Lithium (medication)

<h2 id="medical-uses">Medical uses</h2>

In 1970, lithium was approved by the United States <a href="/facts/Food_and_Drug_Administration/rCEnh9WB">Food and Drug Administration</a> (FDA) for the treatment of bipolar disorder, which remains its primary use in the US.<a class="footnote-ref" id="fnref:24" href="#fn:24">24</a><a class="footnote-ref" id="fnref:25" href="#fn:25">25</a> It is sometimes used when other treatments are not effective in a number of other conditions, including <a href="/facts/Major_depression/l2lQeWqr">major depression</a>,<a class="footnote-ref" id="fnref:26" href="#fn:26">26</a> <a href="/facts/Schizophrenia/FMP4lQ57">schizophrenia</a>, disorders of impulse control, and some psychiatric disorders in children.<a class="footnote-ref" id="fnref:27" href="#fn:27">27</a> Because the FDA has not approved lithium for the treatment of other disorders, such use is <a href="/facts/Off-label_use/0PDs5VWS">off-label</a>.<a class="footnote-ref" id="fnref:28" href="#fn:28">28</a><a class="footnote-ref" id="fnref:29" href="#fn:29">29</a>

<h3>Bipolar disorder</h3>
Lithium is primarily used as a maintenance drug in the treatment of bipolar disorder to stabilize mood and prevent <a href="/facts/Mania/qYV8BBbt">manic episodes</a>, but it may also be helpful in the acute treatment of manic episodes.<a class="footnote-ref" id="fnref:30" href="#fn:30">30</a> Although recommended by treatment guidelines for the treatment of depression in bipolar disorder, the evidence that lithium is superior to placebo for acute depression is low-quality;<a class="footnote-ref" id="fnref:31" href="#fn:31">31</a><a class="footnote-ref" id="fnref:32" href="#fn:32">32</a> <a href="/facts/Atypical_antipsychotics/PQYUYXMu">atypical antipsychotics</a> are considered more effective for treating acute depressive episodes.<a class="footnote-ref" id="fnref:33" href="#fn:33">33</a> <a href="/facts/Lithium_carbonate/soupEeC1">Lithium carbonate</a> treatment was previously considered to be unsuitable for children; however, more recent studies show its effectiveness for treatment of early-onset bipolar disorder in children as young as eight. The required dosage is slightly less than the toxic level (representing a low <a href="/facts/Therapeutic_index/h311pqE5">therapeutic index</a>), requiring close monitoring of blood levels of lithium carbonate during treatment.<a class="footnote-ref" id="fnref:34" href="#fn:34">34</a> Within the therapeutic range there is a dose-response relationship.<a class="footnote-ref" id="fnref:35" href="#fn:35">35</a> A limited amount of evidence suggests lithium carbonate may contribute to the treatment of substance use disorders for some people with bipolar disorder.<a class="footnote-ref" id="fnref:36" href="#fn:36">36</a><a class="footnote-ref" id="fnref:37" href="#fn:37">37</a><a class="footnote-ref" id="fnref:38" href="#fn:38">38</a> Although it is believed that lithium prevents suicide in people with bipolar disorder, a 2022 systematic review found that "Evidence from randomised trials is inconclusive and does not support the idea that lithium prevents suicide or suicidal behaviour."<a class="footnote-ref" id="fnref:39" href="#fn:39">39</a>

<h3>Schizophrenic disorders</h3>
Lithium is recommended for the treatment of schizophrenic disorders only after other antipsychotics have failed; it has limited effectiveness when used alone.<a class="footnote-ref" id="fnref:40" href="#fn:40">40</a> The results of different clinical studies of the efficacy of combining lithium with antipsychotic therapy for treating schizophrenic disorders have varied.<a class="footnote-ref" id="fnref:41" href="#fn:41">41</a>

<h3>Major depressive disorder</h3>
Lithium is widely prescribed as an adjunct treatment for depression.<a class="footnote-ref" id="fnref:42" href="#fn:42">42</a> 

<h4>Augmentation</h4>
If therapy with antidepressants (such as <a href="/facts/Selective_serotonin_reuptake_inhibitor/L6jjcmEH">selective serotonin reuptake inhibitors</a> [SSRIs]) does not fully treat and discontinue<a class="footnote-ref" id="fnref:43" href="#fn:43">43</a> the symptoms of <a href="/facts/Major_depressive_disorder/l2lQeWqr">major depressive disorder</a> (MDD) (also known as refractory depression or treatment resistant depression [TRD])<a class="footnote-ref" id="fnref:44" href="#fn:44">44</a> then a second <a href="/facts/Augmentation_agent/HdnruR6f">augmentation agent</a> is sometimes added to the therapy.<a class="footnote-ref" id="fnref:45" href="#fn:45">45</a> Lithium is one of the few augmentation agents for antidepressants to demonstrate efficacy in treating MDD in multiple randomized controlled trials and it has been prescribed (<a href="/facts/Off-label_use/0PDs5VWS">off-label</a>) for this purpose since the 1980s.<a class="footnote-ref" id="fnref:46" href="#fn:46">46</a> A 2019 systematic review found some evidence of the clinical utility of adjunctive lithium, but the majority of supportive evidence is dated.<a class="footnote-ref" id="fnref:47" href="#fn:47">47</a>
While <a href="/facts/Selective_serotonin_reuptake_inhibitor/L6jjcmEH">SSRIs</a> have been mentioned above as a drug class in which lithium is used to augment, there are other classes in which lithium is added to increase effectiveness. Such classes are <a href="/facts/Antipsychotic/7bNTg7T3">antipsychotics</a> (used for bipolar disorder) as well as <a href="/facts/Antiepileptic/uR8cxJbj">antiepileptic</a> drugs (used for both psychiatric and epileptic cases). <a href="/facts/Lamotrigine/mRmmMuj2">Lamotrigine</a> and <a href="/facts/Topiramate/Bv5gScRt">topiramate</a> are two specific antiepileptic drugs in which lithium is used to augment.<a class="footnote-ref" id="fnref:48" href="#fn:48">48</a>

<h4>Monotherapy</h4>
There are a few old studies indicating efficacy of lithium for acute depression with lithium having the same efficacy as <a href="/facts/Tricyclic_antidepressant/vpBLER2Q">tricyclic antidepressants</a>.<a class="footnote-ref" id="fnref:49" href="#fn:49">49</a> A recent study concluded that lithium works best on chronic and recurrent depression when compared to modern antidepressant (i.e. citalopram) but not for patients with no history of depression.<a class="footnote-ref" id="fnref:50" href="#fn:50">50</a> A 2019 systemic review found no evidence to support the use of lithium for monotherapy.<a class="footnote-ref" id="fnref:51" href="#fn:51">51</a>

<h3>Prevention of suicide</h3>
Lithium is widely believed to prevent suicide and is often used in clinical practice towards that end. However, meta-analyses, faced with evidence base limitations, have yielded differing results, and it therefore remains unclear whether or not lithium is efficacious in the prevention of suicide.<a class="footnote-ref" id="fnref:52" href="#fn:52">52</a><a class="footnote-ref" id="fnref:53" href="#fn:53">53</a><a class="footnote-ref" id="fnref:54" href="#fn:54">54</a><a class="footnote-ref" id="fnref:55" href="#fn:55">55</a><a class="footnote-ref" id="fnref:56" href="#fn:56">56</a><a class="footnote-ref" id="fnref:57" href="#fn:57">57</a> However, some evidence suggests it is effective in significantly reducing the risk of <a href="/facts/Self-harm/CKkaTnjK">self-harm</a> and <a href="/facts/Accident/udpQ3oAD">unintentional injury</a> for bipolar disorder in comparison to no treatment and to <a href="/facts/Antipsychotic/7bNTg7T3">anti-psychotics</a> or <a href="/facts/Valproate/q31XYzd9">valporate</a>.<a class="footnote-ref" id="fnref:58" href="#fn:58">58</a><a class="footnote-ref" id="fnref:59" href="#fn:59">59</a> According to meta-analyses, the increased presence of lithium in drinking water is correlated with lower overall suicide rates, especially among men. It is noted that further testing is needed to confirm this benefit.<a class="footnote-ref" id="fnref:60" href="#fn:60">60</a><a class="footnote-ref" id="fnref:61" href="#fn:61">61</a> 

<h3>Alzheimer's disease</h3>
Alzheimer's disease affects forty-five million people and is the fifth leading cause of death in the 65-plus population.<a class="footnote-ref" id="fnref:62" href="#fn:62">62</a> There is no complete cure for the disease, currently. However, lithium is being evaluated for its effectiveness as a potential therapeutic measure. One of the leading causes of Alzheimer's is the hyperphosphorylation of the tau protein by the enzyme GSK-3, which leads to the overproduction of amyloid peptides that cause cell death.<a class="footnote-ref" id="fnref:63" href="#fn:63">63</a> To combat this toxic amyloid aggregation, lithium upregulates the production of neuroprotectors and neurotrophic factors, as well as inhibiting the GSK-3 enzyme.<a class="footnote-ref" id="fnref:64" href="#fn:64">64</a> Lithium also stimulates neurogenesis within the hippocampus, making it thicker.<a class="footnote-ref" id="fnref:65" href="#fn:65">65</a> Yet another cause of Alzheimer's disease is the dysregulation of calcium ions within the brain.<a class="footnote-ref" id="fnref:66" href="#fn:66">66</a> Too much or too little calcium within the brain can lead to cell death.<a class="footnote-ref" id="fnref:67" href="#fn:67">67</a> Lithium can restore intracellular calcium homeostasis by inhibiting the wrongful influx of calcium upstream.<a class="footnote-ref" id="fnref:68" href="#fn:68">68</a> It also promotes the redirection of the influx of calcium ions into the lumen of the endoplasmic reticulum of the cells to reduce the oxidative stress within the mitochondria.<a class="footnote-ref" id="fnref:69" href="#fn:69">69</a>
In 2009, a study was performed by Hampel and colleagues<a class="footnote-ref" id="fnref:70" href="#fn:70">70</a> that asked patients with Alzheimer's to take a low dose of lithium daily for three months; it resulted in a significant slowing of cognitive decline, benefitting patients being in the prodromal stage the most.<a class="footnote-ref" id="fnref:71" href="#fn:71">71</a> Upon a secondary analysis, the brains of the Alzheimer's patients were studied and shown to have an increase in BDNF markers, meaning they had actually shown cognitive improvement.<a class="footnote-ref" id="fnref:72" href="#fn:72">72</a> Another study, a population study this time by Kessing et al.,<a class="footnote-ref" id="fnref:73" href="#fn:73">73</a> showed a negative correlation between Alzheimer's disease deaths and the presence of lithium in drinking water.<a class="footnote-ref" id="fnref:74" href="#fn:74">74</a> Areas with increased lithium in their drinking water showed less dementia overall in their population.<a class="footnote-ref" id="fnref:75" href="#fn:75">75</a>

