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Buy Lithium Online

lithium antidepressant
Active Ingredient: Lithium Carbonat

Lithium is indicated for the treatment of manic episodes of manic-depressive illness. It is prescribed at maniacal and hypomaniacal states of various genesis, affective psychoses, alcoholism, migraine, Menyer's syndrome, sexual frustration, medicinal dependence.

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Lithium for the treatment of exaggerated emotions, excessive excitability, hypomania, mood changes with alternating periods of happiness and depression, aggressive and independent harm behavior, low white blood cell count as a result of cancer treatment and other conditions. Detailed information on the use, side effects, interactions, contra-indications and reviews of Lithium is presented below:

Lithium compounds are commonly used as psychiatric drugs. Some lithium salts are used as mood-stabilizing drugs, primarily for the treatment of bipolar disorder; they play a role in the treatment of depression and especially mania, both acute and prolonged. As a mood stabilizer, lithium is probably more effective in preventing mania than depression, and also reduces the risk of suicide in patients with bipolar disorder. With depression (unipolar disorder), lithium can be used to enhance the effects of other antidepressants. Lithium carbonate (Li2CO3), which is sold under different trade names, is most often used among lithium preparations. Lithium citrate (Li3C6H5O7) is also often used. As an alternative to these drugs, lithium sulfate (Li2SO4), lithium orotate (C5H3LiN2O4) and lithium aspartate are used. In the past, lithium bromide and lithium chloride were used, but in the 1940s, their possible toxicity was discovered, and these substances disappeared. In addition, there are many other lithium salts and compounds, such as lithium fluoride and lithium iodide, but they are considered toxic substances and have never been tested as pharmacological agents. After entering the esophagus, lithium widely spreads in the central nervous system and interacts with a number of neurotransmitters and receptors, reducing the release of norepinephrine and increasing the synthesis of serotonin.

Medical Use of Lithium

Lithium is used to treat mania in bipolar disorder. Initially, lithium was often used in combination with antipsychotic drugs, since it may sometimes take a month to manifest its effect. Lithium is also used to prevent depression and mania in bipolar disorder. Sometimes lithium is used in the case of other psychiatric disorders, such as cycloid psychosis and major depressive disorder. Lithium has a very important anti-suicidal effect that other stabilizing drugs do not have, such as anticonvulsants. The drug is rarely used for non-psychiatric purposes, however, it has proven itself in the prevention of certain types of headaches associated with a cluster headache, especially nocturnal headaches. In the Italian pilot study conducted in 2005-06, it was stated that lithium can reduce the symptoms of neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS). However, a randomized, double-blind, placebo-controlled trial comparing safety and efficacy of lithium in combination with riluzole for the treatment of ALS failed to demonstrate the benefits of combination therapy compared to riluzole. Lithium is sometimes used as a means to enhance the effect of standard drugs used to treat unipolar depression. Previously, lithium was considered unsuitable for children as a drug, but later studies have shown its effectiveness for the treatment of early bipolar disorder in children aged eight years. The required dose (15-20 mg per kg of body weight) is slightly less than the toxicity level, so during treatment should carefully monitor the levels of lithium in the blood. To assign the right dosage, the entire medical history of the patient, both physically and psychologically, should be taken into account. The initial dose of lithium should be 400-600 mg at night and weekly increase depending on the monitoring of serum. Patients taking lithium should regularly check serum levels and monitor the functioning and possible abnormalities of the thyroid and kidneys, as the substance interferes with the regulation of sodium and water levels in the body and can cause dehydration. Dehydration, aggravated by exposure to heat, can lead to increased levels of lithium. Dehydration is due to inhibition of the action of anti-diuretic hormone by lithium, which provides renal absorption of water from urine. This leads to an inability to concentrate urine, which leads to a subsequent loss of water in the body and thirst. The combination of lithium with high doses of haloperidol, fluphenazine or flupenthixol can be dangerous; there were reports of irreversible toxic encephalopathy caused by the combined use of these drugs.

