Lithium isn’t Only for Mental Health Problems
Besides its use for mental health problems most notably bipolar syndrome you may be interested in lithiums many other positive effects our health.
Low-dose lithium supplementation can be considered by anyone with PTSD, OCD, alcoholism, bipolar depression, unipolar depression, migraine/cluster headaches, improving low white blood cell count, juvenile convulsive disease, liver disorders, recovery from stroke, traumatic brain injury, mild cognitive impairment, Alzheimer's disease, histamine reactions contracting the airways in the lungs, metal toxicity, inflammatory bowel disease and hyperthyroidism.
Lithium Grows and Regenerates Brain Cells
Lithium is involved in the repair, regeneration and maintenance of brain cells. You can consider supplementing low-dose lithium to help to maintain the long term health of your brain, just as little as 0.5 to 1 mg (elemental lithium from lithium-orotate) could be added to your food or drinking water to achieve this. Alternatively you can consider supplementing higher but still low-doses say 2 to 5 or even up to 10 mg to stimulate more intensive period of brain repair and regeneration.
Shrinkage of the brain is observed in many conditions including Alzheimer's disease, mild cognitive impairment, bipolar and chronic depression, for simplicity you can think of there being two things happening, there can be an increased net loss of brain cells and the branches (dendrites) on the remaining cells wither away.
The good news is that we now know at least some parts of the brain actually grow new brain cells, the current estimate is that the region of the brain called the hippocampus produces perhaps 7000 new brain cells per day which means that by the time you're 50 you've actually produce enough new brain cells to regrow the hippocampus which is a pretty large structure within the brain, when the process of growing new brain cells is inhibited as it is for example when people take anti-cancer drugs designed to stop new cell growth people often experience depression and it’s believed that it's the inhibition of the brain's ability to grow new cells but actually causes the depression, if this is true and I believe it is it has quite big implications, it's saying that depression is not due to a lack of chemicals such as serotonin within the synapses but rather due to a lack of actual synapses themselves.
Furthermore the withered dendritic branches are very capable of regrowing when we create the right healthy conditions in the brain. the growth of new cells is called neurogenesis and the growth of dendritic branches is called neuroplasticity. I'm not sure that lithium increases neurogenesis -the growth of new cells- (does anyone know of any evidence for this?) however there is evidence that it slows down the death of brain cells, incidentally the best thing known for increasing, neurogenesis is exercise particularly short burst of vigourous exercise. when it comes to neuroplasticity -the ability of brain cells to grow new connections- however lithium is fantastic stuff.
So whether you've had shrinkage of your dendrites due to prolonged stress and mental illness or damage to a part of the brain due to a stroke and you want to stimulate your existing brain cells to grow new connection you want to supplement lithium. , oOhe did the right nutrition such as omega-3 oils and
supplementation stimulates repair and regeneration of brain cells, it also
Lithium supplementation can have a powerful effect on repairing and protecting the brain it combats the brain shrinkage is seen in cognitive decline, Alzheimer's disease, bipolar syndrome and chronic depression; it also promotes repair and regeneration in the brain following strokes or traumatic brain injury.
Lithium supplementation protects against shrinkage of the brain and can even regenerate the grey and white matter in the brain, improve cognitive function and assist recovery from not only brain injury but also the shrinkage in parts of brain observed in people with chronic stress, depression, bipolar, OCD and PTSD.
I believe supplementing lithium is one of the most powerful things you can do to not only to maintain memory and cognitive function but also regenerate an unhealthy brain.
