Lithium Prescribing and Monitoring in Clinical Practice – A Practical Guide (2025 Update)

Acute mania:

Several clinical trials have shown that lithium monotherapy is significantly better than valproate, olanzapine, or risperidone. [Malhi et al., 2013]

However, a response to lithium monotherapy is longer than most atypical antipsychotics (6-10 days), and therefore, lithium is often administered in combination with an antipsychotic for faster symptom relief. [Malhi et al., 2013]

Recent data continue to support lithium as comparable to antipsychotics for acute mania, but with stronger effects in euphoric mania rather than mixed or rapid-cycling presentations. [Gitlin & Bauer, 2024].

Predictors of better lithium response include a classical euphoric presentation, fewer prior episodes, and a positive family history of lithium responsiveness. [Gitlin & Bauer, 2024].

Acute bipolar depression:

Lithium is evidence-based in the management of acute bipolar depression; however, the evidence base is less impressive than that for Mania.

Nonetheless, it is included as an option in the recent RANZCP guidelines for the treatment of acute bipolar depression. [Malhi et al, 2021]

The paucity of a strong evidence base may be because lithium’s antidepressant effect can take 6-8 weeks, which may be perceived by patients as lacking efficacy, resulting in high drop-out rates, which can skew trial results.

Lithium monotherapy remains limited in evidence for bipolar depression; however, its use is supported particularly in patients with suicidal risk, where its anti-suicidal effect provides additional benefit.  [Gitlin & Bauer, 2024].

Prophylaxis and Maintenance:

Lithium monotherapy is effective against manic, depressive, mixed relapse and suicidal behaviours. It also has better evidence for the prevention of new episodes than other agents and has a more substantial evidence base documenting the risks of prolonged exposure. [Goodwin et al., 2016]

The real-world effectiveness of Lithium was demonstrated in the BALANCE study (Bipolar Affective Disorder: Lithium/Anticonvulsant Evaluation). [Balance Investigators, 2010]

More recently, the real-world effectiveness study in a Finnish cohort of 18018 patients found that lithium use was associated with the lowest risk of rehospitalisation because of mental or physical illness compared to antipsychotics or other mood stabilisers. [Lähteenvuo et al., 2018]

Recent observational cohorts continue to show superior outcomes with lithium compared to valproate, lamotrigine, or antipsychotics, particularly for mania prevention. [Gitlin & Bauer, 2024].

Evidence also suggests that the earlier lithium is initiated in the illness course, the stronger its prophylactic and neuroprotective effects, reinforcing its role as a first-line therapy. [Bortolozzi et al., 2024]

Rapid cycling and mixed states

Lithium is less effective in rapid cycling and mixed states, although it decreases symptom severity and reduces morbidity.

Lithium therapy, therefore, is advocated in rapid cycling as a combination therapy with other psychotropics.

Anti-suicidal properties:

Patients treated with lithium demonstrate a reduction in suicidal behaviour even in the absence of complete mood stabilisation, likely mediated through reduced aggression and impulsivity.

Meta-analyses consistently show an approximately 60% reduction in suicide risk and 70% reduction in self-harm with long-term lithium use. [Smith & Cipriani, 2017]

A recent systematic review specifically examining interventions in Bipolar disorder in the early phases of treatment concluded that lithium treatment may be associated with a lower risk of recurrence of mood episodes compared with several other agents among those in the early course of illness. [Ratheesh et al., 2023]

Although a few recent studies have reported null findings, these are generally attributable to methodological limitations such as subtherapeutic dosing or insufficient follow-up, and the broader evidence base continues to affirm lithium’s anti-suicidal effect [Gitlin & Bauer, 2024].

Summary of Evidence: 

In contrast to antipsychotics, which are primarily indicated for acute treatment, lithium’s unique strength lies in maintenance therapy and long-term prevention, particularly when introduced early in the illness course.

Most recently, a 2025 Delphi expert panel confirmed with over 85% agreement that lithium should remain the first-choice treatment for patients with bipolar disorder, especially for the prevention of both manic/hypomanic and depressive episodes. [Sampogna et al, 2025]

This consensus reflects accumulating evidence that lithium significantly reduces the risk of new episodes compared with placebo.

Optimal long-term efficacy is achieved at target serum levels of 0.6–0.8 mmol/L.

For patients unable to adhere to lithium, second-generation antipsychotics such as olanzapine, risperidone, or aripiprazole may be considered as alternatives.