Lithium salts have a narrow therapeutic / toxic ratio, so they should not be prescribed in the absence of means to monitor plasma concentrations. Patients should be carefully tested. The doses are adjusted to achieve plasma concentrations of 0.4 to 1.2 mmol Li + / L (the lower limit of the range for maintenance therapy and in elderly patients, a higher level for pediatric patients) in samples taken 12 hours after the previous dose. Overdose at a plasma concentration of more than 1.5 mmol Li + / L, can be fatal; toxic effects include tremor, ataxia, dysarthria, nystagmus, renal failure, confusion and convulsions. If these potentially dangerous symptoms occur, treatment should be stopped immediately, the plasma concentrations of lithium should be clarified, and steps taken to reverse the toxicity of lithium should be taken. The toxicity of lithium is aggravated by the depletion of sodium. Simultaneous administration of diuretics that inhibit sodium uptake in the distal tubules (eg, thiazides) is dangerous and should be avoided, as this can result in increased lithiation resorption in proximal convoluted tubules, which leads to elevated, potentially toxic levels of lithium in the body. Sometimes, with a slight poisoning, toxicity can reverse when lithium is stopped taking up and a large amount of sodium and liquid is prescribed. Plasma concentrations of more than 2.5 mmol Li + / L are generally associated with serious toxicity requiring emergency care. At toxic concentrations, maximum toxicity may occur after one to two days. With prolonged use of lithium in therapeutic concentrations, histological and functional changes in the kidney can be observed. The significance of such changes is not clear, long-term lithium intake is not recommended. If kidney problems occur, doctors can change the treatment of a patient with bipolar disorder and prescribe a different mood stabilizing drug, for example, valproate (Depakote) instead of Lithium. An important potential consequence of long-term use of lithium is the development of renal insipid diabetes (inability to concentrate urine). Therefore, for three to five years, lithium should be used only if there is a visible positive effect. Traditional tablets and sustained-release tablets are commercially available. Drugs differ in bioavailability, and a change in the composition used requires the same precautions as the start of treatment. It is possible to give preference to a single simple lithium salt; carbonate is used more widely, citrate is also available. Lithium can be used as an agent for the treatment of seborrheic dermatitis (8% gel lithium gluconate). In addition, lithium increases the production of white blood cells in the bone marrow and can be prescribed to patients suffering from leukopenia. A limited amount of evidence suggests that lithium may be useful in the treatment of substance abuse in some patients with a double disorder. In 2009, Japanese researchers from the University of Oita reported that low levels of natural lithium in drinking water correlated with low suicide rates. In a previous report, similar data was demonstrated in the US state of Texas. In response, psychiatrist Peter Kramer raised the issue of the hypothetical possibility of adding lithium to drinking water as a mineral supplement, and not as a therapeutic agent (therapeutic dose of lithium carbonate (tablet, capsule) or citrate (liquid), "usually in the range from 900-1200 mg / day "and is adjusted according to the patient's response and blood levels.It is similar to niacin when low doses of multivitamins in tablets are taken as a vitamin supplement to prevent pellagra disease associated with q niacin, while a high dose is prescribed as therapeutic to increase levels of high-density lipoproteins ("good" cholesterol).

Side Effects of Lithium

Below is a list of possible side effects that can be caused by drugs containing Lithium. This list is not final. These side effects were fixed earlier, but not always fixed with the drug. Some of these side effects can occur extremely rarely, but have incredibly serious consequences. If any side effects are found, contact your doctor immediately. Especially in case of observing side effects for a long time.

The most common side effects of lithium are general retardation and a slight hand tremor. These side effects are usually present throughout the continuation of treatment, but sometimes some patients may disappear. Other common side effects, such as nausea and headache, are usually eliminated with higher water intake. Lithium causes an imbalance of electrolytes; to avoid this, it is recommended to increase water consumption. According to the Australian study, "the incidence of hypothyroidism in patients taking lithium is six times higher than in the general population. Hypothyroidism, in turn, increases the likelihood of developing clinical depression. "Lithium contributes to weight gain of 1-2 kg. Weight gain may be the cause of low self-esteem in clinical depression. Because lithium competes with receptors for an anti-diuretic hormone in the kidneys, it increases the yield of water in the urine, causing nephrogenic diabetes insipidus. The excretion of lithium by the kidneys is usually successful with the administration of certain diuretics, including amiloride and triamterene. This increases appetite and thirst (polydipsia) and reduces the activity of thyroid hormones (hypothyroidism). The latter is treated with thyroxine. Lithium continuously affects the functioning of the kidneys, although this is not always its property. Lithium can cause the development of nystagmus, to get rid of which it may take several months of abstinence from taking the drug. Most of the side effects of lithium depend on the dose. To limit the risk of side effects, it is recommended to use the lowest effective doses.

- If you experience side effects not listed above, contact your doctor for advice. In addition, you can report the detected side effects to the local Food and Drug Administration.


