Why Lithium Ascorbate?
Lithium Ascorbate is a Synergistic Combination of two active substances in One Molecule: Lithium and Vitamin C (ascorbic acid) with No Side Effects
Stabilizes your emotions
(The Normotim Effect)
Supports antidepressant activity
Lessens anxiety
Prevents stress
Lithium carries with it a superhero cloak in the realm of neuroscience—it’s known as a neuroprotective agent, guarding the precious neurons within our brains.
Extended lithium treatment has a knack for dialing down the toxicity brought on by glutamate, which is mediated through N-methyl-D-aspartate (NMDA) receptors. This impressive feat is partly due to lithium’s ability to suppress calcium influx, which plays a pivotal role in the dance of NMDA receptor activity (Peek into the research here: PMC).
What's more, lithium’s potential benefits may stretch far and wide, possibly extending a helping hand to conditions such as mood disorders, Alzheimer’s disease, diabetes, cancer, and even inflammatory and autoimmune diseases (Explore more on PMC). With such a versatile profile, lithium might just be the unsung hero in the pharmacological fight against these conditions.
Lithium has been documented to elevate the levels of neurotrophic factors including Brain-Derived Neurotrophic Factor (BDNF), Nerve Growth Factor (NGF), and Glial cell line-Derived Neurotrophic Factor (GDNF).
Chronic exposure to lithium in neuronal culture has been shown to induce BDNF activity. BDNF stands as a critical neurotrophic agent, essential for cognitive development, synaptic plasticity, and neuronal survival, and it also exhibits antidepressant and anxiolytic effects (Further information can be found in the article: PubMed).
The increase in BDNF levels is likely a result of the inhibition of glycogen synthase kinase-3 (GSK-3) by lithium (This mechanism is explored in depth in the same source: PubMed).
Additionally, lithium is reported to raise levels of NGF and GDNF in the hippocampus, frontal cortex, occipital regions, and the striatum (The findings are published here: PubMed). Both NGF and GDNF are known to contribute to increased neuronal survival and plasticity, enhancing the regenerative capacity and formation of new synaptic connections among dopaminergic, cholinergic, and serotonergic neurons within the central nervous system.
Lithium enhances neurogenesis and improves cognitive function
Lithium has been found to stimulate progenitor cells and stem cells in hippocampal neuron cultures of the brain (neurons from the memory center). Additionally, lithium prevents the loss of proliferation caused by glutamate or cortisol (glucocorticoids). Furthermore, long-term treatment with lithium promotes the transformation of these progenitor cells into neurons (PubMed).
Moreover, the application of lithium not only enhances the process of neurogenesis in the hippocampus (memory center) in healthy mice but also restores neurogenesis in the brain of an animal model of Down syndrome (PubMed).
The drug also intensifies neurogenesis (the formation of new neurons) in the subventricular zone, the only area, in addition to the hippocampus (memory center), where such an effect was observed, resulting in a sustained increase in gray matter volume in patients (PubMed).
Lithium increases the level of N-acetyl aspartate (NAA) (PubMed), which can be considered an indicator of creativity and correlates with IQ scores (PubMed). One likely consequence of this may be more effective communication between the two hemispheres of the brain, leading to improved brain activity (PubMed).
Lithium's use also increases long-term potentiation (LTP) in hippocampal neurons, which renders the nerve cells more functional and thus aids in learning and memory (PubMed).
Lithium enhances the regeneration of vascular structures within the brain and heart, mediated by the upregulation of Vascular Endothelial Growth Factor (VEGF), a key molecule in angiogenesis. The augmented production of VEGF by lithium administration promotes cellular growth and the regeneration of blood vessels that have been compromised following an ischemic stroke. This is detailed further in the literature, highlighting lithium's potential for expediting recovery from cerebral ischemic events (Refer to the study on PMC).
By increasing VEGF levels, lithium may aid in hastening the recuperation process post-stroke or after a cardiac event, such as a myocardial infarction. The probable mechanism suggested involves the inhibition of glycogen synthase kinase-3 (GSK-3) by lithium, which is instrumental in the modulation of VEGF expression and subsequent angiogenesis (This is elaborated upon in the same source: PMC).
The therapeutic implications of this GSK-3 inhibition by lithium suggest a promising role in the enhancement of VEGF-mediated vascular repair, particularly in the context of neurovascular and cardiovascular pathologies (PMC).
Lithium, a chemical element primarily known for its psychiatric applications, particularly in the management of bipolar disorder, appears to have a beneficial effect on human bone tissue as well.
A comparative study assessed the bone mineral density (BMD) of the hip and lumbar spine in 75 volunteers who were administered lithium and 75 healthy controls who were not. These groups were matched for confounding factors such as age, gender, and body mass index. The study revealed that individuals on lithium had lower bone turnover markers. In terms of BMD, volunteers taking lithium exhibited a significant increase: 4.5% in the lumbar spine, 5.3% in the femoral neck, and 7.5% in the trochanteric region of the femur (Investigate the details on PubMed).
Moreover, lithium therapy has been correlated with a reduced risk of bone fractures and enhanced osteogenesis (Bone formation processes are elaborated in these sources: PubMed, PMC Article 1, PMC Article 2). These findings position lithium as a potential osteoprotective agent, offering new perspectives on its therapeutic applications beyond neuropsychiatry.
Lithium can calm and stabilize mood
In animals, lithium consistently reduces exploratory activity and aggression (PubMed).
It is known that in humans, lithium also has a calming effect and stabilizes mood, and is used for the treatment of depression, bipolar disorder, and schizophrenia (PubMed).
Lithium carbonate is the standard of care in bipolar affective disorders (BAD), reducing the frequency of manic episodes (PubMed, PubMed, PubMed). However, more modern lithium salts with a better safety and efficacy profile are known, for example, lithium ascorbate.
It has also been shown that lithium is effective in mitigating aggressive behavior in people with attention deficit hyperactivity disorder (ADHD) (PubMed).
An increased natural lithium content in drinking water may reduce the frequency of suicides (PubMed). Partly this may be explained by the fact that lithium increases the synthesis and release of serotonin (it also reduces the level of norepinephrine) (PubMed).
Lithium increases the level of CCK in the brain, and this is part of the mechanism by which lithium prevents mania in bipolar disorder.
Lithium fights depression
The prescription of lithium is one of the most studied approaches in the treatment of depression resistant to standard therapy (PubMed).
Lithium increases postsynaptic sensitivity to serotonin through the 5-HT1A receptor, which partly explains its antidepressant activity. (PubMed)
Lithium also increases the level of BDNF, which helps with depression.
The role of lithium in the body
Your brain will function at max power with the help of Normotim
Your brain will function at max power with the help of Normotim