However, cohort data indicate that lithium remains at least comparable, if not superior, in relapse prevention. [Lintunen et al, 2025].

Other Indications: 

Emerging evidence indicates potential roles for lithium beyond mood disorders, including in mild cognitive impairment, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, stroke, and traumatic brain injury.

However, results remain preliminary and optimal dosing is not yet established. [Bortolozzi et al., 2024]

After a single dose, the body distributes lithium throughout most of the tissues and fluids of the body.

Besides the serum and the brain, lithium is found in the bone, thyroid, and red blood cells.

Moreover, magnetic resonance spectroscopy shows that brain concentrations of lithium are about half those found in the serum (0.5:1 ratio of Brain: Serum lithium concentrations). Lithium peaks in the brain approximately 24 hours after ingestion. [Malhi et al., 2012]

Lithium is exclusively excreted through the kidneys without undergoing any known in vivo metabolic transformations. Approximately, 80% of administered lithium is re-absorbed by passive diffusion in the proximal tubes, although there is high inter-individual variability.

The half-life of lithium is between 18-36 hours.

The absorption and bioavailability of lithium differ based on the various formulations available.

Lithium is administered as a salt in the form of lithium carbonate, lithium citrate, lithium chloride or lithium sulfate. 

Lithium is available in Australia as:

• Immediate-release lithium carbonate capsules – 250 mg tablets. Peak concentration is reached in 1 to 3 hours with a bioavailability of 95% to 100%
• Extended-release lithium carbonate – 450 mg tablets. Peak concentration is reached in 3 to 6 hours with a bioavailability of 60% to 90%

Lithium citrate oral solution is also available in other countries.

Due to the delay (7-10 days) in the anti-manic effect of lithium, it is usually combined with an antipsychotic in the treatment of mania, which provides more acute symptom relief.

Lithium can be prescribed as a single dose or multiple dose schedule. A single-dose regime can be associated with higher peaks in plasma lithium levels (associated with side effects) and deeper troughs (higher likelihood of breakthrough symptoms).

After initiation, lithium levels should be checked after 7 days, then 7 days after every dose change until the desired level is reached. [The Maudsley Prescribing Guidelines in Psychiatry, 12th edition] (See levels below)

In the elderly or patients with impaired renal function, the time to steady-state increases, implying that the lithium level should also be measured after 10‐12 days.

Advantages of single dosing schedule:

• Since lithium has a longer half-life in neural tissues, once-daily dosing may be sufficient to maintain an effective brain lithium concentration for prophylaxis.
• A single dosing schedule causes less polyuria and decreases the chances of permanent renal damage.
• Since lithium clearance is lower overnight, a single daily dose can be reduced by 25%, which reduces the likelihood of side effects, which in turn can enhance compliance.

The efficacy of lithium correlates with serum lithium levels (trough levels). (See later).

Trough levels are best measured when tested just before the next dose.

The consensus from the International Society of bipolar disorder (ISBD) and International Study Group on Lithium (IGSLI): [Nolen et al., 2019]

Twice daily dosing:

• Sampling should be in the morning 12 ± 1 hrs after intake of the (last) evening dose and before the morning dose.

Once-daily dosing in the evening:

• Sampling should be in the morning, 12 + 1 hours after intake of the evening dose.

A cross-sectional study, however, suggested that in patients with once-daily dosing, a 24-hour post-dose may offer a more accurate trough level and may prevent underdosing. [Reddy & Reddy, 2014]

The study showed that measuring serum lithium levels at 12 hrs in case of OD dosing gave a value 1.3 times higher than the actual trough value.

Thus, in a patient taking a once-daily evening dose, to avoid the inconvenience of an evening blood test, a 12 hr sample can be obtained and then adjusted by 1.3 to calculate an actual trough level at 24 hours.

The dosing properties of lithium can vary in special situations due to its potential for toxicity:

Pregnancy:

Lithium in pregnancy should be used only after a careful risk-benefit analysis.

Lithium can cross the placenta and can increase the risk of Ebstein’s anomaly with exposure in the first trimester (4-12% risk).

