Lithium (medication)

Source: Wikipedia, the free encyclopedia.

Lithium carbonate
Lithium carbonate, an example of a lithium salt
Clinical data
Trade namesMany[1]
License data
  • AU: D
Drug classMood stabilizer
ATC code
Legal status
Legal status
Pharmacokinetic data
BioavailabilityDepends on formulation
Protein bindingNone
Elimination half-life24 h, 36 h (elderly)[2]
Excretion>95% kidney
  • Lithium(1+)
  • [Li+]
  • InChI=1S/Li/q+1

Certain lithium compounds, also known as lithium salts, are used as psychiatric medication,[2] primarily for bipolar disorder and for major depressive disorder.[2] Lithium is taken orally.[2]

Common side effects include

teratogenic, especially during the first trimester of pregnancy and at higher dosages. The use of lithium while breastfeeding is controversial; however, many international health authorities advise against it, and the long-term outcomes of perinatal lithium exposure have not been studied.[3] The American Academy of Pediatrics lists lithium as contraindicated for pregnancy and lactation.[4] The United States Food and Drug Administration categorizes lithium as having positive evidence of risk for pregnancy and possible hazardous risk for lactation.[4][5]

Lithium salts are classified as mood stabilizers.[2] Lithium's mechanism of action is not known.[2]

In the nineteenth century, lithium was used in people who had gout,

generic medication.[2] In 2020, it was the 197th most commonly prescribed medication in the United States, with more than 2 million prescriptions.[10][11] It appears to be under-utilised in older people,[12]
though the reason for that is unclear.

Medical uses

In 1970, lithium was approved by the United States

major depression,[14] schizophrenia, disorders of impulse control, and some psychiatric disorders in children.[2] Because the FDA has not approved lithium for the treatment of other disorders, such use is off-label.[15][14]

Bipolar disorder

Lithium is primarily used as a maintenance drug in the treatment of bipolar disorder to stabilize mood and prevent manic episodes, but it may also be helpful in the acute treatment of manic episodes.[16] Lithium carbonate 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 therapeutic index), requiring close monitoring of blood levels of lithium carbonate during treatment.[17] A limited amount of evidence suggests lithium carbonate may contribute to treatment of substance use disorders for some people with bipolar disorder.[18][19][20]

Schizophrenic disorders

Lithium is recommended for the treatment of schizophrenic disorders only after other antipsychotics have failed; it has limited effectiveness when used alone.[2] The results of different clinical studies of the efficacy of combining lithium with antipsychotic therapy for treating schizophrenic disorders have varied.[2]

Major depressive disorder

Lithium is widely prescribed as a treatment for depression.[15]


If therapy with antidepressants does not fully treat the symptoms of

augmentation agent is sometimes added to the therapy. 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 (off-label) for this purpose since the 1980s.[14]


There are a few old studies indicating efficacy of lithium for acute depression with lithium having the same efficacy as tricyclic antidepressants.[21] 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.[22]

Prevention of suicide

Lithium is widely believed to prevent suicide, and 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.[23][24][25][26][27][28]

Alzheimer's disease

Alzheimer's disease affects forty-five million people and is the fifth leading cause of death in the 65 plus population.[29] 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.[29] To combat this toxic amyloid aggregation, Lithium upregulates the production of neuroprotectors and neurotrophic factors, as well as it inhibits the GSK-3 enzyme.[30] Lithium also stimulates neurogenesis within the hippocampus, making it thicker.[30] Yet another cause of Alzheimer's Disease is the dysregulation of Calcium ions within the brain.[31] Too much or too little Calcium within the brain can lead to cell death.[31] Lithium is able to restore the intracellular Calcium homeostasis through inhibiting the wrongful influx of Calcium upstream.[31] It also promotes the redirection of the influx of the Calcium ions into the lumen of the endoplasmic reticulum of the cells to reduce the oxidative stress within the mitochondria.[31]