<h3>Monitoring</h3>
Those who use lithium should receive regular serum level tests and should monitor thyroid and kidney function for abnormalities, as it interferes with the regulation of <a href="/facts/Sodium/eYuSPu2V">sodium</a> and water levels in the body, and can cause <a href="/facts/Dehydration/2RXJ8GGI">dehydration</a>. Dehydration, which is compounded by heat, can result in increasing lithium levels. The dehydration is due to lithium inhibition of the action of <a href="/facts/Antidiuretic_hormone/B1EksWWY">antidiuretic hormone</a>, which normally enables the kidney to reabsorb water from urine. This causes an inability to concentrate urine, leading to consequent loss of body water and thirst.<a class="footnote-ref" id="fnref:76" href="#fn:76">76</a>
Lithium concentrations in whole blood, plasma, serum, or urine may be measured using instrumental techniques as a guide to therapy, to confirm the diagnosis in potential poisoning victims, or to assist in the forensic investigation in a case of fatal overdosage. Serum lithium concentrations are usually in the range of 0.5–1.3 <a href="/facts/Mmol/L/P2WL5b9q">mmol/L</a> (0.5–1.3 <a href="/facts/MEq/L/ksgd425g">mEq/L</a>) in well-controlled people, but may increase to 1.8–2.5 mmol/L in those who accumulate the drug over time and to 3–10 mmol/L in acute overdose.<a class="footnote-ref" id="fnref:77" href="#fn:77">77</a><a class="footnote-ref" id="fnref:78" href="#fn:78">78</a>
Lithium salts have a narrow therapeutic/toxic ratio, so should not be prescribed unless facilities for monitoring <a href="/facts/Blood_plasma/oHuwwugG">plasma</a> concentrations are available. Doses are adjusted to achieve plasma concentrations of 0.4 <a class="footnote-ref" id="fnref:79" href="#fn:79">79</a> <a class="footnote-ref" id="fnref:80" href="#fn:80">80</a> to 1.2 mmol/L<a class="footnote-ref" id="fnref:81" href="#fn:81">81</a> on samples taken 12 hours after the preceding dose.
Given the rates of thyroid dysfunction, thyroid parameters should be checked before lithium is instituted and monitored after 3–6 months and then every 6–12 months.<a class="footnote-ref" id="fnref:82" href="#fn:82">82</a>
Given the risks of kidney malfunction, serum creatinine, and eGFR should be checked before lithium is instituted and monitored after 3–6 months at regular intervals. Patients who have a rise in creatinine on three or more occasions, even if their eGFR is > 60 ml/min/
1.73m2 require further evaluation, including a urinalysis for haematuria, and proteinuria, a review of their medical history with attention paid to cardiovascular, urological, and medication history, and blood pressure control and management. Overt proteinuria should be further quantified with a urine protein-to-creatinine ratio.<a class="footnote-ref" id="fnref:83" href="#fn:83">83</a>

<h4>Discontinuation</h4>
For patients who have achieved long-term remission, it is recommended to discontinue lithium gradually and in a controlled fashion.<a class="footnote-ref" id="fnref:84" href="#fn:84">84</a><a class="footnote-ref" id="fnref:85" href="#fn:85">85</a>
In patients stopping the medication, discontinuation symptoms including irritability or restlessness, and somatic symptoms like vertigo, dizziness, or lightheadedness may occur. Symptoms occur within the first week and are generally mild and self-limiting within weeks.<a class="footnote-ref" id="fnref:86" href="#fn:86">86</a>

<h3>Cluster headaches, migraine, and hypnic headache</h3>
Studies testing <a href="/facts/Prophylactic/pWGlacXu">prophylactic</a> use of lithium in cluster headaches (when compared to <a href="/facts/Verapamil/q1IoBwyf">verapamil</a>), <a href="/facts/Migraine/5XaE1W25">migraine</a> attacks, and <a href="/facts/Hypnic_headache/AWVwsC3C">hypnic headache</a> indicate good efficacy.<a class="footnote-ref" id="fnref:87" href="#fn:87">87</a>

<h2 id="adverse-effects">Adverse effects</h2>
The adverse effects of lithium include:<a class="footnote-ref" id="fnref:88" href="#fn:88">88</a><a class="footnote-ref" id="fnref:89" href="#fn:89">89</a><a class="footnote-ref" id="fnref:90" href="#fn:90">90</a><a class="footnote-ref" id="fnref:91" href="#fn:91">91</a><a class="footnote-ref" id="fnref:92" href="#fn:92">92</a><a class="footnote-ref" id="fnref:93" href="#fn:93">93</a><a class="footnote-ref" id="fnref:94" href="#fn:94">94</a>

Very Common (> 10% incidence) adverse effects
<ul><li><a href="/facts/Confusion/Pcvw6deb">Confusion</a></li>
<li><a href="/facts/Constipation/l4DHHM6L">Constipation</a> (usually transient, but can persist in some)</li>
<li>Decreased <a href="/facts/Memory/zucwQIEX">memory</a></li>
<li><a href="/facts/Diarrhea/6TBHaRdA">Diarrhea</a> (usually transient, but can persist in some)</li>
<li><a href="/facts/Dry_mouth/aKMwe59z">Dry mouth</a></li>
<li><a href="/facts/Electrocardiography/YpVswJ0W">EKG</a> changes – usually benign changes in T waves</li>
<li>Hand <a href="/facts/Tremor/rD6ogM7X">tremor</a> (usually transient, but can persist in some) with an incidence of 27%. If severe, psychiatrist may lower lithium dosage, change lithium salt type or modify lithium preparation from long to short-acting (despite lacking evidence for these procedures) or use pharmacological help<a class="footnote-ref" id="fnref:95" href="#fn:95">95</a></li>
<li>Headache</li>
<li><a href="/facts/Hyperreflexia/rmlQuemy">Hyperreflexia</a> — overresponsive reflexes</li>
<li><a href="/facts/Leukocytosis/RNyMWBzl">Leukocytosis</a> — elevated white blood cell count</li>
<li><a href="/facts/Muscle_weakness/H5FEnEBF">Muscle weakness</a> (usually transient, but can persist in some)</li>
<li><a href="/facts/Myoclonus/Xkax4g4w">Myoclonus</a> — muscle twitching</li>
<li><a href="/facts/Nausea/dyhkcbeD">Nausea</a> (usually transient)<a class="footnote-ref" id="fnref:96" href="#fn:96">96</a></li>
<li><a href="/facts/Polydipsia/aYTYCDDb">Polydipsia</a> — increased <a href="/facts/Thirst/bVLNkyqR">thirst</a></li>
<li><a href="/facts/Polyuria/KIJNqUu9">Polyuria</a> — increased urination</li>
<li>Renal (kidney) toxicity which may lead to <a href="/facts/Chronic_kidney_failure/4YKH9wpo">chronic kidney failure</a>, although some cases may be misattributed<a class="footnote-ref" id="fnref:97" href="#fn:97">97</a></li>
<li>Vomiting (usually transient, but can persist in some)</li>
<li><a href="/facts/Vertigo/2RDjIkuh">Vertigo</a></li></ul>
Common (1–10%) adverse effects
<ul><li><a href="/facts/Acne/TKJxhHSd">Acne</a></li>
<li><a href="/facts/Extrapyramidal_side_effects/5d3lLrto">Extrapyramidal side effects</a> — movement-related problems such as muscle rigidity, <a href="/facts/Parkinsonism/orfkyX69">parkinsonism</a>, <a href="/facts/Dystonia/j0jeA0XD">dystonia</a>, etc.</li>
<li>Euthyroid <a href="/facts/Goitre/0kNGMcb6">goitre</a> — i.e. the formation of a goitre despite normal thyroid functioning</li>
<li><a href="/facts/Hypothyroidism/oqtQDu2F">Hypothyroidism</a> — a deficiency of thyroid hormone. Common among bipolar patients; lithium increases rates.<a class="footnote-ref" id="fnref:98" href="#fn:98">98</a></li>
<li><a href="/facts/Hair_loss/uEPKUafl">Hair loss</a>/hair thinning</li>
<li><a href="/facts/Weight_gain/jVbY8Eao">Weight gain</a><a class="footnote-ref" id="fnref:99" href="#fn:99">99</a> — 5% incidence, tends to start fast and then plateau. Usually ends at 1–2 kg.<a class="footnote-ref" id="fnref:100" href="#fn:100">100</a></li></ul>
Unknown incidence
<ul><li>Sexual dysfunction<a class="footnote-ref" id="fnref:101" href="#fn:101">101</a></li>
<li><a href="/facts/Hypoglycemia/BlAmuP6k">Hypoglycemia</a><a class="footnote-ref" id="fnref:102" href="#fn:102">102</a></li>
<li><a href="/facts/Glycosuria/af605y5o">Glycosuria</a></li></ul>
In addition to tremors, lithium treatment appears to be a risk factor for development of <a href="/facts/Parkinsonism/orfkyX69">parkinsonism</a>-like symptoms, although the causal mechanism remains unknown.<a class="footnote-ref" id="fnref:103" href="#fn:103">103</a>
In the average bipolar patient, chronic lithium use is not associated with cognitive decline.<a class="footnote-ref" id="fnref:104" href="#fn:104">104</a> Depending on dosage and duration of use, lithium can be either pro-convulsant, or as its historical use suggests, anti-convulsant.<a class="footnote-ref" id="fnref:105" href="#fn:105">105</a>
Most side effects of lithium are dose-dependent. The lowest effective dose is used to limit the risk of side effects.