Key points about Lithium in Pregnancy: [Fornaro et al., 2019]

• Lithium prescribed during pregnancy was associated with higher odds of any congenital anomaly (NNH -33; Odds ratio 1.810).
• Odds of a cardiac anomaly (NNH -71; Odds ratio – 1.86).
• Lithium exposure during the first trimester was associated with higher odds of spontaneous abortion (NNH -15; Odds ratio 3.77).
• Lithium was more effective than no lithium in preventing postpartum relapse (NNT -3; Odds ratio – 0.16).
• The qualitative synthesis showed that mothers with serum lithium levels <0.64 mEq/L and dosages <600 mg/day had more reactive newborns without an increased risk of cardiac malformations.

When evaluating adverse reactions to lithium, the following three factors should always be considered:

1. Misattribution of psychiatric symptoms for drug-related side effects
2. Effect of the depressed mood state increasing subjective analysis of side effects
3. The additive effect of multiple pharmacotherapies on side effect rates

Common side effects of lithium include:

Gastrointestinal side-effects :

• Typically, nausea, vomiting, indigestion, diarrhoea, and abdominal cramping are relatively common, particularly in the initial stages of therapy.
• Administration of lithium after meals, using a multiple daily dose regimen, or using sustained-release formulations can reduce nausea.

Neurological side-effects:

• Tremor is one of the most common lithium-induced side effects, affecting roughly 25% of patients. It is typically symmetric, fine, and postural, becoming most noticeable during intentional tasks such as writing, drinking, or holding objects.  [Gitlin M. 2016].
• Lithium tremor is distinct from Parkinsonian tremor, which is usually asymmetric and seen at rest, but patients on both lithium and dopamine-blocking agents may develop a mixed tremor of multiple origins.
• Tremor severity is dose-dependent and correlates with higher serum lithium levels. Additional risk factors include advancing age (due to additive effects of essential tremor), anxiety, alcohol withdrawal, caffeine intake, and concomitant medications such as some antidepressants.
• Tremor can occur at any point in treatment, though it is more common early on. In some patients, it improves spontaneously after years of therapy. Extended-release formulations do not reduce prevalence but may smooth fluctuations in plasma levels.
• In the setting of lithium toxicity, tremor becomes coarse, irregular, more severe, and often spreads beyond the hands, accompanied by ataxia, dysarthria, or confusion.
• Management is usually conservative: keep lithium levels within the low–medium therapeutic range, reduce caffeine and stimulant use, and address additive factors.  [Gitlin M. 2016]
• If tremor remains functionally impairing or socially embarrassing, pharmacological treatments can be considered. Propranolol is the most widely used agent, with effective daily doses typically under 120 mg, though the therapeutic range extends from 20 to 320 mg.
• Other options include primidone, benzodiazepines (especially when anxiety contributes), and vitamin B6, all supported by smaller studies and clinical experience.
• In rare, refractory cases where tremor is severe and persistent, a change to another mood stabiliser may be necessary if the side effect significantly affects quality of life.

Cognitive dysfunction:

• Lithium can cause mental slowing, subtle memory impairment, and reduced creativity, which patients often describe as “dullness.” [Gitlin M. 2016].
• Deficits are most evident in verbal learning, working memory, and psychomotor speed, and they follow a dose–response relationship, being more pronounced at higher serum levels.
• These effects can be difficult to separate from the cognitive dysfunction inherent to bipolar disorder or from co-prescribed medications such as antipsychotics, antidepressants, and benzodiazepines. [Wingo et al., 2009]
• Management starts with lowering lithium to the lowest effective therapeutic range and reassessing concomitant psychotropics.
• For persistent impairment, modafinil or armodafinil may improve alertness and concentration without increasing switch risk; in carefully selected cases, dopaminergic stimulants may be considered with caution. [Gitlin M. 2016].

Dermatological Side Effects: 

• Lithium can cause or exacerbate acne, psoriasis, and folliculitis, with onset often within the first months of therapy. [Gitlin M. 2016].
• Acne and folliculitis are more frequent in younger patients, particularly males, possibly due to androgen influence.
• Psoriasis may worsen significantly with lithium, sometimes requiring discontinuation in severe or refractory cases.
• Mechanism is thought to involve altered neutrophil chemotaxis, keratinocyte proliferation, and inositol depletion within skin cells.
• Prevalence rates vary, but skin reactions are reported in up to 45% of lithium-treated patients in some cohorts.
• Clinical impact ranges from mild cosmetic issues to severe lesions associated with marked psychosocial distress.

Management includes:[Gitlin M. 2016].