ADD
Lithium attenuate excessive glutamate
Research explains lithium’s dual anti-manic/ anti-depressive effect July 1, 1998 Researchers at the UW Medical School have solved the puzzle of how one drug — lithium — can effectively stabilize both the wild euphoria and the crushing melancholy that are the hallmark of manic depression, or bipolar disorder. As reported in the July 7 Proceedings of the National Academy of Sciences, the researchers found that in mice brains, lithium exerts a push/pull effect on the neurotransmitter glutamate, eventually causing it to level off in a stable zone where it can control both extremes. “Glutamate is the primary excitatory neurotransmitter, carrying messages instantaneously from one nerve cell to another in 85 percent of the brain,” said UW Medical School professor of pharmacology Dr. Lowell Hokin, who directed the research. Other neurotransmitters include serotonin, dopamine, norepinephrine and acetylcholine. Under normal circumstances, an impulse from a nerve cell releases a flood of message-bearing glutamate aimed at a neighboring neuron across the synapse. A structure on the end of the releasing nerve cell, called a reuptake transporter, then shuts off the signal by reabsorbing the glutamate, pumping it back into the cell for reuse. If the reuptake mechanism malfunctions, inappropriate concentrations of neurotransmitter remain in the synapse. Hokin postulates abnormally low glutamate levels are involved in depression, while elevated levels are responsible for mania. Nearly a half century ago, Australian psychiatrist John F. Cade discovered lithium’s mood-stabilizing effect. It has long been the drug of choice in treating bipolar disorder, which affects approximately 2.5 million Americans. Despite some side effects, lithium usually successfully dampens the mood swings that in the most severe cases end in suicide, the dire result for one in five untreated or unresponsive bipolar patients. In an earlier study (reported in PNAS, Aug. 30, 1994), Hokin and his colleague showed that lithium causes glutamate to accumulate in synapses of mice and monkey brain slices, but exactly how it worked remained unclear until now. In the current study, functioning slices of mice brain were examined following exposure to lithium, while control slices were not exposed to the drug. The researchers observed that lithium raised the glutamate level by slowing its reuptake. The higher the lithium dose, the greater the inhibition, they found. To study the chronic effect of the lithium, the UW team administered it to live mice for two weeks. To their surprise, they saw that glutamate reuptake increased. This “up-regulation” resulted in less neurotransmitter in the synapse, which would produce an anti-manic effect. “We were especially interested to find that the reuptake mechanism in the 18 lithium-treated mice was stabilized in a very narrow range, compared to the 18 controls,” he said. Hokin speculates a compensatory mechanism in the reuptake system strives over time to reset raised glutamate levels down into a fixed range. When the levels are too low, as postulated in depression, lithium brings them up into the stable region. The research findings support clinical observations, he noted. “It takes a few weeks before lithium begins to relieve depression and mania in bipolar patients,” he said. “It’s now apparent an adaptive reuptake mechanism that brings glutamate within a ‘normal’ range works over time to curb both the highs and lows.” What’s more, he added, lithium doesn’t change the moods of people who aren’t bipolar, suggesting that their glutamate levels may be positioned consistently within the set zone, and therefore would not be affected by the drug. - See more at: http://news.wisc.edu/research-explains-lithiums-dual-anti-manic-anti-depressive-effect/#sthash.DQ6C2WLI.dpuf
Neuropharmacology. 2002 Dec;43(7):1173-9.
Lithium induces brain-derived neurotrophic factor and activates TrkB in rodent cortical neurons: an essential step for neuroprotection against glutamate excitotoxicity.
Hashimoto R1, Takei N, Shimazu K, Christ L, Lu B, Chuang DM.
Author information
- 1Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-1363, USA.
Mechanisms underlying the therapeutic effects of lithium for bipolar mood disorder remain poorly understood. Recent studies demonstrate that lithium has neuroprotective actions against a variety of insults in vitro and in vivo. This study was undertaken to investigate the role of the brain-derived neurotrophic factor (BDNF)/TrkB signaling pathway in mediating neuroprotection of lithium against glutamate excitotoxicity in cortical neurons. Pretreatment with either lithium or BDNF protected rat cerebral cortical neurons from glutamate excitotoxicity. The duration of treatment required to elicit maximal neuroprotection by BDNF (1 day) was much shorter than that by lithium (6 days). K252a, an inhibitor of Trk tyrosine kinases, and a BDNF neutralizing antibody suppressed the neuroprotective effect of lithium. Treatment of cortical neurons with lithium increased the cellular BDNF content in 3 days and the phosphorylation of TrkB at Tyr490 in 5 days, suggesting that long-term lithium administration enhances BDNF expression/secretion, leading to the activation of TrkB receptor. Lithium failed to protect against glutamate excitotoxicity in cortical neurons derived from homozygous and heterozygous BDNF knockout mice, although lithium fully protected cortical neurons prepared from wild type mice littermates. Taken together, these data suggest that the BDNF/TrkB pathway plays an essential role in mediating the neuroprotective effect of lithium.