<h3>Hypothyroidism</h3>
The rate of <a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a> is around six times higher in people who take lithium. Low thyroid hormone levels in turn increase the likelihood of developing depression. People taking lithium thus should routinely be assessed for hypothyroidism and treated with synthetic thyroxine if necessary.<a class="footnote-ref" id="fnref:106" href="#fn:106">106</a>
Because lithium competes with the <a href="/facts/Antidiuretic_hormone/B1EksWWY">antidiuretic hormone</a> in the kidney, it increases water output into the urine, a condition called nephrogenic <a href="/facts/Diabetes_insipidus/mtAXABCU">diabetes insipidus</a>. Clearance of lithium by the kidneys is usually successful with certain diuretic medications, including <a href="/facts/Amiloride/JlcLDbvd">amiloride</a> and <a href="/facts/Triamterene/yappgL4p">triamterene</a>.<a class="footnote-ref" id="fnref:107" href="#fn:107">107</a> It increases the appetite and thirst ("polydypsia") and reduces the activity of <a href="/facts/Thyroid_hormone/9k4xJtCq">thyroid hormone</a> (<a href="/facts/Hypothyroidism/oqtQDu2F">hypothyroidism</a>).<a class="footnote-ref" id="fnref:108" href="#fn:108">108</a><a class="footnote-ref" id="fnref:109" href="#fn:109">109</a> The latter can be corrected by treatment with <a href="/facts/Thyroxine/9k4xJtCq">thyroxine</a> and does not require the lithium dose to be adjusted. Lithium is also believed to cause renal dysfunction, although this does not appear to be common.<a class="footnote-ref" id="fnref:110" href="#fn:110">110</a>
Lambert et al. (2016), comparing the rate of hypothyroidism in patients with bipolar disorder treated with 9 different medications, found that lithium users do not have a particularly high rate of hypothyroidism (8.8%) among BD patients – only 1.39 times the rate in <a href="/facts/Oxcarbazepine/jstz7RYM">oxcarbazepine</a> users (6.3%, the lowest group). Lithium and quetiapine are not statistically different in terms of hypothyroidism rates. However, lithium users are tested much more frequently for hypothyroidism than those using other drugs. The authors write that there may be an element of surveillance bias in understanding lithium's effects on the thyroid glands, as lithium users are tested 2.3–3.1 times as often. Furthermore, the authors argue that because hypothyroidism is common among BD patients regardless of lithium treatment, regular thyroid testing should be applied to all BD patients, not just those on lithium.<a class="footnote-ref" id="fnref:111" href="#fn:111">111</a><a class="footnote-ref" id="fnref:112" href="#fn:112">112</a>

<h3>Pregnancy</h3>
Lithium is a <a href="/facts/Teratogen/j4BN6lsB">teratogen</a>, which can cause birth defects in a small number of newborns. <a href="/facts/Case_report/gIQnMGCR">Case reports</a> and several <a href="/facts/Retrospective_cohort_study/xcHxdpvu">retrospective studies</a> have demonstrated possible increases in the rate of a <a href="/facts/Congenital_heart_defect/QsuPPC2Y">congenital heart defects</a> (CHDs) including <a href="/facts/Ebstein%27s_anomaly/FW4hu3Cc">Ebstein's anomaly</a> if taken during the first trimester of pregnancy. The risk is dose-dependent: in the 2017 AMX registry study, the risk of "any malformations" is increased by 11+152−47% in those taking no more than 600 mg of lithium carbonate daily, by 60+220−93% in those taking 601–900 mg daily, and by 222+380−75% in those taking more than 900 mg daily. The first two numbers do not indicate a statistically significant association.<a class="footnote-ref" id="fnref:113" href="#fn:113">113</a> In a 2018 meta-analysis, there was a statistically significant 62+71−50% increase in congenital malformations in general, but not for cardiac malformations specifically (54+216−90% increase).<a class="footnote-ref" id="fnref:114" href="#fn:114">114</a> Exposure during any part of the pregnancy is associated with a slight but statistically significant increase in the risks of preterm birth and of a larger-than-usual baby at birth.<a class="footnote-ref" id="fnref:115" href="#fn:115">115</a>
Lithium is effective for preventing relapse during and after pregnancy.<a class="footnote-ref" id="fnref:116" href="#fn:116">116</a> As the risks of stopping Lithium can be significant, patients are sometimes recommended to stay on this medicine while pregnant. Careful weighing of the risks and benefits should be made in consultation with a <a href="/facts/Psychiatrist/hS7EnAU6">psychiatric physician</a>.<a class="footnote-ref" id="fnref:117" href="#fn:117">117</a> The relatively low teratogenic risk of lithium allows such a choice.<a class="footnote-ref" id="fnref:118" href="#fn:118">118</a> The decision should be made before the start of pregnancy, as there is no reason for stopping lithium once the pregnancy has started.<a class="footnote-ref" id="fnref:119" href="#fn:119">119</a>
For patients who are exposed to lithium, or plan to stay on the medication throughout their pregnancy, fetal <a href="/facts/Echocardiography/X0rQzVe3">echocardiography</a> is routinely performed to monitor for cardiac anomalies.<a class="footnote-ref" id="fnref:120" href="#fn:120">120</a> Pregnancy is associated with a decrease in blood lithium levels (especially in the first and second trimesters), so more frequent monitoring with an increase in dose may be required to maintain control of symptoms. To prevent postpatrum psychosis, a higher blood lithium level may be desirable in the third trimester.<a class="footnote-ref" id="fnref:121" href="#fn:121">121</a>
While lithium is typically the most effective treatment, possible alternatives to Lithium include <a href="/facts/Lamotrigine/mRmmMuj2">Lamotrigine</a> and <a href="/facts/Atypical_antipsychotic/PQYUYXMu">Second generation Antipsychotics</a> for the treatment of acute <a href="/facts/Bipolar_depression/aMDwXbV0">bipolar depression</a> or for the management of bipolar patients with <a href="/facts/Euthymia_(medicine)/IgWGjuQC">normal mood</a> during pregnancy.<a class="footnote-ref" id="fnref:122" href="#fn:122">122</a>
Initiating lithium immediately after delivery is also effective for preventing postpartum psychosis and postpartum bipolar relapse. This is an acceptable treatment option for women with a history of psychosis limited to the postpartum period. For women with diagnosed bipolar disorder, this provides less protection than maintaining lithium therapy during pregnancy.<a class="footnote-ref" id="fnref:123" href="#fn:123">123</a>

<h3>Breastfeeding</h3>
While only small amounts of Lithium are transmitted to the infant in breastmilk, there is limited data on the safety of <a href="/facts/Breastfeeding/cdWXyYDX">Breastfeeding</a> while on Lithium. Medical evaluation and monitoring of infants consuming breastmilk during maternal prescription may be indicated.<a class="footnote-ref" id="fnref:124" href="#fn:124">124</a><a class="footnote-ref" id="fnref:125" href="#fn:125">125</a>

<h3>Kidney damage</h3>
Lithium has been associated with several forms of kidney injury.<a class="footnote-ref" id="fnref:126" href="#fn:126">126</a><a class="footnote-ref" id="fnref:127" href="#fn:127">127</a> It is estimated that impaired urinary concentrating ability is present in at least half of individuals on chronic lithium therapy, a condition called lithium-induced <a href="/facts/Nephrogenic_diabetes_insipidus/BsRYCfze">nephrogenic diabetes insipidus</a>.<a class="footnote-ref" id="fnref:128" href="#fn:128">128</a> Continued use of lithium can lead to more serious <a href="/facts/Kidney_damage/koq79A75">kidney damage</a> in an aggravated form of <a href="/facts/Diabetes_insipidus/mtAXABCU">diabetes insipidus</a>.<a class="footnote-ref" id="fnref:129" href="#fn:129">129</a><a class="footnote-ref" id="fnref:130" href="#fn:130">130</a> In rare cases, some forms of lithium-caused kidney damage may be progressive and lead to end-stage kidney failure with a reported incidence of 0.2% to 0.7%.<a class="footnote-ref" id="fnref:131" href="#fn:131">131</a>
Some reports of kidney damage may be wrongly attributed to lithium, increasing the apparent rate of this adverse effect.<a class="footnote-ref" id="fnref:132" href="#fn:132">132</a> Nielsen et al. (2018), citing 6 large observational studies since 2010, argue that findings of decreased kidney function are partially inflated by surveillance bias. Furthermore, modern data does not show that lithium increases the risk of end-stage kidney disease.<a class="footnote-ref" id="fnref:133" href="#fn:133">133</a> Davis et al. (2018), using literature from a wider timespan (1977–2018), also found that lithium's association with chronic kidney disease is unproven with various contradicting results. They also find contradicting results regarding end-stage kidney disease.<a class="footnote-ref" id="fnref:134" href="#fn:134">134</a>
A 2015 nationwide study suggests that chronic kidney disease can be avoided by maintaining the serum lithium concentration at a level of 0.6–0.8 mmol/L and by monitoring <a href="/facts/Serum_creatinine/gkebqj2L">serum creatinine</a> every 3–6 months.<a class="footnote-ref" id="fnref:135" href="#fn:135">135</a>

<h3>Hyperparathyroidism</h3>
Lithium-associated <a href="/facts/Hyperparathyroidism/WnCEnPUP">hyperparathyroidism</a> is the leading cause of <a href="/facts/Hypercalcemia/kdEeLaVd">hypercalcemia</a> in lithium-treated patients. Lithium may lead to exacerbation of pre-existing <a href="/facts/Primary_hyperparathyroidism/4JbGepnw">primary hyperparathyroidism</a> or cause an increased set-point of calcium for parathyroid hormone suppression, leading to <a href="/facts/Parathyroid_hyperplasia/Dh7Uld78">parathyroid hyperplasia</a>.

