (18 in total assessing 1,317 persons) found no evidence to support an improvement in sleep quality in either healthy persons or those with insomnia as assessed by rating scales and empirical sleep measurements (actinography), and these null results were not associated with any publication bias but associated with many (40%) trials having less than ideal methodological structure due to having a Jadad score of less than 3. When benefit was noted to a significant degree, it was solely on the subjective (yes/no) rating scale of whether persons felt that their sleep was improved where the RR was 1.37 and the 95% CI 1.05-1.78. Two reviews published on valerian after the publication of this meta-analysis do not overturn its conclusions.
The one meta-analysis to date has failed to find a significant benefit of valerian to sleep quality relative to placebo when assessing empirical and survey data, although there was benefit solely on the measurement as to whether persons felt if they had a more restful sleep than not
Valerian at 750mg (root extract) daily for eight weeks in persons with diagnosed OCD noted a reduction in symptoms assessed by the Y-BOCS (rating scale) prominent after four weeks and to the end of the study ultimately reaching a 10 (out of 40) point reduction while placebo reached a 5 point reduction. There were no significant differences at two weeks time, and there were no significant side-effects aside from somnolence (sleepiness) which occurred in 53.3% of the valerian subjects yet only 18.75% of the placebo.
One pilot study has noted that a slightly larger than normal dose of valerian showed benefits to OCD when taken as a daily supplement, although the benefits relative to placebo were moderate at best
Supplementation of 100mg/kg valerian root or an equivalent amount of valerenic acid (340μg/kg) for three weeks in rats cognitive aged with D-galactose beforehand appears to improve memory and learning associated with a decrease in corticosterone in serum and a decrease in lipid peroxidation in the hippocampus.
One study reported that the most common side effect (16% of a sample of 19) was 'vivid dreams' induced by 600mg Valerian extract.
Oral intake of 100mg/kg of valerian root or an equivalent amount of valerenic acid (340μg/kg) appears to reduce corticosterone levels in the plasma of aged rats.
Sleep disorders during cancer therapies appears to be significantly larger than in the standard population, with a prevalence between 23%–61%. As sleep is a major determinant of quality of life in this cohort as well, improving sleep during cancer therapy is sought out and valerian is of interest due to its relatively safe history of usage as a dietary supplement.
Supplementation of valerian root (450mg with 0.8% valerenic acid an hour before bed) for eight weeks in persons undergoing cancer therapy (not limited to one cancer nor type of therapy) was able to beneficially influence the time required to fall asleep relative to placebo and reduced reports of disturbed sleep from 84% (placebo) down to 60%. Despite the aforementioned, no benefit to sleep was seen on the PSQI yet as assessed by the BFI and POMS there were reductions in self-reported fatigue seen with valerian without any reported drowsiness.
There appears to be less impairments to sleep in cancer patients taking valerian, but reducing these impairments has failed to occur alongside per se improvements to sleep quality
Dysmenorrhea (presence of spasmodic pain in the abdomen during menstruation) is known to affect 42-72% of women of menstruating age and is a known impairment to quality of life. Due to valerian having antispasmolytic properties in vitro due to activating potassium channels while inhibiting calcium channels (menstrual pain being spasmodic in nature) it is investigated for being a potential aid to dysmenorrhea.
Supplementation of valerian root at 225mg thrice daily for two menstrual cycles was able to reduce the magnitude of pain as assessed by a 10 point rating scale (73.3% reduction; from 7.45 to 1.99) to a greater degree than placebo (37.6%; from 7.06 to 4.41) while valerian also reduced self-reported duration of pain.
Possible related to spasmolytic properties, valerian has once been associated with reducing abdominal pain associated with menstruation
Valerian is sometimes recommended for menopausal symtoms mostly pertaining to sleep and anxiety, and one trial using supplementation of valerian (225mg of the root extract thrice daily for eight weeks) noted that supplementation was able to reduce hot flash frequency and severity by 29.3% after 4 weeks and 47.5% after 8 weeks. This study used a custom questionnaire rather than a standardized test.
One study using 530mg of valerian root twice daily in postmenopausal women reporting insomnia has noted that while 4% of the placebo group found benefit, valerian was assocaited with a 30% reduction in reported insomnia as assessed by the PSQI; another study has assessed valerian and its effects on sleep after menopause which noted benefits relative to placebo (also assessed by PSQI) although valerian (160mg) was confounded with lemon balm (80mg).
One study has noted benefit with valerian in regards to aiding sleep in menopausal women, although due to this result being at odds with the effects of valerian in general (see 'sleep and sedation') the results should be taken with a grain of salt
Licorice (Glycyrrhiza species) is known to be a traditional medicine for the purpose of enhancing absorption of other herbal bioactives beyond its own purposes (cognitive protection, usually).
25mg/kg of a licorice extract (from glycyrrhiza glabra) alongside 50mg/kg of valerian root in mice appears to potentiate the anxiolytic properties of valerian when consumed at subactive doses despite itself being inactive.
Preliminary evidence suggests that licorice enhances the anxiolytic properties of valerian
Valerian is generally regarded as highly safe, with few side-effects reported to be significantly different than placebo. A meta-analysis noted a significant difference in regards to diarrhea instance and while drowsiness is sometimes reported as a side-effect with night-time dosing this it not always the case in isolated trials nor a meta-analysis of side-effects.
Side-effects of drowsiness during the day tend to be reported when valerian is taken at the higher doses that require day-time dosing (ie. 450mg thrice a day), and while the 'hangover' effect does not tend to occur with 450mg of the supplement before sleep it has been noted with 900mg.
In general, valerian at the recommended dose is highly safe. Drowsiness has been reported in instances where a higher than normal dose of valerian is taken at nighttime and in instances where daytime dosing have used valerian
Valerian root has been implicated in a case of hyponatremia (low blood sodium) in a psychiatric patient who consumed an excess (3.5L) of valerian containing beverages purported to reduce anxiety, although it was thought that the excess water intake was the main factor in this case of hyponatremia.
(Common misspellings for Valerian include valerian root, valrian, valerin)
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