In 2009, a study was performed by Hampel and colleagues[32] 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.[30] 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.[30] Another study, a population study this time by Kessing et al.,[33] showed a negative correlation between Alzheimer's Disease deaths and the presence of Lithium in drinking water.[30] Areas with increased Lithium in their drinking water showed less dementia overall in their population.[30]


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

antidiuretic hormone, 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.[34]

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 

mEq/L) 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.[35][36]

Lithium salts have a narrow therapeutic/toxic ratio, so should not be prescribed unless facilities for monitoring plasma concentrations are available. Doses are adjusted to achieve plasma concentrations of 0.4[37][38] to 1.2 mmol Li+
/L [39] 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.[40]

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 interval. 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, 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.[41]


For patients who have achieved long term remission, it is recommended to discontinue lithium gradually and in a controlled fashion.[42][21]

Discontinuation symptoms may occur in patients stopping the medication including irritability, restlessness and somatic symptoms like vertigo, dizziness or lightheadedness. Symptoms occur within the first week and are generally mild and self-limiting within weeks. [43]

Cluster headaches, migraine and hypnic headache

Studies testing

prophylactic use of lithium in cluster headaches (when compared to verapamil), migraine attacks and hypnic headache indicate good efficacy.[21]

Adverse effects

Sources for the following lists.[44][45][46][47][48][49][50]

Very Common (> 10% incidence) adverse effects of lithium include
  • Confusion
  • Constipation (usually transient, but can persist in some)
  • Decreased memory
  • Diarrhea (usually transient, but can persist in some)
  • Dry mouth
  • EKG changes — usually benign changes in T waves
  • Hand tremor (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[51]
  • Headache
  • Hyperreflexia — overresponsive reflexes
  • Leukocytosis — elevated white blood cell count
  • Muscle weakness (usually transient, but can persist in some)
  • Myoclonus — muscle twitching
  • Nausea (usually transient)[40]
  • Polydipsia — increased thirst
  • Polyuria — increased urination
  • Renal (kidney) toxicity which may lead to
    chronic kidney failure
  • Vomiting (usually transient, but can persist in some)
  • Vertigo
  • Weight gain
Common (1–10%) adverse effects include

Lithium carbonate can induce a 1–2 kg of weight gain.[53]

In addition to tremors, lithium treatment appears to be a risk factor for development of parkinsonism-like symptoms, although the causal mechanism remains unknown.[54]

Most side effects of lithium are dose-dependent. The lowest effective dose is used to limit the risk of side effects.

In a systematic literature review, the authors found 250 reports containing 1100 individuals who developed lithium-related movement disorders. The abnormal movements encountered were parkinsonism, dyskinesia, myoclonus, dystonia, Creutzfeldt-Jakob-like syndrome, akathisia, restless legs syndrome symptoms, tics, cerebellar syndromes, and stuttering.[55]


The rate of hypothyroidism 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.[53]

Because lithium competes with the

thyroxine and does not require the lithium dose to be adjusted. Lithium is also believed to permanently affect renal function[how?], although this does not appear to be common.[59]

Pregnancy and breast feeding

Lithium is a

also tend to be associated with teratogenicity.

While it appears to be safe to use while breastfeeding a number of guidelines list it as a contraindication[65] including the British National Formulary.[66]

Kidney damage

Lithium has been associated with several forms of kidney injury.

kidney damage in an aggravated form of diabetes insipidus.[69][70] Chronic kidney disease caused by lithium has not been proven with various contradicting results presented by a 2018 review.[71] 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%.[71][72]



parathyroid hyperplasia



Lithium is primarily

proximal tubule. Its levels are therefore sensitive to water and electrolyte balance.[74] 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.[74][75] 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.[74]

There are also drugs that can increase the clearance of lithium from the body, which can result in decreased lithium levels in the blood. These drugs include theophylline, caffeine, and acetazolamide. Additionally, increasing dietary sodium intake may also reduce lithium levels by prompting the kidneys to excrete more lithium.[76]