PMID:
12504924
[PubMed - indexed for MEDLINE]
- Share on Facebook
- Share on Twitter
- Share on Google+
Reduced Violent Crime and Suicide
There’s evidence that when people have a higher intake of lithium from their diet and water they are less likely to commit suicide {The British Journal of Psychiatry Apr 2011, 198 (5) 346-350; DOI: 10.1192/bjp.bp.110.091041} and violent crimes, so just tiny amounts of this little mineral can have remarkable life saving effects on improving mental health.
See How to use low-dose lithium for more on suicide.
There is also some evidence that an increased dietary intake of lithium increases life expectancy and the increasing life expectancy is not just because of the reduced rate of suicide. {doi:10.1007/s00394-011-0171-x}
Lithium and Longevity
A new paper was published this week - Low-dose lithium uptake promotes longevity in humans and metazoans. Now, as a psychiatrist, I'm a lithium fan. Apparently, it is an essential trace micronutrient (who knew) aside from the uses for decreasing suicide and helping mood stabilization. Want a primer - look at my blog post here. (Here is the original lithium for treating mania paper by John Cade if you are interested.)
Decreasing suicide? Yes, well lithium is actually very good at keeping people alive. Even those with bipolar disorder or major depression who have no real symptomatic improvement seem to have less suicidal thoughts and suicides while on lithium. Very interesting. But why?
Let's start with some observational studies. Back in 1989, Schrauzer and Shrestha published a paper called "Lithium in Drinking Water and the Incidences of Crimes, Suicides, and Arrests Related to Drug Addictions." They took information about the lithium level in the water of 27 counties in the Great State of Texas. Seems that counties with higher lithium levels in the water had a statistically significant decrease in the incidence of homicide, suicide, arrests for opiates and cocaine, and violent criminal behavior. Now to put things into perspective, a high lithium water content translates to about 2mg of lithium a day. Psychiatric doses start at 300mg daily.
Reduced GSK3
Lithium reduces an enzyme called GSK3B which is a good thing. Elevated GSK3b promotes inflammation and chronic degeneration, its associated with the development of TAU proteins in the brain involved in the development of Alzheimer's disease, elevated GSK3B increases the risk of developing type II diabetes and abnormal expression of the GSK3B gene looks like it's involved in causing disturbances in the timing of the biological clock/sleep cycles common in bipolar syndrome and in possibly causing bipolar syndrome itself. (references for all of this are so easy to find I'll let you look yourself).
I think it would be useful in the future if we could test for GSK3B levels like we test for high cholesterol today.
lithium and cognitive decline
Lithium and risk for Alzheimer's disease in elderly patients with bipolar disorder
Paula V. Nunes, Orestes V. Forlenza, Wagner F. Gattaz
DOI: 10.1192/bjp.bp.106.029868 Published 30 March 2007
Abstract
Bipolar disorder is associated with increased risk for dementia. We compared the prevalence of Alzheimer's disease between 66 elderly euthymic patients with bipolar disorder who were on chronic lithium therapy and 48 similar patients without recent lithium therapy. The prevalence of dementia in the whole sample was19% v. 7% in an age-comparable population. Alzheimer's disease was diagnosed in 3 patients (5%) on lithium and in 16 patients (33%) who were not on lithium (P<0.001). Our case–control data suggest that lithium treatment reduced the prevalence of Alzheimer's disease in patients with bipolar disorder to levels in the general elderly population. This is in accordance with reports that lithium inhibits crucial processes in the pathogenesis of Alzheimer's disease.
- © 2007 Royal College of Psychiatrists
Curr Alzheimer Res. 2013 Jan;10(1):104-7.
Microdose lithium treatment stabilized cognitive impairment in patients with Alzheimer's disease.
Nunes MA1, Viel TA, Buck HS.
Author information
Abstract
A lower incidence of dementia in bipolar patients treated with lithium has been described. This metal inhibits the phosphorylation of glycogen-synthase-kinase 3-α and β, which are related to amyloid precursor protein processing and tau hyperphosphorylation in pathological conditions, respectively. Following the same rationale, a group just found that lithium has disease-modifying properties in amnestic mild cognitive impairment with potential clinical implications for the prevention of Alzheimer's Disease (AD) when a dose ranging from 150 to 600 mg is used. As lithium is highly toxic in regular doses, our group evaluated the effect of a microdose of 300 μg, administered once daily on AD patients for 15 months. In the evaluation phase, the treated group showed no decreased performance in the mini-mental state examination test, in opposition to the lower scores observed for the control group during the treatment, with significant differences starting three months after the beginning of the treatment, and increasing progressively. This data suggests the efficacy of a microdose lithium treatment in preventing cognitive loss, reinforcing its therapeutic potential to treat AD using very low doses.
