Some studies have demonstrated that bottled water from different manufactures can reach high concentrations of Li [ 67]. In one Slovakian product, a Li concentration reached as much as nearly 10,000 μg/L. The mean concentration of Li in European bottled waters, however, was estimated at 0.94 μg/L [ 67]. The mean Li content in tap water and bottled water in Scandinavia (Norway, Sweden, Finland, Iceland) accounted for 0.54 and 0.64 μg/L, respectively [ 69]. Długaszek and Połeć (2012) reported 2.1–14.9 mg/L of Li in spring and medicinal waters produced in Poland with the higher values observed for the latter [ 70]. In German, mineral waters were reported to contain 1.5–1320 μg/L of Li [ 71]; while in Romania, the highest concentration was as low as 0.0719 μg/L [ 72]. These differences in Li concentrations are likely caused by different ambient Li contents in various geographical regions.

Do you have a specific question that this article didn’t answered? Send us a message and we’ll answer Jathar VS, Pendharkar PR, Pandey VK, Raut SJ, Doongaji DR, Bharucha MP, Satoskar RS Manic depressive psychosis in India and the possible role of lithium as a natural prophylactic. II—Lithium content of diet and some biological fluids in Indian subjects. J Postgrad Med 1980, 26:39–44

The therapy with Li has also been shown to increase density of the gray matter and increase the size of the amygdala and hippocampus. Li is also known to stimulate the production of neural stem cells and has protective effects against oxidative stress and its consequences [ 25, 35]. Daunderer M (September 1982). "Lithium aspartate in drug dependence". Fortschr. Med. 100 (33): 1500–2. PMID 7129311. You see on a molecular basis, lithium is almost the same as sodium. Both have the same number of electrons. When supplied in the form of soluble salts, Li is absorbed virtually entirely in the small intestine through sodium channels and evenly distributed in the body, although differences in its concentrations in tissues, plasma, and the brain have been detected [ 10, 23, 35, 45]. It is likely that the absorption process can be modified depending on the other components of the diet; however, a thorough study of chemical compounds that increase and reduce the absorption of Li in the digestive system requires more detailed investigation [ 44]. There is an established body of evidence supporting the use of lithium medication for treating depression. Researchers have found that lithium may be protective against future episodes of depression and suicidality in those who have had a previous episode of depression. In addition, lithium’s anti-suicidal effects have been consistently reported for more than 40 years.

Sugawara N, Yasui-Furukori N, Ishii N, Iwata N, Terao T (2013) Lithium in tap water and suicide mortality in Japan. Int J Environ Res Public Health 10:6044–6048 Because several studies have shown pSN FW to be a disease-progression biomarker in PD ( Ofori et al., 2015, Burciu et al., 2017), the monoamine oxidase B (MAO-B) inhibitor rasagiline, which has several neuroprotective actions, was recently studied in a randomized controlled trial in PD to assess its effects on this outcome ( Arpin et al., 2021). The results showed rasagiline to not significantly affect longitudinal pSN FW progression; however, the placebo group did have over a 4-fold higher 1-year increase in pSN FW compared to the rasagiline group. Our findings of longitudinal reductions in pSN FW associated with medium-dose lithium aspartate therapy for 24 weeks contrasts the findings from this study with rasagiline. Although rasagiline has several neuroprotective mechanisms of action, it has never been shown to affect Nurr1 expression. Lithium, on the other hand, does not inhibit MAO-A or MAO-B and robustly increases Nurr1 expression in PC12 cells ( Nag, 2004; Zhang et al., 2016). Lithium also has anti-inflammatory and autophagy-enhancing actions that have not been described for rasagiline.

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Lithium has been discovered to inhibit the GSK3 enzyme. This enzyme plays a role in the amyloid cascade whereby amyloid beta accumulation in the brains of Alzheimer’s disease patients causes hyperphosphorylation of tau protein, which results in the formation of tangles that contribute to cognitive decline. 2,3 Lithium also supports autophagy, a metabolic process that can help break down harmful tau and amyloid beta proteins. 2 In rodent studies, lithium helped maintain memory and cognitive performance. 4 Fischl B., van der Kouwe A., Destrieux C., Halgren E., Segonne F., Salat D.H., Busa E., Seidman L.J., Goldstein J., Kennedy D., Caviness V., Makris N., Rosen B., Dale A.M. Automatically parcellating the human cerebral cortex. Cereb. Cortex. 2004; 14:11–22. [ PubMed] [ Google Scholar] The risk of intentional abuse of the supplement or accidental poisoning due to interaction in the gastrointestinal tract or as a result of reduced Li of lithium from the body (low-sodium diet, renal failure) also constitutes an obstacle to increasing the intake of this element at a population level [ 46, 89]. Higher doses of Li could potentially lead to exacerbation of symptoms of some diseases, e.g., psoriasis in sensitive individuals [ 90]. It is also relevant to consider the possible side effects of low-dose Li on the functioning of the thyroid gland and kidneys, as well as on pregnancy and fetal development, although the risk of low-dose teratogenicity is considered to be relatively low [ 7, 74]. The University at Buffalo’s Institutional Review Board approved the study prior to patient enrollment (Clinicaltrials.gov: {"type":"clinical-trial","attrs":{"text":"NCT04273932","term_id":"NCT04273932"}}NCT04273932). Eligible patients were 45–80 years old diagnosed with PD by the UK Brain Bank Diagnostic Criteria under the care of the principal investigator, did not have dementia or formed visual hallucinations, no history of stroke or brain surgery, had stable PD medications for >30 days and psychiatric medications for >60 days with no current need for adjustments, stable or no diuretic or NSAID use for >30 days, no history of prescription or dietary supplement lithium use, no history of nilotinib or a glucagon-like peptide-1 agonist use, no use of tobacco for >1 year, normal thyroid stimulating hormone (TSH) level and estimated glomerular filtration rate ≥50. After providing written informed consent, 16 patients were randomized using a random number table to either “high-dose” ( n=5, lithium carbonate titrated to achieve a trough serum level of 0.4–0.5mmol/L), “medium-dose” ( n=6, 45mg/day elemental lithium aspartate) or “low-dose” ( n=5, 15mg/day elemental lithium aspartate) lithium therapy for 24 weeks. Three additional PD patients who chose not to receive lithium therapy served as controls. Fasting blood samples were obtained at baseline, 12 and 24 weeks. For the high-dose group, dose titration was based on trough serum lithium levels assessed by Kaleida Health Laboratories, Williamsville, NY. For all patient groups, trough serum lithium levels were assessed by inductively coupled plasma mass spectrometry (ICPMS) by the UB Chemistry Instrument Center using 6-lithium as an internal standard, which provided a limit of quantification of 1.0µg/L.