Lithium is known to be a potential precipitant of

antidepressants, buspirone and certain opioids such as pethidine (meperidine), tramadol, oxycodone, fentanyl and others.[44][77] Lithium co-treatment is also a risk factor for neuroleptic malignant syndrome in people on antipsychotics and other antidopaminergic medications.[78]

High doses of

flupenthixol may be hazardous when used with lithium; irreversible toxic encephalopathy has been reported.[79]
Indeed, these and other
antipsychotics have been associated with increased risk of lithium neurotoxicity, even with low therapeutic lithium doses.[80][81]


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 that are taking lithium in which the lithium levels are affected by drug interactions in the body.

In acute toxicity, people have primarily gastrointestinal symptoms such as vomiting and diarrhea, which may result in volume depletion. During acute toxicity, lithium distributes later into the central nervous system resulting in mild neurological symptoms, such as dizziness.[40]

In chronic toxicity, people have primarily neurological symptoms which include nystagmus, tremor, hyperreflexia, ataxia, and change in mental status. During chronic toxicity, the gastrointestinal symptoms seen in acute toxicity are less prominent. The symptoms are often vague and nonspecific.[82]

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.

Mechanism of action

The specific biochemical mechanism of lithium action in stabilizing mood is unknown.[2]

Upon ingestion, lithium becomes widely distributed in the central nervous system and interacts with a number of neurotransmitters and receptors, decreasing norepinephrine release and increasing serotonin synthesis.[83]

Unlike many other

euphoria) in normal individuals at therapeutic concentrations.[83]
Lithium may also increase the release of serotonin by neurons in the brain.[84] In vitro studies performed on serotonergic neurons from rat raphe nuclei have shown that when these neurons are treated with lithium, serotonin release is enhanced during a depolarization compared to no lithium treatment and the same depolarization.[85]

Lithium both directly and indirectly inhibits


Another mechanism proposed in 2007 is that lithium may interact with nitric oxide (NO) signalling 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.[94][95] It was also reported that NMDA receptor blockage augments antidepressant-like effects of lithium in the mouse forced swimming test,[96] indicating the possible involvement of NMDA receptor/NO signaling in the action of lithium in this animal model of learned helplessness.

Lithium possesses neuroprotective properties by preventing apoptosis and increasing cell longevity.[97]

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.[98]

Oxidative metabolism

Evidence suggests that

mitochondrial dysfunction is present in patients with bipolar disorder.[97]

Dopamine and G-protein coupling

During mania, there is an increase in

autopsies (which do not necessarily reflect living people), people with bipolar disorder had increased G-protein coupling compared to people without bipolar disorder.[97] Lithium treatment alters the function of certain subunits of the dopamine associated G-protein, which may be part of its mechanism of action.[97]

Glutamate and NMDA receptors

neurons, leading to a homeostatic increase in glutamate re-uptake which reduces glutamatergic transmission.[97]
The NMDA receptor is also affected by other
monovalent ions such as rubidium and caesium.[97]

GABA receptors

proteins and stimulating release of neuroprotective proteins.[97] Lithium's regulation of both excitatory dopaminergic and glutamatergic systems through GABA may play a role in its mood stabilizing effects.[100]

Cyclic AMP secondary messengers

Lithium's therapeutic effects are thought to be partially attributable to its interactions with several signal transduction mechanisms.

Inositol depletion hypothesis

Lithium treatment has been found to inhibit the enzyme

Neurotrophic Factors

Various neurotrophic factors such as BDNF and mesencephalic astrocyte-derived neurotrophic factor have been shown to be modulated by various mood stabilizers.[104]


Lithium was first used in the 19th century as a treatment for

William Alexander Hammond in New York City[8]
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, a number of lithium preparations were still produced for the control of renal calculi and uric acid diathesis.

table salt (sodium chloride). This practice and the sale of lithium itself were both banned in the United States in February 1949, following publication of reports detailing side effects and deaths.[106]

Also in 1949, the

tranquilizers. 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.[108]