J Clin Psychiatry. 2009 Jun;70(6):922-31.
Lithium trial in Alzheimer's disease: a randomized, single-blind, placebo-controlled, multicenter 10-week study.
Hampel H1, Ewers M, Bürger K, Annas P, Mörtberg A, Bogstedt A, Frölich L, Schröder J, Schönknecht P, Riepe MW, Kraft I, Gasser T, Leyhe T, Möller HJ, Kurz A, Basun H.
Author information
Abstract
OBJECTIVE:
Lithium, a first-line drug for the treatment of bipolar depression, has recently been shown to regulate glycogen synthase kinase-3 (GSK-3), a kinase that is involved in the phosphorylation of the tau protein. Since hyperphosphorylation of tau is a core pathological feature in Alzheimer's disease, lithium-induced inhibition of GSK-3 activity may have therapeutic effects in Alzheimer's disease. In the current study, we tested the effect of short-term lithium treatment in patients with Alzheimer's disease.
METHOD:
A total of 71 patients with mild Alzheimer's disease (Mini-Mental State Examination score > or = 21 and < or = 26) were successfully randomly assigned to placebo (N = 38) or lithium treatment (N = 33) at 6 academic expert memory clinics. The 10-week treatment included a 6-week titration phase to reach the target serum level of lithium (0.5-0.8 mmol/L). The primary outcome measures were cerebrospinal fluid (CSF) levels of phosphorylated tau (p-tau) and GSK-3 activity in lymphocytes. Secondary outcome measures were CSF concentration of total tau and beta-amyloid(1-42) (Abeta(1-42)), plasma levels of Abeta(1-42), Alzheimer's Disease Assessment Scale (ADAS)-Cognitive summary scores, MMSE, and Neuropsychiatric Inventory (NPI). Patients were enrolled in the study from November 2004 to July 2005.
RESULTS:
No treatment effect on GSK-3 activity or CSF-based biomarker concentrations (P > .05) was observed. Lithium treatment did not lead to change in global cognitive performance as measured by the ADAS-Cog subscale (P = .11) or in depressive symptoms.
CONCLUSIONS:
The current results do not support the notion that lithium treatment may lead to reduced hyperphosphorylation of tau protein after a short 10-week treatment in the Alzheimer's disease target population.
TRIAL REGISTRATION:
(Controlled-Trials.com) Identifier: ISRCTN72046462.
Drugs Aging. 2012 May 1;29(5):335-42. doi: 10.2165/11599180-000000000-00000.
Does lithium prevent Alzheimer's disease?
Forlenza OV1, de Paula VJ, Machado-Vieira R, Diniz BS, Gattaz WF.
Author information
Abstract
Lithium salts have a well-established role in the treatment of major affective disorders. More recently, experimental and clinical studies have provided evidence that lithium may also exert neuroprotective effects. In animal and cell culture models, lithium has been shown to increase neuronal viability through a combination of mechanisms that includes the inhibition of apoptosis, regulation of autophagy, increased mitochondrial function, and synthesis of neurotrophic factors. In humans, lithium treatment has been associated with humoral and structural evidence of neuroprotection, such as increased expression of anti-apoptotic genes, inhibition of cellular oxidative stress, synthesis of brain-derived neurotrophic factor (BDNF), cortical thickening, increased grey matter density, and hippocampal enlargement. Recent studies addressing the inhibition of glycogen synthase kinase-3 beta (GSK3B) by lithium have further suggested the modification of biological cascades that pertain to the pathophysiology of Alzheimer's disease (AD). A recent placebo-controlled clinical trial in patients with amnestic mild cognitive impairment (MCI) showed that long-term lithium treatment may actually slow the progression of cognitive and functional deficits, and also attenuate Tau hyperphosphorylation in the MCI-AD continuum. Therefore, lithium treatment may yield disease-modifying effects in AD, both by the specific modification of its pathophysiology via inhibition of overactive GSK3B, and by the unspecific provision of neurotrophic and neuroprotective support. Although the clinical evidence available so far is promising, further experimentation and replication of the evidence in large scale clinical trials is still required to assess the benefit of lithium in the treatment or prevention of cognitive decline in the elderly.
lithium and cognitive decline
HOW TO ENLARGE YOUR BRAIN AND IMPROVE BRAIN PERFORMANCE
By Dr. James Howenstine, MD.