Lithium is also a teratogenic substance that can cause birth defects in a small number of newborns. The available data and a number of retrospective studies suggest that when taking lithium during pregnancy, an increase in the risk of congenital heart disease, known as Ebstein's anomaly, is possible. In this regard, pregnant women who take lithium, it is necessary to regularly carry out echocardiography of the fetus in order to exclude the possibility of cardiac anomalies. Lamotrigine is a possible alternative to lithium for pregnant women. Gabapentin and Clonazepam are also prescribed as anti-panic medications in childbearing age and during pregnancy. Valproic acid and carbamazepine are also teratogenic substances.


Patients taking lithium salts may experience very dangerous dehydration, especially in combination with lithium-induced nephrogenic diabetes insipidus with polyuria. Such situations can occur with preoperative fluid intake restriction or in other cases of lack of fluid, warm weather conditions, sporting events and hiking. Another danger is that rapid dehydration can very quickly cause hyponatraemia with dangerous toxic concentrations of lithium in the plasma.

Overdose Lithium

Lithium toxicity can be observed in individuals who accidentally or intentionally take excessive amounts of lithium, either at the same time or by accumulating high levels during ongoing chronic therapy. Manifestations of toxicity include nausea, vomiting, diarrhea, weakness, ataxia, confusion, inhibition, polyuria, seizures and to whom. Other toxic effects of lithium include large-amplitude tremors, muscle twitches, seizures and kidney failure. People who survived poisoning can develop persistent neurotoxicity. Some authors describe the "irreversible lithium neurotoxicity syndrome" (SILENT) associated with episodes of acute lithium toxicity or long-term treatment in the appropriate dose range. Symptoms include cerebellar dysfunction.

Measurements in Body Fluids

The concentrations of lithium in whole blood, plasma, serum or urine can be measured using instrumental methods, as a guide to therapy, to confirm the diagnosis from potential victims of poisoning or to assist in forensic examination in the event of a fatal overdose. The lithium concentrations in serum are generally in the range of 0.5-1.3 mmol / L in controlled patients, but may increase to 1.8-2.5 mmol / L in patients who accumulate the drug over time and up to 3-10 mmol / l in victims of acute overdose.

Mechanism of Action

Unlike other psychoactive substances, the intake of Li + in therapeutic concentrations usually does not produce any obvious psychotropic effects (eg, euphoria) in healthy people. Li + can act by interfering with the transport of monovalent or divalent cations in neurons. However, since the substance is a poor substrate on the sodium pump, it can not maintain the membrane potential and only maintains a small gradient through the biological membranes. Li + is fairly similar to Na +, so under experimental conditions it can replace Na + to produce a single action potential in neurons. Recent research shows that the effect of this ion on mood stabilization, jointly or separately, manifests three different mechanisms. The activating neurotransmitter glutamate, as well as other mood stabilizers such as valproate and lamotrigine may be involved in the action of lithium, affecting glutamate, which may serve as a possible biological explanation for a phenomenon such as mania. Other mechanisms by which lithium can regulate mood include changes in gene expression. Lithium can also increase the release of serotonin by brain neurons. Laboratory studies performed on serotonergic neurons of the weld nuclei in rats showed that when these neurons are treated with lithium, the release of serotonin during depolarization is enhanced in comparison with the absence of lithium and the same depolarization. A variant of an unbound mechanism of action was suggested in which lithium deactivates the enzyme GSK3-beta. This enzyme usually phosphorylates the protein factor of transcription of Rev-Erb-alpha, preventing its degradation. Rev-Erb-alpha, in turn, suppresses BMAL1, a component of the circadian clock. Thus, lithium, by inhibiting GSK3beta, causes degradation of Rev-Erb-alpha and increases the expression of BMAL, which extinguishes the circadian clock. With the help of this mechanism, lithium is able to block the reset of the "timer" in the brain, as a result of which the natural cycle of the organism is disturbed. If the cycle is violated, the schedule of many functions (metabolism, sleep, body temperature) is violated. Lithium can, in this way, restore the normal functioning of the brain after disturbances in some people. Some authors suggest that pAp-phosphatase may be one of the therapeutic purposes of lithium. This hypothesis is supported by a low Ki lithium for human pAp-phosphatase compatible within the therapeutic concentration of lithium in patients plasma (0.8-1 mM). It is important to note that human KpAp-phosphatase is ten times lower than that of GSK3beta (glycogen synthase kinase 3beta). Inhibition of pAp-phosphatase by lithium leads to an increase in the level of pAp (3'-5 'phosphoadenisine phosphate), which inhibits PARP-1. Another theory proposed in 2007 is that lithium can interact with the signal pathway of nitric oxide (NO) in the central nervous system, which plays a decisive role in neuronal plasticity. The NO system may play an important role in the antidepressant effect of lithium in the Porsolt test in mice. In addition, it is reported that the blockade of NMDA receptors increases the antidepressant effect of lithium in the Porsolt test in mice ("despair behavior" test, when animals are placed in a closed container of water for 15 minutes and then, 24 hours after the antidepressant is exposed, an animal is placed in the same capacity for 5 minutes already, and measure the time when the animal is at rest and does not even try to escape), which indicates the possible involvement of the NMDA / NO signaling receptors in lithium action in this animal model of learned helplessness. Lithium inhibits the enzyme inositol monophosphatase, which leads to an increase in the levels of inositol triphosphate. This effect is enhanced by a reuptake inhibitor of synosite triphosphate. The destabilization of inositol is associated with memory impairment and depression.