The rest of the world was slow to adopt this treatment, largely because of deaths which resulted from even relatively minor overdosing, including those reported from use of lithium chloride as a substitute for table salt. Largely through the research and other efforts of Denmark's Mogens Schou and Paul Baastrup in Europe,[105] and Samuel Gershon and Baron Shopsin in the U.S., this resistance was slowly overcome. Following the recommendation of the APA Lithium Task Force (William Bunney, Irvin Cohen (Chair), Jonathan Cole, Ronald R. Fieve, Samuel Gershon, Robert Prien, and Joseph Tupin[109]), the application of lithium in manic illness was approved by the United States Food and Drug Administration in 1970,[110] becoming the 50th nation to do so.[15] In 1974, this application was extended to its use as a preventive agent for manic-depressive illness.

Fieve, who had opened the first lithium clinic in North America in 1966, helped popularize the psychiatric use of lithium through his national TV appearances and his bestselling book, Moodswing. In addition, Fieve and David L. Dunner developed the concept of "rapid cycling" bipolar disorder based on non-response to lithium.

Lithium has now become a part of Western popular culture. Characters in

South African artist Koos Kombuis, "Lithium" by Evanescence, "Lithium" by Nirvana, "Lithium and a Lover" by Sirenia, "Lithium Sunset", from the album Mercury Falling by Sting,[111] and "Lithium" by Thin White Rope

7 Up

As with

Painesville Telegraph still carried an advertisement for a lithiated lemon beverage.[114]

Salts and product names

Many different lithium salts can be used as medication, including

lithium gluconate

Lithium carbonate (Li
), sold under several trade names, is the most commonly prescribed, while lithium citrate (Li
) is also used in conventional pharmacological treatments.
Lithium orotate (C
), has been presented as an alternative.[115] Lithium bromide and lithium chloride have been used in the past as table salt; however, they fell out of use in the 1940s, when it was discovered they were toxic in those large doses. Many other lithium salts and compounds exist, such as lithium fluoride and lithium iodide, but they are presumed to be as toxic or more so than the chloride and have never been evaluated for pharmacological effects.

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, D-Gluconsäure, Lithiumsalz, 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.[1]


Tentative evidence in

amyotrophic lateral sclerosis (ALS), but a study showed lithium had no effect on ALS outcomes.[118]