May 5, 2004
NewsWithViews.com
Conventional medical thinking concerning the brain have always believed that the brain steadily decreased in size with aging and that when brain neurones (nerve cells) died they were lost forever. This explains why elderly persons generally have slightly smaller brains than younger individuals.
Preserving And Renewing Brain Cells With Lithium
Medical students are taught that there is a slow steady loss of brain cells with aging culminating in gradual shrinkage of the brain. Lithium has long been known to be an effective therapy for Bipolar Disorder (manic depression) when taken in high doses. However, recent research has shown that low doses of lithium preserve and renew[1] brain cells. Eight of ten persons given lithium showed an increase in brain grey matter of 3 % after only 4 weeks. By promoting brain cell regeneration and increasing brain size lithium can function as an anti-aging nutrient for the brain.
Lithium also accomplishes the following benefits for brain cells:
- Lithium enhances DNA replication which is the first step to formation of new cells.
- The damaging effects of excitotoxins. (monosodium glutamate (MSG), aspartame (Nutrasweet) etc. can be blocked by lithium.[2]
- Animal research shows that lithium can decrease the areas of cell death after induced strokes by 56 %.
- Lithium protects rat brain cells from the. increased levels of brain cell death caused by anti-convulsant drugs (Dilantin phenytoin , Tegretol, carbamazepine etc.)
- Lithium may protect against adverse effects from mood altering drugs, alcohol, tobacco, caffeine, 'uppers"and "downers", and marihuana all of which cause brain damage with long term use.
- Abnormally functioning signaling pathways may become repaired by lithium.
- The aluminum felt to be a possible cause of Alzheimer's Disease (AD). is chelated[3] by lithium so it can be more easily removed from the body.
Ten years of research by 27 counties in Texas disclosed that the incidence of homicide, rape, robbery, burglary, arrests for drug possession, and suicide[4] were higher in counties whose drinking water contained little or no lithium. Counties whose drinking water naturally contained higher amounts of lithium had significantly lower rates of all these crimes. These counties with higher levels of lithium in their tap water experienced fewer hospitalizations for homicides, mental illness[5], psychosis, neurosis, schizophrenia, and personality disorder. Low dosage lithium benefits alcoholism and mood disorders seen in heavy users of alcohol and their relatives. This therapy is often obvious to family members[6] when depression, premenstrual tension, temper flareups and irritability cease affecting the individual. Lithium has been helpful in reducing aggressive[7] behavior in children. High dosages of lithium helped two adult women with severe anorexia nervosa[8] regain 26 and 20 pounds in six weeks. Both women experienced improvement in behavioral problems.
Low dosages of lithium have been found to be safe.[9] Dr. Jonathan Wright suggests 20 to 30 mg. of lithium aspartate or lithium-orotate daily as an appropriate dose to stop brain aging. This is 1/3 to 1/6 the dosage of lithium-carbonate used to treat manic depressive disorder. Dr. Hans Nieper of Germany has learned that lithium-orotate or lithium aspartate penetrate cells more effectively than lithium-carbonate so smaller doses can be used. One tablespoon of flaxseed oil daily along with 400 I.U. of vitamin E ensures that no lithium toxicity can develop. These lithium products can be obtained from Tehama Clinic 425-264-0059.
Should Lithium Be Added To The Water Supply In The U.S.?
The answer is yes, particularly for parts of the country where lithium water levels are low. Placing lithium in the water supply would almost certainly lower crime rates and would also improve the productivity of many emotionally troubled persons.
Is this likely to occur? Probably not because there is no large corporation that would profit from the placing of lithium in water. To understand the political environment surrounding an issue like this it is important to have an awareness of how fluoride was placed in U.S. water supplies.
Why did fluoride get placed in U.S. community water supplies? A politically important industry (aluminum manufacture) had an enormous problem disposing of the very toxic sodium fluoride created as a byproduct of the production of aluminum. Other than use as a rat poison, sodium fluoride had no economic value.