For the first time, lithium began to be used in the 19th century to treat gout, after scientists discovered that lithium under laboratory conditions is capable of dissolving uric acid crystals isolated from the kidneys. However, the levels of lithium needed to dissolve uric acid in the body were toxic. Because of the proliferation of theories linking excess uric acid with disorders, including depressive and manic disorders, Carl Lange in Denmark and William Alexander Hammond in New York City have begun using lithium to treat mania since the 1870s, although the use of lithium-spring waters for the treatment of mania were known even in ancient Greece and Rome. At the turn of the 20th century, the use of lithium was abandoned, according to Susan Greenfield, due to the reluctance of the pharmaceutical industry to invest in a drug that can not be patented. The accumulated knowledge testifies to the role of excess sodium intake in the development of hypertension and heart diseases. Lithium salts are prescribed to patients as a substitute for dietary salt (sodium chloride). This practice was discontinued in 1949, when reports of side effects and deaths were reported as a result of taking the drug, which led to a ban on the Sale of Lithium. The use of lithium salts for the treatment of mania was rediscovered by Australian psychiatrist John Cade in 1949. Cade injected rodents with urine extracts taken from patients with schizophrenia in an attempt to isolate the metabolic compound that may be the cause of the development of mental symptoms. Since it was known that uric acid is a psychoactive substance in gout (it stimulates adenosine receptors on neurons, they are blocked by caffeine), to control Khed needed soluble urates. He used lithium urates, which, as already known, are the most soluble urate compounds, and it turned out that these compounds acted as rodents as tranquilizers. Cade followed the influence on lithium ions separately. Soon, Kade suggested using lithium salts as tranquilizers. With the help of lithium salts, he managed to control mania in chronically hospitalized patients. This was one of the first successful applications of the drug for the treatment of mental illness, and this opened the way for the development of drugs to treat other mental problems in the coming decades. The rest of the world did not hurry to accept this method of treatment, mainly because of deaths occurring even with a relatively small overdose, including when using lithium chloride as a substitute for table salt. Largely due to the research and efforts of Mogens Schou from Denmark, Paul Baastrup in Europe, Samuel Gershon and Baron Shopsin in the US, this resistance is gradually being overcome. In 1970, the US FDA approves the use of lithium in manic diseases. In 1974, the drug was approved for use as a preventive for manic-depressive psychosis. Lithium became part of Western pop culture. The main characters of the films "Pi", "Presentiment", "Memories of Stardust", "American Psycho", "Country of Gardens" "Unmarried woman", all take lithium. Sirius XM Satellite Radio in North America in the 1990s had an alternative rock station called Lithium. In addition, there are songs about lithium preparations. These include the compositions of Mac Lethal Lithium Lips, Koos Kombuis Equilibrium met Lithium, Evanescence Lithium, Nirvana Lithium, Sirenia Lithium and a Lover, Sting Lithium Sunset and Thin White Rope Lithium.

Use of lithium in the drink "7Up"

It is known that before cocaine was a part of Coca-Cola, and Lithium - in the refreshing drink 7Up. In 1920, Charles Leipur Griegg, who founded the company "The Howdy Corporation" in St. Louis, invented the formula of a soft drink with a taste of lemon-lime. The product, originally called "Bib-Label Lithiated Lemon-Lime Soda", was launched on the market two weeks before the stock market crash of 1929. The drink included a mood stabilizer lithium citrate, and this drink was one of the patented medicinal products popular in the late 19th and early 20th century. Its name was soon changed to "7Up"; in 1948 all American beverage producers were forced to withdraw lithium from its composition.


Lithium preparations are used to treat the manic phase of bipolar psychosis, to prevent exacerbations of manic-depressive psychosis, aggressiveness in psychopathies and chronic alcoholism, addiction to psychotropic drugs, sexual deviations, Meniere's syndrome, migraine. The drug is dispensed from pharmacies on prescription. But in the pharmacy from our site you can buy lithium online without a prescription.