See also


  1. ^ a b "Lithium brands". Archived from the original on 5 April 2017. Retrieved 4 April 2017.
  2. ^ a b c d e f g h i j k l m n o p "Lithium Salts". The American Society of Health-System Pharmacists. Archived from the original on 8 December 2015. Retrieved 1 December 2015.
  3. PMID 30506447
  4. ^ .
  5. ^ "Lithium Carbonate Medication Guide" (PDF). U.S. FDA. Archived (PDF) from the original on 27 January 2022. Retrieved 27 January 2022.
  6. ^ from the original on 8 September 2017.
  7. ^ .
  8. ^
    PMID 10885179. Archived from the original
    (PDF) on 1 April 2012.
  9. . WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  10. ^ "The Top 300 of 2020". ClinCalc. Retrieved 7 October 2022.
  11. ^ "Lithium - Drug Usage Statistics". ClinCalc. Retrieved 7 October 2022.
  12. S2CID 257824414
  13. .
  14. ^ .
  15. ^ .
  16. .
  17. ^ Semple, David "Oxford Hand Book of Psychiatry" Oxford Press. 2005.[page needed]
  18. S2CID 26227696
  19. .
  20. .
  21. ^ . Retrieved 17 July 2021.
  22. .
  23. .
  24. .
  25. .
  26. .
  27. .
  28. .
  29. ^ .
  30. ^ .
  31. ^ .
  32. .
  33. .
  34. ^ Healy D. 2005. Psychiatric Drugs Explained. 4th ed. Churchhill Livingstone: London.[page needed]
  35. .
  36. .
  37. mmol/L plasma lithium level in adults for prophylaxis of recurrent affective bipolar manic-depressive illness Camcolit 250 mg Lithium Carbonate Archived 4 March 2016 at the Wayback Machine
    Revision 2 December 2010, Retrieved 5 May 2011
  38. PMID 12091193.) concluded the higher rate of relapse for the "low" dose was due to abrupt changes in the lithium serum levels[improper synthesis?
  39. .
  40. ^ .
  41. .
  42. .
  43. .
  44. ^ a b c DrugPoint® System (Internet). Truven Health Analytics, Inc. Greenwood Village, CO: Thomsen Healthcare. 2013.
  45. .
  46. .
  47. ^ "lithium (Rx) - Eskalith, Lithobid". Medscape. WebMD. Archived from the original on 4 December 2013. Retrieved 7 October 2013.
  48. ^ "Lithobid (lithium carbonate) tablet, film coated, extended release". National Library of Medicine. Noven Therapeutics, LLC. Archived from the original on 5 October 2013. Retrieved 7 October 2013 – via DailyMed.
  49. ^ "Product Information Lithicarb (Lithium carbonate)". TGA eBusiness Services. Aspen Pharmacare Australia Pty Ltd. Archived from the original on 22 March 2017. Retrieved 7 October 2013.
  50. S2CID 9496408
  51. .
  52. .
  53. ^ .
  54. .
  55. .
  56. .
  57. ^ Keshavan MS, Kennedy JS (2001). Drug-induced dysfunction in psychiatry. .
  58. ^ "Safer lithium therapy". NHS National Patient Safety Agency. 1 December 2009. Archived from the original on 30 January 2010.
  59. ^ 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.
    PMID 19940841
  60. .
  61. .
  62. .
  63. .
  64. .
  65. ^ "Lithium use while Breastfeeding". LactMed. 10 March 2015. Archived from the original on 8 December 2015. Retrieved 1 December 2015.
  66. ^ "Lithium carbonate". Archived from the original on 25 October 2016. Retrieved 25 May 2016.
  67. PMID 18519084
  68. ^ .
  69. .
  70. .
  71. ^ .
  72. .
  73. ^ "Lithium". WebMD. Archived from the original on 2 November 2014. Retrieved 1 November 2014.
  74. ^
    PMID 8834421
  75. .
  76. .
  77. ^ Boyer EW. "Serotonin syndrome". UpToDate. Wolters Kluwer. Archived from the original on 16 December 2013. Retrieved 8 October 2013.
  78. ^ Wijdicks EF. "Neuroleptic malignant syndrome". UpToDate. Wolters Kluwer. Archived from the original on 23 October 2013. Retrieved 8 October 2013.
  79. PMID 9296146
  80. .
  81. .
  82. .
  83. ^ .
  84. .
  85. .
  86. ^ .
  87. .
  88. .
  89. .
  90. .
  91. .
  92. .
  93. .
  94. .
  95. .
  96. .
  97. ^ .
  98. .
  99. .
  100. .
  101. .
  102. .
  103. .
  104. .
  105. ^ .
  106. ^ "Lithium: Discovered, Forgotten and Rediscovered". Retrieved 12 March 2023.
  107. ^ "Obituary - Shirley Aldythea Andrews - Obituaries Australia". Retrieved 26 October 2022.
  108. (PDF) from the original on 25 May 2006.
  109. .
  110. (PDF) from the original on 25 May 2006.
  111. ^ Agassi T (12 March 1996). "Sting is now older, wiser and duller". The Jerusalem Post. Archived from the original on 13 May 2012. Retrieved 25 June 2009.
  112. ^ "7 UP: The Making of a Legend". Cadbury Schweppes: America's Beverages.
  113. ^ "Urban Legends Reference Pages: 7Up". Retrieved 13 November 2007.
  114. ^ anonymous (13 July 1950). "ISALLY'S (ad)". Painesville Telegraph. Retrieved 8 September 2013.
  115. PMID 4607169
  116. .
  117. .
  118. .

Further reading

External links