• Dose reduction when feasible.
• Conventional dermatological treatments (topical retinoids, antibiotics, keratolytics for acne; emollients, corticosteroids, vitamin D analogues for psoriasis).
• Inositol supplementation (6 g/day) has shown benefit in reducing psoriasis severity in small controlled studies.
• For severe or socially impairing reactions, switching to an alternative mood stabiliser should be considered.

Endocrine side-effects:

Lithium can affect the thyroid and parathyroid glands.

• Lithium reduces thyroxine secretion, leading to an increase in TSH and the associated clinical picture of hypothyroidism, resulting in lethargy, depression, weight gain, and dry skin.
• Lithium’s antithyroid effects are mediated through multiple mechanisms, primarily by inhibiting thyroid hormone release. Additional mechanisms include reduced iodine uptake and impaired thyroid hormone synthesis.
• Clinically significant hypothyroidism occurs in 8-19% of patients on lithium compared to 0.5-1% of the general population. Women and the elderly are particularly prone. [Özerdem et al., 2013]
• Subclinical hypothyroidism, marked by elevated TSH with normal T4 and absence of symptoms, is observed in up to 23% of patients. [Gitlin M. 2016].

Key risk factors for lithium-induced hypothyroidism include: [Gitlin M. 2016].

• Presence of antithyroid antibodies, which increases the risk eightfold
• Female sex (which correlates with higher antithyroid antibody prevalence)
• Older age
• Family history of thyroid dysfunction

Given the high incidence of thyroid dysfunction in lithium-treated patients, thyroid function should be assessed before initiating treatment, followed by monitoring at 3–6 months and then at 6–12 month intervals.

TSH measurement is the primary screening tool, with some clinicians also recommending T3, T4, antithyroid peroxidase (TPO) antibodies, and thyroid ultrasound for comprehensive evaluation.

Clinical Management: [Gitlin M. 2016].

• Lithium-induced hypothyroidism does not warrant discontinuation of lithium therapy.

Treatment recommendations based on TSH levels:

• TSH >10 mU/L (confirmed on two occasions): Initiate levothyroxine therapy, even if asymptomatic.
• TSH 4–10 mU/L: Consider levothyroxine if the patient has refractory depression or significant fatigue.
• Asymptomatic patients may be monitored, though some experts recommend early levothyroxine initiation.
• Discontinuation of lithium may allow cessation of thyroid hormone replacement, but persistent hypothyroidism suggests lithium may have unmasked an underlying thyroid disorder.
• Ongoing monitoring is essential to determine long-term thyroid function and treatment needs.

Parathyroid Dysfunction: 

• Lithium increases calcium reabsorption and parathyroid hormone release, causing hypercalcaemia/hyperparathyroidism (~10%).
• Symptoms may include weakness, renal stones, renal impairment, and osteoporosis.
• Annual calcium monitoring is prudent; treat persistent elevations with cinacalcet or parathyroidectomy.

The diagnosis and management are covered in more detail in this article: Lithium-Induced Hyperparathyroidism – Clinical Features and Management

Renal side-effects :

Long-term lithium therapy remains associated with an increased risk of renal impairment. Approximately 26% of patients may develop chronic kidney disease (CKD) stage 3.

However, the absolute risk of end-stage renal disease (ESRD) remains relatively small despite a clearly elevated relative risk compared with controls.

Key risk factors include treatment duration, older age at initiation, and prior episodes of lithium toxicity. Importantly, polyuria does not appear to correlate directly with progression to CKD. [Gitlin & Bauer, 2024].

Frequent urination (polyuria) and excessive thirst (polydipsia) are consistently reported during the initial stages of lithium therapy and are also likely to be related to each other (i.e. thirst is secondary to renal-mediated polyuria).

It is caused by lithium inhibiting the action of antidiuretic hormone (ADH).

The decreased ability of the kidney to concentrate urine predisposes patients to diabetes insipidus, which affects approximately 10% of lithium-treated patients. This can be moderated by amiloride and potentially by the carbonic anhydrase inhibitor acetazolamide.

Lithium levels > 0.8 mmol/L are associated with a higher risk of renal toxicity.

End-stage renal failure occurs in 0.53% of lithium-treated patients compared to 0.2% of the general population.

512 bipolar patients followed up showed that lithium tended to begin to decrease estimated GFR (eGFR) after 10–15 years, and the risk of low values typically required 30 years of treatment, although no patient went on to end-stage renal failure requiring dialysis. The following are risk factors for low eGFR: [Post, 2018]

• Longer lithium treatment
• Lower lithium dose
• Higher serum lithium concentration
• Older age (starting lithium at age ⩾40 years)
• Medical comorbidity
• Low initial baseline eGFR.