Iglesias J.E., Insausti R., Lerma-Usabiaga G., Bocchetta M., Van Leemput K., Greve D.N., van der Kouwe A., Alzheimer's Disease Neuroimaging I., Fischl B., Caballero-Gaudes C., Paz-Alonso P.M. A probabilistic atlas of the human thalamic nuclei combining ex vivo MRI and histology. Neuroimage. 2018; 183:314–326. [ PMC free article] [ PubMed] [ Google Scholar] Aral H, Vecchio-Sadus A (2008) Toxicity of lithium to humans and the environment. Ecotoxicol Environ Saf 70:349–356 The biochemical mechanism of Li action seems to be multifactorial and interdependent with the function of various enzymes, hormones, and vitamins [ 23]. Numerous studies conducted so far on the exact mechanism of its function in the human body still leave many gaps yet to be fully elucidated [ 1, 3, 7]. It is possible that the action of Li + ions in cells is based on competition with Na + and Mg 2+ ions, resulting from the similarity of their atomic radius. It is also postulated that the key to the therapeutic effect of Li lies in the inhibition of enzymes, dependent on the above cations, which regulate intracellular processes and participate in specific nerve transmission pathways. The synthesis and release of neurotransmitters in the cell membrane and the entire cellular metabolism can therefore be modified by the action of Li [ 3, 7, 24, 25].Lithium orotate has been researched as a treatment for alcoholism, and it showed promise since this addictive behavior is propelled by mood swings. Low-dose lithium could also be used to augment treatment for severe depression. Elimination of Li from the body occurs within 24 h after its oral intake and is facilitated by the kidneys. To a small extent (2–3%), it is also excreted with feces and sweat [ 23, 45, 46]. The rate of elimination depends on its concentration in plasma, which is proportional to its daily intake. The amount of Li excreted with urine serves as an indicator of the supply of this element [ 10, 44]. In addition, Li excretion depends on the glomerular filtration rate, and can therefore be reduced with age and in renal disease (e.g., chronic renal failure) [ 10]. Typical range of Li concentration falls within 4.6–219 μg/L limits [ 44, 47], and according to some observations, it remains in significant relation to its concentration in the consumed water [ 10]. However, a psychiatrist may prescribe lithium orotate to people who have gone off lithium therapy or experience milder symptoms. Lithium Orotate: Weight Loss

Torshin I.Y., Gromova O.A., Ostrenko K.S., Filimonova M.V., Gogoleva I.V., Demidov V.I., Kalacheva A.G. Lithium ascorbate as a promising neuroprotector: fundamental and experimental studies of an organic lithium salt. Molecules. 2022:27. [ PMC free article] [ PubMed] [ Google Scholar] Decressac M., Volakakis N., Bjorklund A., Perlmann T. NURR1 in Parkinson disease--from pathogenesis to therapeutic potential. Nat. Rev. Neurol. 2013; 9:629–636. [ PubMed] [ Google Scholar] In its purest form, lithium is a soft, light and silvery-white metal belonging to the alkali group on the periodic table. Knowing this, it may seem strange that the lithium salts lithium carbonate, lithium citrate and lithium sulfate, all inorganic substances, are often prescribed by psychiatrists for oral ingestion. So why exactly do professionals suggest eating metallic compounds to overcome psychiatric conditions, and what are the risks? Lithium in Your Body Hou L., Xiong N., Liu L., Huang J., Han C., Zhang G., Li J., Xu X., Lin Z., Wang T. Lithium protects dopaminergic cells from rotenone toxicity via autophagy enhancement. BMC Neurosci. 2015; 16:82. [ PMC free article] [ PubMed] [ Google Scholar] While ingesting metallic substances can be dangerous, a dosage of 15–20 mg of lithium per kg of body weight falls below the level of toxicity for anyone eight years old and over, though in children the levels of lithium in the blood need to be closely monitored. In addition, when taken in the correct dosage, lithium is processed and released by the body usually within 24 hours, meaning that the metal will not become a part of your body in any harmful way if you take no more than the required dose.Where can I go to learn more about Jacobson’s relaxation technique and other similar methods? – Anonymous patient Answer: Cui J, Shao L, Young LT, Wang JF (2007) Role of glutathione in neuroprotective effects of mood stabilizing drugs lithium and valproate. Neuroscience 144(4):1447–1453