<h2 id="interactions">Interactions</h2>
Lithium <a href="/facts/Blood_plasma/oHuwwugG">plasma</a> <a href="/facts/Concentrations/wqBmz5od">concentrations</a> are known to be increased with concurrent use of <a href="/facts/Diuretics/x3j4I1Tg">diuretics</a>—especially <a href="/facts/Loop_diuretics/eEgJ4qpf">loop diuretics</a> (such as furosemide) and <a href="/facts/Thiazides/y0xU4l4F">thiazides</a>—and <a href="/facts/Non-steroidal_anti-inflammatory_drugs/coIkzl4s">non-steroidal anti-inflammatory drugs</a> (NSAIDs) such as <a href="/facts/Ibuprofen/vsKBTfVl">ibuprofen</a>.<a class="footnote-ref" id="fnref:136" href="#fn:136">136</a> Lithium concentrations can also be increased with concurrent use of <a href="/facts/ACE_inhibitors/cHT1Yxub">ACE inhibitors</a> such as <a href="/facts/Captopril/lcBPW3Xg">captopril</a>, <a href="/facts/Enalapril/b4Wr1lWN">enalapril</a>, and <a href="/facts/Lisinopril/uUz0kGp3">lisinopril</a>.<a class="footnote-ref" id="fnref:137" href="#fn:137">137</a>
Lithium is primarily <a href="/facts/Clearance_(pharmacology)/RqI64paT">cleared</a> from the body through <a href="/facts/Glomerular_filtration/kJKJge0o">glomerular filtration</a>, but some is then reabsorbed together with sodium through the <a href="/facts/Proximal_convoluted_tubule/mkezjse0">proximal tubule</a>. Its levels are therefore sensitive to water and <a href="/facts/Electrolyte/4YE8bIVa">electrolyte</a> balance.<a class="footnote-ref" id="fnref:138" href="#fn:138">138</a> Diuretics act by lowering water and sodium levels; this causes more reabsorption of lithium in the proximal tubules so that the removal of lithium from the body is less, leading to increased blood levels of lithium.<a class="footnote-ref" id="fnref:139" href="#fn:139">139</a><a class="footnote-ref" id="fnref:140" href="#fn:140">140</a> ACE inhibitors have also been shown in a retrospective case-control study to increase lithium concentrations. This is likely due to constriction of the afferent arteriole of the glomerulus, resulting in decreased glomerular filtration rate and clearance. Another possible mechanism is that ACE inhibitors can lead to a decrease in sodium and water. This will increase lithium reabsorption and its concentrations in the body.<a class="footnote-ref" id="fnref:141" href="#fn:141">141</a>
Some drugs can increase the clearance of lithium from the body, which can result in decreased lithium levels in the blood. These drugs include <a href="/facts/Theophylline/qJzjQVB2">theophylline</a>, <a href="/facts/Caffeine/Hx6E2QC5">caffeine</a>, and <a href="/facts/Acetazolamide/kwTvRugT">acetazolamide</a>. Additionally, increasing dietary <a href="/facts/Sodium/eYuSPu2V">sodium</a> intake may also reduce lithium levels by prompting the kidneys to excrete more lithium.<a class="footnote-ref" id="fnref:142" href="#fn:142">142</a>
Lithium is known to be a potential precipitant of <a href="/facts/Serotonin_syndrome/PqLvx901">serotonin syndrome</a> in people concurrently on serotonergic medications such as <a href="/facts/Antidepressants/N62ND3Fa">antidepressants</a>, <a href="/facts/Buspirone/IeoGp3eD">buspirone</a> and certain opioids such as <a href="/facts/Pethidine/3U92Kb1Y">pethidine</a> (meperidine), <a href="/facts/Tramadol/R0tYqres">tramadol</a>, <a href="/facts/Oxycodone/mv95L2c7">oxycodone</a>, <a href="/facts/Fentanyl/MMD9GdD3">fentanyl</a> and others.<a class="footnote-ref" id="fnref:143" href="#fn:143">143</a><a class="footnote-ref" id="fnref:144" href="#fn:144">144</a> Lithium co-treatment is also a risk factor for <a href="/facts/Neuroleptic_malignant_syndrome/g80RuABy">neuroleptic malignant syndrome</a> in people on antipsychotics and other antidopaminergic medications.<a class="footnote-ref" id="fnref:145" href="#fn:145">145</a>
High doses of <a href="/facts/Haloperidol/ue4TJKmu">haloperidol</a>, <a href="/facts/Fluphenazine/7MfU4Uq7">fluphenazine</a>, or <a href="/facts/Flupenthixol/lx3rT6tU">flupenthixol</a> may be hazardous when used with lithium; irreversible <a href="/facts/Toxic_encephalopathy/SGDRYmR8">toxic encephalopathy</a> has been reported.<a class="footnote-ref" id="fnref:146" href="#fn:146">146</a>
Indeed, these and other <a href="/facts/Antipsychotics/7bNTg7T3">antipsychotics</a> have been associated with an increased risk of lithium <a href="/facts/Neurotoxicity/FrgTICfX">neurotoxicity</a>, even with low therapeutic lithium doses.<a class="footnote-ref" id="fnref:147" href="#fn:147">147</a><a class="footnote-ref" id="fnref:148" href="#fn:148">148</a>
Classical psychedelics such as <a href="/facts/Psilocybin/0jGynLUX">psilocybin</a> and <a href="/facts/LSD/o5qq0grH">LSD</a> may cause seizures if taken while using lithium, although further research is needed.<a class="footnote-ref" id="fnref:149" href="#fn:149">149</a>

<h2 id="overdose">Overdose</h2>
Main article: <a href="/facts/Lithium_toxicity/wlPELAqG">Lithium toxicity</a>
Lithium toxicity, which is also called lithium overdose and lithium poisoning, is the condition of having too much lithium in the blood. This condition also happens in persons who are taking lithium in which the lithium levels are affected by <a href="/facts/Drug_interaction/T5VcSVGd">drug interactions</a> in the body.
In acute toxicity, people have primarily gastrointestinal symptoms such as vomiting and <a href="/facts/Diarrhea/6TBHaRdA">diarrhea</a>, which may result in <a href="/facts/Hypovolemia/MmP8TsPw">volume depletion</a>. During acute toxicity, lithium distributes later into the central nervous system resulting in mild neurological symptoms, such as dizziness.<a class="footnote-ref" id="fnref:150" href="#fn:150">150</a>
In chronic toxicity, people have primarily neurological symptoms which include <a href="/facts/Nystagmus/7Djf4Itt">nystagmus</a>, <a href="/facts/Tremor/rD6ogM7X">tremor</a>, <a href="/facts/Hyperreflexia/rmlQuemy">hyperreflexia</a>, <a href="/facts/Ataxia/suENWGS6">ataxia</a>, and <a href="/facts/Delirium/f1zdzAc5">change in mental status</a>. During chronic toxicity, the gastrointestinal symptoms seen in acute toxicity are less prominent. The symptoms are often vague and nonspecific.<a class="footnote-ref" id="fnref:151" href="#fn:151">151</a>
If the lithium toxicity is mild or moderate, lithium dosage is reduced or stopped entirely. If the toxicity is severe, lithium may need to be removed from the body.

<h2 id="mechanism-of-action">Mechanism of action</h2>
The specific biochemical mechanism of lithium action in stabilizing mood is unknown.<a class="footnote-ref" id="fnref:152" href="#fn:152">152</a>
Upon ingestion, lithium becomes widely distributed in the <a href="/facts/Central_nervous_system/k8I6To97">central nervous system</a> and interacts with a number of <a href="/facts/Neurotransmitter/LlpYFSU3">neurotransmitters</a> and <a href="/facts/Receptor_(biochemistry)/tjTAC76a">receptors</a>, decreasing <a href="/facts/Norepinephrine/AjTIC9ox">norepinephrine</a> release and increasing <a href="/facts/Serotonin/EzY58q4a">serotonin</a> synthesis.<a class="footnote-ref" id="fnref:153" href="#fn:153">153</a>
Unlike many other <a href="/facts/Psychoactive_drugs/dNXrUmsx">psychoactive drugs</a>, Li+ typically produces no obvious psychotropic effects (such as <a href="/facts/Euphoria_(emotion)/u4cnbWC4">euphoria</a>) in normal individuals at therapeutic concentrations.<a class="footnote-ref" id="fnref:154" href="#fn:154">154</a>
Lithium may also increase the release of <a href="/facts/Serotonin/EzY58q4a">serotonin</a> by neurons in the brain.<a class="footnote-ref" id="fnref:155" href="#fn:155">155</a> In vitro studies performed on serotonergic neurons from rat <a href="/facts/Raphe_nuclei/DCmphm59">raphe nuclei</a> have shown that when these neurons are treated with lithium, <a href="/facts/Serotonin/EzY58q4a">serotonin</a> release is enhanced during a <a href="/facts/Depolarization/qGX8lFXE">depolarization</a> compared to no lithium treatment and the same depolarization.<a class="footnote-ref" id="fnref:156" href="#fn:156">156</a>
Lithium has a plethora of proposed molecular targets:

<ul><li>Lithium both directly and indirectly inhibits <a href="/facts/GSK3B/SnSqURUH">GSK3β (glycogen synthase kinase 3β)</a> which results in the activation of <a href="/facts/MTOR/5l2dVa1p">mTOR</a>. This leads to an increase in neuroprotective mechanisms by facilitating the <a href="/facts/Akt/PKB_signaling_pathway/S22sQFUq">Akt signaling pathway</a>.<a class="footnote-ref" id="fnref:157" href="#fn:157">157</a> GSK-3β is a downstream target of monoamine systems. As such, it is directly implicated in cognition and mood regulation.<a class="footnote-ref" id="fnref:158" href="#fn:158">158</a><a class="footnote-ref" id="fnref:159" href="#fn:159">159</a> During mania, GSK-3β is activated via dopamine overactivity.<a class="footnote-ref" id="fnref:160" href="#fn:160">160</a> GSK-3β inhibits the transcription factors <a href="/facts/Beta-catenin/5eQzonk1">β-catenin</a> and cyclic AMP (cAMP) response element binding protein (CREB), by phosphorylation. This results in a decrease in the transcription of important genes encoding for <a href="/facts/Neurotrophin/NwuESuUa">neurotrophins</a>. Inhibiton of GSK3β reverses this change.<a class="footnote-ref" id="fnref:161" href="#fn:161">161</a><a class="footnote-ref" id="fnref:162" href="#fn:162">162</a><a class="footnote-ref" id="fnref:163" href="#fn:163">163</a></li>
<li>In addition, several authors proposed that pAp-phosphatase could be one of the therapeutic targets of lithium.<a class="footnote-ref" id="fnref:164" href="#fn:164">164</a><a class="footnote-ref" id="fnref:165" href="#fn:165">165</a> This hypothesis was supported by the low Ki of lithium for human pAp-phosphatase compatible within the range of therapeutic concentrations of lithium in the plasma of people (0.8–1 mM). The Ki of human pAp-phosphatase is ten times lower than that of <a href="/facts/GSK3B/SnSqURUH">GSK3β (glycogen synthase kinase 3β)</a>. Inhibition of pAp-phosphatase by lithium leads to increased levels of pAp (3′-5′ phosphoadenosine phosphate), which was shown to inhibit <a href="/facts/PARP-1/ct3W2NDG">PARP-1</a>.<a class="footnote-ref" id="fnref:166" href="#fn:166">166</a></li>
<li>Another mechanism proposed in 2007 is that lithium may interact with <a href="/facts/Nitric_oxide/UvhdvDzp">nitric oxide</a> (NO) signaling pathway in the central nervous system, which plays a crucial role in neural plasticity. The NO system could be involved in the antidepressant effect of lithium in the Porsolt forced swimming test in mice.<a class="footnote-ref" id="fnref:167" href="#fn:167">167</a><a class="footnote-ref" id="fnref:168" href="#fn:168">168</a></li>
<li>It was also reported that <a href="/facts/NMDA_receptor/BqMhXEbU">NMDA receptor</a> blockage augments antidepressant-like effects of lithium in the mouse forced swimming test,<a class="footnote-ref" id="fnref:169" href="#fn:169">169</a> indicating the possible involvement of NMDA receptor/NO signaling in the action of lithium in this animal model of <a href="/facts/Learned_helplessness/m7obuyPx">learned helplessness</a>.</li></ul>
Lithium possesses <a href="/facts/Neuroprotection/BcbsTfN0">neuroprotective</a> properties by preventing <a href="/facts/Apoptosis/8dVzSm4y">apoptosis</a> and increasing cell longevity.<a class="footnote-ref" id="fnref:170" href="#fn:170">170</a>
Although the search for a novel lithium-specific receptor is ongoing, the high concentration of lithium compounds required to elicit a significant pharmacological effect leads mainstream researchers to believe that the existence of such a receptor is unlikely.<a class="footnote-ref" id="fnref:171" href="#fn:171">171</a>

<h3>Oxidative metabolism</h3>
Evidence suggests that <a href="/facts/Mitochondria/ErHqrdJ1">mitochondrial</a> dysfunction is present in patients with bipolar disorder.<a class="footnote-ref" id="fnref:172" href="#fn:172">172</a>
<a href="/facts/Oxidative_stress/HX7dfUUb">Oxidative stress</a> and reduced levels of <a href="/facts/Anti-oxidants/4TG4MQ83">anti-oxidants</a> (such as <a href="/facts/Glutathione/5bSxjusL">glutathione</a>) lead to cell death. Lithium may protect against oxidative stress by up-regulating complexes I and II of the <a href="/facts/Mitochondrial_electron_transport_chain/QjcIkgeR">mitochondrial electron transport chain</a>.<a class="footnote-ref" id="fnref:173" href="#fn:173">173</a>

<h3>Dopamine and G-protein coupling</h3>
During mania, there is an increase in <a href="/facts/Neurotransmission/9H38LExu">neurotransmission</a> of <a href="/facts/Dopamine/5gNy8Xkd">dopamine</a> that causes a secondary <a href="/facts/Homeostasis/rloTGAHa">homeostatic</a> down-regulation, resulting in decreased neurotransmission of dopamine, which can cause depression.<a class="footnote-ref" id="fnref:174" href="#fn:174">174</a> Additionally, the post-synaptic actions of dopamine are mediated through <a href="/facts/G-protein_coupled_receptors/0arUMkQc">G-protein coupled receptors</a>. Once dopamine is coupled to the G-protein receptors, it stimulates other secondary messenger systems that modulate neurotransmission. Studies found that in <a href="/facts/Autopsies/GzSXuCH2">autopsies</a> (which do not necessarily reflect living people), people with bipolar disorder had increased G-protein coupling compared to people without bipolar disorder.<a class="footnote-ref" id="fnref:175" href="#fn:175">175</a> Lithium treatment alters the function of certain subunits of the dopamine-associated G-protein, which may be part of its mechanism of action.<a class="footnote-ref" id="fnref:176" href="#fn:176">176</a>

<h3>Glutamate and NMDA receptors</h3>
<a href="/facts/Glutamate/7oXbNcvu">Glutamate</a> levels are observed to be elevated during <a href="/facts/Mania/qYV8BBbt">mania</a>. Lithium is thought to provide long-term mood stabilization and have anti-<a href="/facts/Mania/qYV8BBbt">manic</a> properties by modulating glutamate levels.<a class="footnote-ref" id="fnref:177" href="#fn:177">177</a> It is proposed that lithium competes with magnesium for binding to <a href="/facts/NMDA_receptor/BqMhXEbU">NMDA glutamate receptor</a>, increasing the availability of glutamate in <a href="/facts/Postsynaptic_potential/jAaRvdwN">post-synaptic</a> <a href="/facts/Neurons/G7CyTVdH">neurons</a>, leading to a homeostatic increase in glutamate re-uptake which reduces glutamatergic transmission.<a class="footnote-ref" id="fnref:178" href="#fn:178">178</a>
The NMDA receptor is also affected by other <a href="/facts/Neurotransmitters/LlpYFSU3">neurotransmitters</a> such as <a href="/facts/Serotonin/EzY58q4a">serotonin</a> and <a href="/facts/Dopamine/5gNy8Xkd">dopamine</a>. Effects observed appear exclusive to lithium and have not been observed by other <a href="/facts/Monovalent_ion/ck7cHByj">monovalent</a> ions such as <a href="/facts/Rubidium/KDHSe2HM">rubidium</a> and <a href="/facts/Cesium/dXKN1S5k">cesium</a>.<a class="footnote-ref" id="fnref:179" href="#fn:179">179</a>

<h3>GABA receptors</h3>
<a href="/facts/GABA/vRTeQQUG">GABA</a> is an inhibitory <a href="/facts/Neurotransmitter/LlpYFSU3">neurotransmitter</a> that plays an important role in regulating <a href="/facts/Dopamine/5gNy8Xkd">dopamine</a> and <a href="/facts/Glutamate/7oXbNcvu">glutamate</a> <a href="/facts/Neurotransmission/9H38LExu">neurotransmission</a>.<a class="footnote-ref" id="fnref:180" href="#fn:180">180</a> It was found that patients with bipolar disorder had lower GABA levels, which results in <a href="/facts/Excitotoxicity/DKnHA79x">excitotoxicity</a> and can cause <a href="/facts/Apoptosis/8dVzSm4y">apoptosis</a> (cell loss). Lithium has been shown to increase the level of GABA in plasma and cerebral spinal fluid.<a class="footnote-ref" id="fnref:181" href="#fn:181">181</a> Lithium counteracts these degrading processes by decreasing pro-apoptotic <a href="/facts/Proteins/Jxmagu3E">proteins</a> and stimulating release of <a href="/facts/Neuroprotection/BcbsTfN0">neuroprotective</a> proteins.<a class="footnote-ref" id="fnref:182" href="#fn:182">182</a> Lithium's regulation of both excitatory dopaminergic and glutamatergic systems through GABA may play a role in its mood-stabilizing effects.<a class="footnote-ref" id="fnref:183" href="#fn:183">183</a>