Review of Lithium-Induced Renal Dysfunction – Pathophysiology | Diagnosis | Management

Metabolic side-effects

Calabrese reported that the mean weight change over one year in a double-blind study of lithium-treated patients was 4.2 kg. [Calabrese et al., 2003]

Traditional concerns about weight gain with lithium have been nuanced by more recent analyses.

A meta-analysis of 20 studies found no significant weight gain relative to placebo. [Gomes-da-Costa S et al,2022]

Nonetheless, appetite increase and patient-reported weight gain remain clinically relevant. Emerging evidence supports the role of metformin as a countermeasure, while ongoing trials are investigating the potential of GLP-1 receptor agonists for lithium-induced weight gain. [McIntyre et al, 2024].  

However, for the majority of bipolar patients, weight gain is more likely to occur due to other psychotropic medications (such as antipsychotics, valproate and some antidepressants).

It is important to understand lithium’s mechanism of action and to determine the effect a patient’s age, body composition, and disease states have on the clinical outcome, side effects, and potential toxicities.

Bringing these clinical insights together, along with awareness of significant drug interactions, can aid in optimising lithium management.

The RANZCP mood disorder guidelines recommend the following timetable for monitoring of side effects.

Acute toxicity:

At levels above 1.5, mmol/L gastrointestinal (increasing nausea, anorexia, diarrhoea) and CNS effects ( muscle weakness, drowsiness, ataxia, coarse tremor and muscle twitching) occur.

Above levels of 2.0, mmol/L increasing disorientation and seizures can occur.

However, in some instances, even such high plasma levels may lead to mild symptoms.

Chronic toxicity:

Because lithium has a longer half-life in brain tissue than in plasma, long-term lithium treatment can lead to lithium accumulation in the brain and lead to chronic toxicity.

Haemodialysis can treat lithium toxicity. Potassium (20-50 mmol/day) is also useful in reducing the effects of lithium toxicity on the kidney. N-acetyl cysteine may prevent lithium-induced renal damage. [Malhi et al., 2012]

Many patients taking lithium will also be taking it in combination with anticonvulsants, antipsychotics, or antidepressants.

It is important to note any clinically relevant drug interactions:

Carbamazepine:

Enhances the neurological effects of lithium including dizziness, tremors, confusion, and hyperreflexia. This can occur even in the absence of detectable serum increases

NSAIDs:

Lithium clearance is reduced with lithium levels increasing from 10% – greater than 4 fold increases.

Thiazide diuretics:

Thiazide diuretics can dramatically increase lithium serum levels (up to 4 fold increases).

Iodides: 

Such as potassium iodide increase the hypothyroid properties of lithium whereby it decreases the release of thyroid hormone from the thyroid gland

Antidepressants:

Lithium increases serotonergic side effects and therefore increases the risk of the patient developing serotonin syndrome

ACE Inhibitors:

Increase sodium and water excretion rates thus actively retaining lithium. Therefore, the increase in lithium serum levels can cause toxicity (up to 4 fold increases).

Initiating:

The recommendation is to commence therapy with a low and divided dose and to increase this until a serum lithium level of 1.2 mmol/L is reached. Patient requires monitoring and assessment for adverse events as the dose is increased closer to the therapeutic range.

Lithium naive patients should have lithium levels of 0.8 – 1.0 mmol/L.

The NICE guidelines propose a starting level of 0.6 -0.8 mmol/L.

The APA proposes a higher level of 0.8-1.0 mmol/L for controlling symptoms but low levels of 0.4-0.6 mmol/L for prophylaxis long term.

Tailoring:

For prophylaxis, a lower dose of 0.4-0.6 mmol/L may be sufficient whereas for stabilizing patients, it is recommended that a serum concentration of 0.6-0.8 mmol/L may be required.

For the control of mania, a serum concentration of 0.8-0.1 mmol/L is more common.

Maintenance:

In clinical practice, the serum concentration of lithium requires the clinician to understand the risk-benefit ratio of lithium maintenance therapy.

Low serum levels (0.4-0.6 mmol/L) may not be as efficacious as a higher serum level (0.8-1.1 mmol/L) however dropout rates are greater due to tolerability issues at this higher serum level.

Patients likely to have depressive episodes may benefit from prophylactic levels of 0.4-0.8 mmol/L, whereas in those more likely to have mania, levels of 0.6 – 1.0 mmol/L may be more effective.