Was there any evidence that fluoride decreases the incidence of cavities? No, not then or since then.
Were any studies conducted to verify if the placing of fluoride in the water was safe for the American public? No.
Did anyone know how much fluoride should be added to water? No. The dose selected one part per million[10] was selected arbitrarily. When the legislation to place fluoride into U.S. water supplies was passed every congressman had bottled water placed in their offices. A prominent senator always carried a flask of spring water in his coat pocket when he dined in a fashionable Washington restaurant. He stated to his dinner companions " Not one drop of fluoridated water will ever pass my lips." Such are the guardians of our nation. Since placing lithium in our water could improve general health and decrease the need for pharmaceutical drugs there is little possibility this will occur.
Preserving Brain Function
An interesting study was done in elderly nuns living in a convent to try to ascertain what factors seem to contribute to declining brain function in the elderly (dementia). What was discovered was that those who were involved in activities that challenged the brain (learning new skills, working crossword puzzles, playing chess, etc.) were less likely to become demented than those who had no interests and were simply vegetating. This fits with "use it or lose it concept regarding brain function in the elderly" which appears to be valid.
Footnotes:
1, Moore G.L. et al Lithium-induced increase in human grey matter. Lancet 2000; 356: 1, 241-1, 242
2, Nanaka S., Chronic lithium treatment robustly protects neurones in the central nervous system against neuro excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx. Proceedings of the National Academy of Sciences of U.S.A. 1998; 95: 2,642-2,647
3, Radesater A., et al, Inhibition of GSK 3 beta by lithium attenuates tau phosphoralation and degeneration. Society for Neuroscience Abstracts 2001: 1, 437
4, Schrauzer,GN et al Lithium in drinking water and the incidence of crimes, suicides, and arrests related to drug addiction. Biological Trace Element Research 1990;105-113
5, Dawson E. B. The relationship of tap water and physiological levels of lithium levels of lithium to mental hospital admission and homicide in Texas. In Schrauzeer GN, Klippel KF (editors) Lithium in Biology and Medicine VCH Publishers, New York, 1991, pp. 170-187
6, Wright Jonathan Lithium Part 2 Other Effects Townsend Letter for Doctors & Patients April 2004 pg.59-60
7, Wright J. Lithium, Part 2: Other Effects Townsend Letter for Doctors & Patients April 2004 pp. 59
8, Bsreai A. Lithium id adult anorexia nervosa. Acta Psychiat Scand 1977; 55:97-101
9, Wright, J., Nutrition & Healing Vol. 10, Issue 7 Augiust 2003 pg.1-4
10, Mullins Eustace Murder By Injection The story of the Medical Conspiracy Against America pp 158 The National Council for Medical Research, P.O. Box 1105, Staunton, Virginia 24401
© 2004 Dr. James Howenstine - All Rights Reserved
Is Lithium Good for Depression
lithium bipolar 2
Biochemical and Physiological Effects of Lithium
Cellular Transport and the Inorganic Biochemistry of Lithium (N.J. Birch)
The chemistry of lithium is unusual. Lithium atoms are very small, highly polarized, and have a high charge density. The chemical and biochemical properties of lithium are similar to those of magnesium, with which it shares a “diagonal relationship” in the periodic table. Because magnesium plays a crucial role in the regulation of biochemical systems, it has been theorized that lithium influences magnesium-dependent processes
Lithium can be transported across membranes in five different ways. Of these, passive flux is important for the entry of lithium into cells, and sodium-lithium countertransport for the extrusion of lithium from cells. Lithium can presumably replace sodium in the sodium-sodium countertransport system, although the biological significance of the latter process is still unclear.
It appears that the concentration of lithium in cells does not reach the levels predicted by the Nernst equation. Rather, the intracellular lithium concentration is considerably lower than its concentration in blood or extracellular fluid. This is important for the models which have been proposed for its mechanism of action, as these must be able to explain the effects of lithium at intracellular concentrations of 0.1 mmol/l (i.e. similar to those seen in patients on lithium prophylaxis).
One hypothesis suggests that the biological effects of lithium are due to the role it plays at the cell periphery, where, for example, it may influence cell recognition, cell signaling mechanisms at the cell membrane, and certain immunological processes.