<h3>Cyclic AMP secondary messengers</h3>
Lithium's therapeutic effects are thought to be partially attributable to its interactions with several signal transduction mechanisms.<a class="footnote-ref" id="fnref:184" href="#fn:184">184</a> The <a href="/facts/Cyclic_AMP/flK2vwUe">cyclic AMP</a> secondary messenger system is shown to be modulated by lithium. Lithium was found to increase the basal levels of cyclic AMP but impair receptor-coupled stimulation of cyclic AMP production.<a class="footnote-ref" id="fnref:185" href="#fn:185">185</a> It is hypothesized that the dual effects of lithium are due to the inhibition of <a href="/facts/G-proteins/HKkcfgGP">G-proteins</a> that mediate cyclic AMP production.<a class="footnote-ref" id="fnref:186" href="#fn:186">186</a> Over a long period of lithium treatment, cyclic AMP and <a href="/facts/Adenylate_cyclase/WnCSuV96">adenylate cyclase</a> levels are further changed by <a href="/facts/Gene_transcription_factor/wro0DPHe">gene transcription factors</a>.<a class="footnote-ref" id="fnref:187" href="#fn:187">187</a>

<h3>Inositol depletion hypothesis</h3>
Lithium treatment has been found to inhibit the enzyme <a href="/facts/Inositol_monophosphatase/Wz8NE48K">inositol monophosphatase</a>, involved in degrading inositol monophosphate to inositol required in <a href="/facts/Phosphatidylinositol_4,5-bisphosphate/Sq6VS4vk">PIP2</a> synthesis. This leads to lower levels of <a href="/facts/Inositol_trisphosphate/TDLGCWuG">inositol triphosphate</a>, created by decomposition of PIP2.<a class="footnote-ref" id="fnref:188" href="#fn:188">188</a> This effect has been suggested to be further enhanced with an inositol triphosphate <a href="/facts/Reuptake_inhibitor/vsrPEUXF">reuptake inhibitor</a>. <a href="/facts/Inositol/FVon023Q">Inositol</a> disruptions have been linked to memory impairment and depression. It is known with good certainty that signals from the receptors coupled to the <a href="/facts/Phosphoinositide/hgKM1RYV">phosphoinositide</a> <a href="/facts/Signal_transduction/1bs0Me6w">signal transduction</a> are affected by lithium.<a class="footnote-ref" id="fnref:189" href="#fn:189">189</a> <a href="/facts/Myo-inositol/FVon023Q">myo-inositol</a> is also regulated by the high affinity <a href="/facts/Solute_carrier_family/Pnuz1TLA">sodium mI transport system</a> (SMIT). Lithium is hypothesized to inhibit mI entering the cells and mitigate the function of SMIT.<a class="footnote-ref" id="fnref:190" href="#fn:190">190</a> Reductions of cellular levels of <a href="/facts/Myo-inositol/FVon023Q">myo-inositol</a> results in the inhibition of the <a href="/facts/Phosphoinositide/hgKM1RYV">phosphoinositide cycle</a>.<a class="footnote-ref" id="fnref:191" href="#fn:191">191</a>

<h3>Neurotrophic factors</h3>
Lithium's actions on Gsk3 result in activation of CREB, leading to higher expression of BDNF. (Valproate, another mood stabilizer, also increases the expression of BDNF.) As expected of increased BDNF expression, chronic lithium treatment leads to increased <a href="/facts/Grey_matter/rqRM0qYY">grey matter</a> volume in brain areas implicated in emotional processing and cognitive control.<a class="footnote-ref" id="fnref:192" href="#fn:192">192</a> Bipolar patients treated with lithium also have higher <a href="/facts/White_matter/mvHqXJYk">white matter</a> integrity compared to those taking other drugs.<a class="footnote-ref" id="fnref:193" href="#fn:193">193</a>
Lithium also increases the expression of <a href="/facts/Mesencephalic_astrocyte-derived_neurotrophic_factor/FFlPmde6">mesencephalic astrocyte-derived neurotrophic factor</a> (MANF), another <a href="/facts/Neurotrophic_factor/bJNG05TQ">neurotrophic factor</a>, via the <a href="/facts/AP-1_transcription_factor/jryICv0m">AP-1 transcription factor</a>. MANF is able to regulate <a href="/facts/Proteostasis/8lHJfaof">proteostasis</a> by interacting with <a href="/facts/GRP78/bFxmuNCJ">GRP78</a>, a protein involved in the <a href="/facts/Unfolded_protein_response/RdxKNXvv">unfolded protein response</a>.<a class="footnote-ref" id="fnref:194" href="#fn:194">194</a>

<h2 id="history">History</h2>
Lithium was first used in the 19th century as a treatment for <a href="/facts/Gout/ktWD69YP">gout</a> after scientists discovered that, at least in the laboratory, lithium could dissolve <a href="/facts/Uric_acid/gPMSfLcT">uric acid</a> crystals isolated from the kidneys. The levels of lithium needed to dissolve urate in the body, however, were toxic.<a class="footnote-ref" id="fnref:195" href="#fn:195">195</a> Because of prevalent theories linking excess uric acid to a range of disorders, including depressive and manic disorders, <a href="/facts/Carl_Lange_(physician)/FwkGzG2T">Carl Lange</a> in Denmark<a class="footnote-ref" id="fnref:196" href="#fn:196">196</a> and <a href="/facts/William_Alexander_Hammond/d7lU9KpD">William Alexander Hammond</a> in New York City<a class="footnote-ref" id="fnref:197" href="#fn:197">197</a> used lithium to treat mania from the 1870s onwards.
By the turn of the 20th century, as theory regarding mood disorders evolved and so-called "brain gout" disappeared as a medical entity, the use of lithium in psychiatry was largely abandoned; however, several lithium preparations were still produced for the control of renal calculi and uric acid diathesis.<a class="footnote-ref" id="fnref:198" href="#fn:198">198</a> As accumulating knowledge indicated a role for excess sodium intake in <a href="/facts/Hypertension/wlAvBfcf">hypertension</a> and <a href="/facts/Heart_disease/HD420nMv">heart disease</a>, lithium salts were prescribed to patients for use as a replacement for dietary <a href="/facts/Table_salt/SCplalQ3">table salt</a> (<a href="/facts/Sodium_chloride/MWcXl3Mb">sodium chloride</a>). This practice and the sale of lithium itself were both banned in the United States in February 1949, following the publication of reports detailing side effects and deaths.<a class="footnote-ref" id="fnref:199" href="#fn:199">199</a>
Also in 1949, the Australian psychiatrist <a href="/facts/John_Cade/xu7vj1e4">John Cade</a> and Australian <a href="/facts/Biochemist/gAWNAY5v">biochemist</a> <a href="/facts/Shirley_Andrews/yLbapgBN">Shirley Andrews</a> rediscovered the usefulness of lithium salts in treating mania while working at the Royal Park Psychiatric Hospital in <a href="/facts/Victoria_(Australia)/76P2nqtz">Victoria.</a><a class="footnote-ref" id="fnref:200" href="#fn:200">200</a> They were injecting rodents with urine extracts taken from manic patients in an attempt to isolate a metabolic compound which might be causing mental symptoms. Since uric acid in gout was known to be psychoactive, (<a href="/facts/Adenosine_receptors/TjlLlUD0">adenosine receptors</a> on neurons are stimulated by it; <a href="/facts/Caffeine/Hx6E2QC5">caffeine</a> blocks them), they needed soluble urate for a control. They used lithium urate, already known to be the most soluble urate compound, and observed that it caused the rodents to become tranquil. Cade and Andrews traced the effect to the lithium-ion itself, and after Cade ingested lithium himself to ensure its safety in humans, he proposed lithium salts as <a href="/facts/Tranquilizer/hBNJDykC">tranquilizers</a>. He soon succeeded in controlling mania in chronically hospitalized patients with them. This was one of the first successful applications of a drug to treat mental illness, and it opened the door for the development of medicines for other mental problems in the next decades.<a class="footnote-ref" id="fnref:201" href="#fn:201">201</a>
The rest of the world was slow to adopt this treatment, largely because of deaths that resulted from even relatively minor overdosing, including those reported from the use of <a href="/facts/Lithium_chloride/mNbthJx2">lithium chloride</a> as a substitute for table salt. Largely through the research and other efforts of Denmark's <a href="/facts/Mogens_Schou/bJ1vhdKe">Mogens Schou</a> and Paul Baastrup in Europe,<a class="footnote-ref" id="fnref:202" href="#fn:202">202</a> and Samuel Gershon and Baron Shopsin in the U.S., this resistance was slowly overcome. Following the recommendation of the <a href="/facts/American_Psychiatric_Association/xn9juNST">APA</a> Lithium Task Force <a href="/facts/William_E._Bunney/WrcgSlFb">(William Bunney</a>, <a href="/facts/Irvin_M._Cohen/CPqKtYTM">Irvin Cohen</a> (Chair), <a href="/facts/Jonathan_Cole_(psychiatrist)/XS1S6f5B">Jonathan Cole</a>, <a href="/facts/Ronald_R._Fieve/dmehoE8c">Ronald R. Fieve</a>, Samuel Gershon, Robert Prien, and Joseph Tupin<a class="footnote-ref" id="fnref:203" href="#fn:203">203</a>), the application of lithium in manic illness was approved by the United States <a href="/facts/Food_and_Drug_Administration/rCEnh9WB">Food and Drug Administration</a> in 1970,<a class="footnote-ref" id="fnref:204" href="#fn:204">204</a> becoming the 50th nation to do so.<a class="footnote-ref" id="fnref:205" href="#fn:205">205</a>
Lithium has now become a part of Western popular culture. Characters in <a href="/facts/Pi_(film)/qXbS3kJ1">Pi</a>, <a href="/facts/Premonition_(2007_film)/tJL7qXRI">Premonition</a>, <a href="/facts/Stardust_Memories/IWTsWN77">Stardust Memories</a>, <a href="/facts/American_Psycho_(film)/auaPsql5">American Psycho</a>, <a href="/facts/Garden_State_(film)/7B3YIo2f">Garden State</a>, and <a href="/facts/An_Unmarried_Woman/Q1MRz5Al">An Unmarried Woman</a> all take lithium. It's the chief constituent of the calming drug in <a href="/facts/Ira_Levin/Vjxf5rGy">Ira Levin</a>'s dystopian <a href="/facts/This_Perfect_Day/oYVAcepF">This Perfect Day</a>. <a href="/facts/Sirius_XM/dHAYI1h6">Sirius XM</a> Satellite Radio in North America has a 1990s alternative rock station called Lithium, and several songs refer to the use of lithium as a mood stabilizer. These include: "Equilibrium met Lithium" by <a href="/facts/South_African_music/vzB7JFQd">South African</a> artist <a href="/facts/Koos_Kombuis/mR7mjxJL">Koos Kombuis</a>, "<a href="/facts/Lithium_(Evanescence_song)/YEWGPP0H">Lithium</a>" by <a href="/facts/Evanescence/3prLkETe">Evanescence</a>, "<a href="/facts/Lithium_(Nirvana_song)/e9lwYugo">Lithium</a>" by <a href="/facts/Nirvana_(band)/LB38lBz8">Nirvana</a>, "Lithium and a Lover" by <a href="/facts/Sirenia_(band)/WUcCmpRK">Sirenia</a>, "Lithium Sunset", from the album <a href="/facts/Mercury_Falling/MAxmTDIN">Mercury Falling</a> by <a href="/facts/Sting_(musician)/zSd0xAPB">Sting</a>,<a class="footnote-ref" id="fnref:206" href="#fn:206">206</a> and "Lithium" by <a href="/facts/Thin_White_Rope/U9tUeGqd">Thin White Rope</a>.