Long-term:

The long-term maintenance of the recommended target plasma lithium level provides effective prophylaxis and the prevention of symptom recurrence.

Adherence rates are often impaired due to weight gain, polyuria, tremor, and fatigue.

Psychoeducation for the patient and their supportive network is crucial as is careful and frequent monitoring of the patient to ensure compliance is maintained.

Below are the serum levels for initiation and prophylaxis based on different guidelines.

A joint International Society for Bipolar Disorders (ISBD) and International Study Group on Lithium (IGSLI) consensus suggested :

For adults with bipolar disorder:

• 0.60‐0.80 mmol/L with the option to reduce it to 0.40‐0.60 mmol/L in case of good response but poor tolerance or to increase it to 0.80‐1.00 mmol/L in case of insufficient response and good tolerance. [Nolen et al., 2019]
• Recent consensus recommendations from the International Society for Bipolar Disorders (ISBD) and the International Group for the Study of Lithium (IGSLI) emphasise target serum lithium levels of 0.6–0.8 mEq/L for most adults, with 0.4–0.6 mEq/L as an appropriate range in older patients or those with tolerability issues. Importantly, these levels apply equally to the prevention of manic, depressive, and mixed states, reinforcing the need to individualise dosing to both efficacy and tolerability. [Gitlin & Bauer, 2024].

Lithium orotate (LiC₅H₃N₂O₄) was initially advocated by Hans Nieper in the 1970s, who proposed that orotic acid was a superior carrier compound that could more readily transport inorganic ions across biological membranes.

Lithium orotate (LO) was found to have greater lithium brain levels than lithium carbonate at equivalent concentrations, thus offering the potential to maintain a lower lithium dose. [Pacholko & Bekar, 2021]

LO fell out of favour due to a greater incidence of renal impairment compared to Lithium carbonate.

LO is available over the counter as a nutraceutical.

Benefits: 

• Increased brain lithium concentrations relative to lithium carbonate at equivalent concentrations
• potential for lower toxicity due to lowered dose requirements
• Potential for greater compliance due to better side effect profile

Disadvantages: 

• Potential greater renal toxicity
• Unknown therapeutic window
• No dosage guidelines
• Lack of randomised clinical trials

The usual dose of LO is 120 mg daily (equivalent to 5 mg of elemental Lithium) [250 mg of Lithium carbonate = 50 mg of elemental Lithium)

Recent work by Pacholko and Bekar highlights critical areas requiring investigation to establish LO’s safety and efficacy, particularly concerning the pharmacological effects of its constituent, orotic acid (OA).

OA, along with its metabolites carnosine and uridine, has demonstrated potential neuroprotective effects; however, OA’s role in promoting oncogenesis at higher concentrations warrants careful scrutiny. Although the oncogenic risk of OA appears confined to supra-therapeutic levels, further evaluation using both animal and cellular models at therapeutic concentrations of LiOr is essential. [Pacholko & Bekar, 2021]

Pacholko and Bekar also emphasise the necessity of extensive toxicity studies, responding to the foundational concerns raised by Smith and Schou (1979) regarding LO’s enhanced membrane transport. [Smith & Schou, 1979]

This characteristic raises the possibility of impacts on peripheral organs beyond the central nervous system.

A recent study suggests that LO may offer greater potency and fewer adverse effects than lithium carbonate (LiCO) due to distinct pharmacokinetics. LO’s efficacy depended on selective transport mechanisms and pentose pathway involvement, differing from LiCO’s action. Unlike LiCO, LO did not cause polydipsia, elevated creatinine, or increased TSH levels. These findings highlight LiOr’s potential for greater tolerability and efficacy, warranting clinical trials to assess its therapeutic role. [Pacholko & Bekar 2023]

Further research is required to support the use of LO in clinical practice; however, clinicians need to be aware of the use of LO in alternative medicine.

Read more about Nutraceuticals in Psychiatry. 

Lithium is considered a gold-standard treatment for bipolar disorders and a first-line mood stabiliser in many clinical guidelines.

It is important that clinicians appreciate the pharmacokinetics and pharmacodynamics of lithium to ensure the greatest efficacy in the absence of overt toxicity.

The utilisation of treatment guidelines, in conjunction with a clinician’s experience, should guide an appropriate and relevant treatment strategy for bipolar disorder that is tailored to the individual.