<h3>7 Up</h3>
As with <a href="/facts/Coca-Cola/wbnCJYb6">cocaine in Coca-Cola</a>, lithium was widely marketed as one of several <a href="/facts/Patent_medicine/BeT1rsEQ">patent medicine</a> products popular in the late 19th and early 20th centuries and was the medicinal ingredient of a refreshment beverage. <a href="/facts/Charles_Leiper_Grigg/5snQsHuj">Charles Leiper Grigg</a>, who launched his St. Louis-based company The Howdy Corporation, invented a formula for a <a href="/facts/Lemon-lime/eoRlSN3L">lemon-lime</a> soft drink in 1920. The product, originally named "Bib-Label Lithiated Lemon-Lime Soda", was launched two weeks before the <a href="/facts/Wall_Street_Crash_1929/MS1LUgko">Wall Street Crash of 1929</a>.<a class="footnote-ref" id="fnref:207" href="#fn:207">207</a> It contained the <a href="/facts/Mood_stabilizer/9sj4E0wx">mood stabilizer</a> <a href="/facts/Lithium_citrate/CAlV5IQX">lithium citrate</a>, and was one of many patent medicine products popular in the late-19th and early-20th centuries.<a class="footnote-ref" id="fnref:208" href="#fn:208">208</a> Its name was soon changed to <a href="/facts/7_Up/ndczDHQt">7 Up</a>. All American beverage makers were forced to remove lithium from beverages in 1948. Despite the ban, in 1950, the <a href="/facts/Painesville_Telegraph/w44fxt7p">Painesville Telegraph</a> still carried an advertisement for a lithiated lemon beverage.<a class="footnote-ref" id="fnref:209" href="#fn:209">209</a>

<h2 id="salts-and-product-names">Salts and product names</h2>
<a href="/facts/Lithium_carbonate/soupEeC1">Lithium carbonate</a> (Li2CO3) is the most commonly used form of <a href="/facts/Lithium_salt/G6Gy0nJU">lithium salts</a>, a <a href="/facts/Carbonic_acid/fjjVAhwt">carbonic acid</a> involving the <a href="/facts/Lithium_element/7vXX6BWA">lithium element</a> and a <a href="/facts/Carbonate_ion/FES1QHkN">carbonate ion</a>. Other lithium salts are also used as medication, such as <a href="/facts/Lithium_citrate/CAlV5IQX">lithium citrate</a> (Li3C6H5O7), <a href="/facts/Lithium_sulfate/0v8N2V3R">lithium sulfate</a>, <a href="/facts/Lithium_chloride/mNbthJx2">lithium chloride</a>, and <a href="/facts/Lithium_orotate/BmRoL5vS">lithium orotate</a>.<a class="footnote-ref" id="fnref:210" href="#fn:210">210</a><a class="footnote-ref" id="fnref:211" href="#fn:211">211</a> <a href="/facts/Nanoparticles/k8kNxX4E">Nanoparticles</a> and <a href="/facts/Microemulsions/IJMquT3A">microemulsions</a> have also been invented as <a href="/facts/Drug_delivery/vDfboXeT">drug delivery</a> mechanisms. As of 2020, there is a lack of evidence that alternate formulations or salts of lithium would reduce the need for monitoring serum lithium levels or lower systemic toxicity.<a class="footnote-ref" id="fnref:212" href="#fn:212">212</a>
As of 2017 lithium was marketed under many brand names worldwide, including Cade, Calith, Camcolit, Carbolim, Carbolit, Carbolith, Carbolithium, Carbolitium, Carbonato de Litio, Carboron, Ceglution, Contemnol, Efadermin (Lithium and Zinc Sulfate), Efalith (Lithium and Zinc Sulfate), Elcab, Eskalit, Eskalith, Frimania, Hypnorex, Kalitium, Karlit, Lalithium, Li-Liquid, Licarb, Licarbium, Lidin, Ligilin, Lilipin, Lilitin, Limas, Limed, Liskonum, Litarex, Lithane, Litheum, Lithicarb, Lithii carbonas, Lithii citras, Lithioderm, Lithiofor, Lithionit, Lithium, Lithium aceticum, Lithium asparagicum, Lithium Carbonate, Lithium Carbonicum, Lithium Citrate, Lithium DL-asparaginat-1-Wasser, Lithium gluconicum, Lithium-D-gluconat, Lithiumcarbonaat, Lithiumcarbonat, Lithiumcitrat, Lithiun, Lithobid, Lithocent, Lithotabs, Lithuril, Litiam, Liticarb, Litijum, Litio, Litiomal, Lito, Litocarb, Litocip, Maniprex, Milithin, Neurolepsin, Plenur, Priadel, Prianil, Prolix, Psicolit, Quilonium, Quilonorm, Quilonum, Téralithe, and Theralite.<a class="footnote-ref" id="fnref:213" href="#fn:213">213</a>

<h2 id="research">Research</h2>
Tentative evidence in <a href="/facts/Alzheimer%27s_disease/w7Ad6tdg">Alzheimer's disease</a> showed that lithium may slow progression.<a class="footnote-ref" id="fnref:214" href="#fn:214">214</a><a class="footnote-ref" id="fnref:215" href="#fn:215">215</a> It has been studied for its potential use in the treatment of <a href="/facts/Amyotrophic_lateral_sclerosis/9fIXnNL4">amyotrophic lateral sclerosis</a> (ALS), but a study showed lithium had no effect on ALS outcomes.<a class="footnote-ref" id="fnref:216" href="#fn:216">216</a>

<h2 id="notes">Notes</h2>

<h2 id="further-reading">Further reading</h2>

<ul><li>Mota de Freitas D, Leverson BD, Goossens JL (2016). "Lithium in Medicine: Mechanisms of Action". In Sigel A, Sigel H, Sigel R (eds.). Metal ions in Life Sciences. Vol. 16. Springer. pp. 557–584. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1007%2F978-3-319-21756-7_15">10.1007/978-3-319-21756-7_15</a>. <a href="/facts/ISBN_(identifier)/15AdSPa9">ISBN</a> 978-3-319-21755-0. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/26860311">26860311</a>.</li>
<li>Phelps J (19 September 2014). <a href="https://psycheducation.org/blog/lithium-basics/">"Lithium Basics"</a>. Psych. <a href="https://web.archive.org/web/20220211060657/https://psycheducation.org/blog/lithium-basics/">Archived</a> from the original on 11 February 2022. Retrieved 11 February 2022.</li>
<li>Phillips ML (16 February 2006). <a href="https://www.the-scientist.com/daily-news/exposing-lithiums-circadian-action-47818">"Exposing lithium's circadian action"</a>. The Scientist. <a href="https://web.archive.org/web/20200808124701/https://www.the-scientist.com/daily-news/exposing-lithiums-circadian-action-47818">Archived</a> from the original on 8 August 2020. Retrieved 17 August 2018.</li></ul>

<h2 id="external-links">External links</h2>
<ul><li><a href="https://web.archive.org/web/20040811012851/http://www.psycheducation.org/depression/meds/moodstabilizers.htm">"Mood Stabilizers: An Updated List and Links"</a>. PsychEducation.org. April 2004. Archived from <a href="http://www.psycheducation.org/depression/meds/moodstabilizers.htm">the original</a> on 11 August 2004.</li></ul>

<h2 id="references">References</h2>

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<li id="fn:78">Baselt R (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. pp. 851–854. ISBN 978-0-9626523-7-0. <a href="978-0-9626523-7-0" target="_blank">978-0-9626523-7-0</a> <a href="#fnref:78" class="footnote-back-ref">↩</a></li>
<li id="fn:79">The UK Electronic Medical Compendium recommends 0.4–0.8 mmol/L plasma lithium level in adults for prophylaxis of recurrent affective bipolar manic-depressive illness "Camcolit 250 mg Lithium Carbonate". 2 December 2010. Archived from the original on 4 March 2016. Retrieved 5 May 2011. <a href="/wiki/Mmol/L" target="_blank">/wiki/Mmol/L</a> <a href="#fnref:79" class="footnote-back-ref">↩</a></li>
<li id="fn:80">One study (Solomon DA, Ristow WR, Keller MB, Kane JM, Gelenberg AJ, Rosenbaum JF, et al. (October 1996). "Serum lithium levels and psychosocial function in patients with bipolar I disorder". The American Journal of Psychiatry. 153 (10): 1301–1307. doi:10.1176/ajp.153.10.1301. PMID 8831438.) concluded a "low" dose of 0.4–0.6 mmol/L serum lithium treatment for patients with bipolar 1 disorder had fewer side effects, but a higher rate of relapse, than a "standard" dose of 0.8–1.0 mmol/L. However, a reanalysis of the same experimental data (Perlis RH, Sachs GS, Lafer B, Otto MW, Faraone SV, Kane JM, et al. (July 2002). "Effect of abrupt change from standard to low serum levels of lithium: a reanalysis of double-blind lithium maintenance data". The American Journal of Psychiatry. 159 (7): 1155–1159. doi:10.1176/appi.ajp.159.7.1155. PMID 12091193.) concluded the higher rate of relapse for the "low" dose was due to abrupt changes in the lithium serum levels[improper synthesis?] <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:80" class="footnote-back-ref">↩</a></li>
<li id="fn:81">Grandjean EM, Aubry JM (2009). "Lithium: updated human knowledge using an evidence-based approach. Part II: Clinical pharmacology and therapeutic monitoring". CNS Drugs. 23 (4). Springer Science and Business Media LLC: 331–349. doi:10.2165/00023210-200923040-00005. PMID 19374461. S2CID 38042857. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:81" class="footnote-back-ref">↩</a></li>
<li id="fn:82">Gitlin M (December 2016). "Lithium side effects and toxicity: prevalence and management strategies". International Journal of Bipolar Disorders. 4 (1): 27. doi:10.1186/s40345-016-0068-y. PMC 5164879. PMID 27900734. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879</a> <a href="#fnref:82" class="footnote-back-ref">↩</a></li>
<li id="fn:83">Davis J, Desmond M, Berk M (November 2018). "Lithium and nephrotoxicity: a literature review of approaches to clinical management and risk stratification". BMC Nephrology. 19 (1). Springer Science and Business Media LLC: 305. doi:10.1186/s12882-018-1101-4. PMC 6215627. PMID 30390660. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215627" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215627</a> <a href="#fnref:83" class="footnote-back-ref">↩</a></li>
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<li id="fn:87">Bauer M, Grof P, Muller-Oerlinghausen B (2006). Lithium in Neuropsychiatry: The Comprehensive Guide. Taylor & Francis. ISBN 978-1-84184-515-9. Retrieved 17 July 2021. <a href="978-1-84184-515-9" target="_blank">978-1-84184-515-9</a> <a href="#fnref:87" class="footnote-back-ref">↩</a></li>
<li id="fn:88">DrugPoint® System (Internet). Truven Health Analytics, Inc. Greenwood Village, CO: Thomsen Healthcare. 2013. <a href="#fnref:88" class="footnote-back-ref">↩</a></li>
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<li id="fn:96">Gitlin M (December 2016). "Lithium side effects and toxicity: prevalence and management strategies". International Journal of Bipolar Disorders. 4 (1): 27. doi:10.1186/s40345-016-0068-y. PMC 5164879. PMID 27900734. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879</a> <a href="#fnref:96" class="footnote-back-ref">↩</a></li>
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<li id="fn:98">Kessing LV (January 2024). "Why is lithium [not] the drug of choice for bipolar disorder? a controversy between science and clinical practice". International Journal of Bipolar Disorders. 12 (1): 3. doi:10.1186/s40345-023-00322-7. PMC 10792154. PMID 38228882. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10792154" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10792154</a> <a href="#fnref:98" class="footnote-back-ref">↩</a></li>
<li id="fn:99">Baptista T, Teneud L, Contreras Q, Alastre T, Burguera JL, de Burguera M, et al. (March 1995). "Lithium and body weight gain". Pharmacopsychiatry. 28 (2): 35–44. doi:10.1055/s-2007-979586. PMID 7624385. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:99" class="footnote-back-ref">↩</a></li>
<li id="fn:100">Malhi GS, Tanious M, Bargh D, Das P, Berk M (2013). "Safe and effective use of lithium". Australian Prescriber. 36: 18–21. doi:10.18773/austprescr.2013.008. <a href="https://doi.org/10.18773%2Faustprescr.2013.008" target="_blank">https://doi.org/10.18773%2Faustprescr.2013.008</a> <a href="#fnref:100" class="footnote-back-ref">↩</a></li>
<li id="fn:101">Gitlin M (December 2016). "Lithium side effects and toxicity: prevalence and management strategies". International Journal of Bipolar Disorders. 4 (1): 27. doi:10.1186/s40345-016-0068-y. PMC 5164879. PMID 27900734. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5164879</a> <a href="#fnref:101" class="footnote-back-ref">↩</a></li>
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<li id="fn:103">Silver M, Factor S (2015). "Chapter 12: VPA, lithium, amiodarone, and other non-DA". In Friedman J (ed.). Medication-Induced Movement Disorders. Cambridge University Press. pp. 131–140. ISBN 978-1-107-06600-7. <a href="978-1-107-06600-7" target="_blank">978-1-107-06600-7</a> <a href="#fnref:103" class="footnote-back-ref">↩</a></li>
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<li id="fn:106">Malhi GS, Tanious M, Bargh D, Das P, Berk M (2013). "Safe and effective use of lithium". Australian Prescriber. 36: 18–21. doi:10.18773/austprescr.2013.008. <a href="https://doi.org/10.18773%2Faustprescr.2013.008" target="_blank">https://doi.org/10.18773%2Faustprescr.2013.008</a> <a href="#fnref:106" class="footnote-back-ref">↩</a></li>
<li id="fn:107">Wetzels JF, van Bergeijk JD, Hoitsma AJ, Huysmans FT, Koene RA (1989). "Triamterene increases lithium excretion in healthy subjects: evidence for lithium transport in the cortical collecting tubule". Nephrology, Dialysis, Transplantation. 4 (11): 939–942. doi:10.1093/ndt/4.11.939. PMID 2516883. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:107" class="footnote-back-ref">↩</a></li>
<li id="fn:108">Keshavan MS, Kennedy JS (2001). Drug-induced dysfunction in psychiatry. Taylor & Francis. p. 305. ISBN 978-0-89116-961-1. <a href="978-0-89116-961-1" target="_blank">978-0-89116-961-1</a> <a href="#fnref:108" class="footnote-back-ref">↩</a></li>
<li id="fn:109">"Safer lithium therapy". NHS National Patient Safety Agency. 1 December 2009. Archived from the original on 30 January 2010. <a href="https://web.archive.org/web/20100130065528/http://www.nrls.npsa.nhs.uk/resources/patient-safety-topics/medication-safety/?entryid45=65426" target="_blank">https://web.archive.org/web/20100130065528/http://www.nrls.npsa.nhs.uk/resources/patient-safety-topics/medication-safety/?entryid45=65426</a> <a href="#fnref:109" class="footnote-back-ref">↩</a></li>
<li id="fn:110">Bendz H, Schön S, Attman PO, Aurell M (February 2010). "Renal failure occurs in chronic lithium treatment but is uncommon". Kidney International. 77 (3): 219–224. doi:10.1038/ki.2009.433. PMID 19940841. <a href="https://doi.org/10.1038%2Fki.2009.433" target="_blank">https://doi.org/10.1038%2Fki.2009.433</a> <a href="#fnref:110" class="footnote-back-ref">↩</a></li>
<li id="fn:111">Lambert CG, Mazurie AJ, Lauve NR, Hurwitz NG, Young SS, Obenchain RL, et al. (May 2016). "Hypothyroidism risk compared among nine common bipolar disorder therapies in a large US cohort". Bipolar Disorders. 18 (3): 247–260. doi:10.1111/bdi.12391. PMC 5089566. PMID 27226264. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5089566" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5089566</a> <a href="#fnref:111" class="footnote-back-ref">↩</a></li>
<li id="fn:112">Kessing LV (January 2024). "Why is lithium [not] the drug of choice for bipolar disorder? a controversy between science and clinical practice". International Journal of Bipolar Disorders. 12 (1): 3. doi:10.1186/s40345-023-00322-7. PMC 10792154. PMID 38228882. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10792154" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10792154</a> <a href="#fnref:112" class="footnote-back-ref">↩</a></li>
<li id="fn:113">"Essential Reads: Lithium and Pregnancy". MGH Center for Women's Mental Health. 4 March 2021. Retrieved 5 December 2024. <a href="https://womensmentalhealth.org/posts/lithium-and-pregnancy-still-a-viable-option/" target="_blank">https://womensmentalhealth.org/posts/lithium-and-pregnancy-still-a-viable-option/</a> <a href="#fnref:113" class="footnote-back-ref">↩</a></li>
<li id="fn:114">Poels EM, Bijma HH, Galbally M, Bergink V (December 2018). "Lithium during pregnancy and after delivery: a review". International Journal of Bipolar Disorders. 6 (1): 26. doi:10.1186/s40345-018-0135-7. PMC 6274637. PMID 30506447. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274637" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274637</a> <a href="#fnref:114" class="footnote-back-ref">↩</a></li>
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<li id="fn:116">Poels EM, Bijma HH, Galbally M, Bergink V (December 2018). "Lithium during pregnancy and after delivery: a review". International Journal of Bipolar Disorders. 6 (1): 26. doi:10.1186/s40345-018-0135-7. PMC 6274637. PMID 30506447. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274637" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274637</a> <a href="#fnref:116" class="footnote-back-ref">↩</a></li>
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</ol>

Lithium (medication) open-in-new

Lithium (medication)