Yas said:
I'll read more about it and decide if it is something I would like to add my supplements.
I had been taking it for a while along with the MTHFR protocol, and it seemed to make a large difference when taken along side the B12. But I'll get to that.
Trying to untangle the relation to the thyroid seems a rather complex subject, but then 99% of the research seems to be based on high dose Lithium Chloride.
So a few things of note:
https://www.psychologytoday.com/blog/evolutionary-psychiatry/201201/could-you-have-lithium-deficiency
Despite the fame and long term, widespread use, no one really knew what lithium actually did. In medical school, I was taught that it had some effect on the regulation of second messenger systems within the neurons (1 (link is external)). Meaning, like every other psychotropic medication, it changes something about the communication in the brain, for good or ill.
A recent article (link is external) sheds some light on lithium's actual mechanism of action. In bipolar disorder, there has been shown to be an increase in inflammatory markers of the frontal cortex of the brain. There is also an increase in the enzymes that regulate the expression of the omega 6 fatty acid derived arachidonic acid. When rats are given lithium-laced or lithium-free food for 6 weeks, the lithium-dosed rats had less arachidonic acid, and more 17-OH DHA, which is an anti-inflammatory metabolite of the fish oil, DHA. 17-OH DHA seems to inhibit all sorts of inflammatory proteins in the brain.
Interestingly enough, lithium has been shown to be the only effective drug (at least to slow the progression down) in another inflammatory, progressive, and invariably fatal neurotoxic disease, ALS, which is also known as Lou Gerhig's disease (2 (link is external)), and lithium is being studied in HIV, dementia and Alzheimer's disease.
(Full paper here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2853431/ )
The 17-OH DHA (17-hydroxy-DHA, known as part of a class called resolvins) thread is an interesting one to pull on (aspirin apparently has the same effect - lithium being the better option osit).
http://lipidlibrary.aocs.org/Primer/content.cfm?ItemNumber=39317
It is now well established that administration of lipoxins, resolvins and protectins in vivo and in vitro in animal models can aid the process of recovery from inflammation without compromising host defences by causing immune suppression. It is evident that such compounds and their metabolism have considerable potential for therapeutic intervention in acute inflammation or chronic inflammatory disease, and they have been tested in a wide range of experimental models, including peritonitis, periodontitis, colitis, arthritis, dry eye, inflammatory pain, cardiovascular disease, asthma and even cancer. A phase III clinical trial of a RvE1 analogue against dry eye syndrome is underway. They also appear to be beneficial towards attack by bacteria, fungi, viruses and parasites, including such debilitating diseases as influenza and malaria. From a nutritional or health standpoint, it has been suggested that dietary supplements of the precursor omega-3 fatty acids, taken together with aspirin, may ameliorate the clinical symptoms of many inflammatory disorders by regulating the time course of resolution via the production of resolvins and protectins
This is the best overview I could find on lithium and the thyroid (based on the High dose lithium therapy)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1584230/
Results
The main findings from this review included: a) lithium definitely affects thyroid function as repeatedly shown by studies on cell cultures, experimental animals, volunteers, and patients; b) inhibition of thyroid hormone release is the critical mechanism in the development of hypothyroidism, goitre, and, perhaps, changes in the texture of the gland which are detected by ultrasonic scanning; c) compensatory mechanisms operate and prevent the development of hypothyroidism in the majority of patients; d) when additional risk factors are present, either environmental (such as iodine deficiency) or intrinsic (immunogenetic background), compensatory potential may be reduced and clinically relevant consequences may derive; e) hypothyroidism may develop in particular during the first years of lithium treatment, in middle-aged women, and in the presence of thyroid autoimmunity; f) thyroid autoimmunity is found in excess among patients suffering from affective disorders, irrespective of lithium exposure; g) in patients who have been on lithium for several years, the outcome of hypothyroidism, goitre, and thyroid autoimmunity do not much differ from those observed in the general population; h) hyperthyroidism and thyroid cancer are observed rarely during lithium treatment.
It should be noted that lithium and iodine compete for absorption in the intestines, so one wonders if the high dose lithium is causing iodine deficiency?
Lithium may be helpful for those who have problems breaking down/producing dopamine, as well as MTHFR problems and/or low B12 levels.
https://chronicdiseaserecovery.wordpress.com/2013/04/30/mthfr-and-lithium/
[..]Why is this important?
There is a connection between lithium and COMT, bipolar disorder and SZ. It is possible that imbalances in the COMT pathway need regulation by low dose lithium in order to get the kind of levels of COMT that you need for proper dopamine processing. When the levels of COMT in the brains of patients with SZ and bipolar disorder were compared with normal controls, the levels of COMT in those affected were lower than in controls. Lithium seems to increase the activity of COMT.
Lithium induces both B12 and folate transport into the cells thus driving the long route. This can happen with just the standing levels of B12 and folate without additional supplementation. B12 binding capacity as well as white count will go up in the presence of lithium. B12 deficiency is known to lead to degeneration of the central nervous system and psychiatric disturbances such as affective disorders and manic psychosis. Violent criminals as a group have the lowest levels of lithium in hair. There is not only a relationship between lithium, B12 and folate, but also between low lithium and anxiety, aggression, bipolar disorder and SZ.
In studies with patients known to be low in B12, the following psychiatric manifestations were reported to remit with vitamin B12 therapy: confusion , hallucinations, delusions, disorientation, confabulation, anxiety, restlessness, fatigue, depression, irritability, sleepiness, psychosis, stupor, slowed ability to process thoughts, decreased memory, acute delirium, mania, apathy, lack of energy, weakness, violent behavior, flight of ideas, negativism and acute paranoid states. These symptoms may occur in the absence of hematological evidence of B12 deficiency.
So certain behavioral problems, depression and learning disability could be caused or aggravated by low nutritional intake of lithium coupled with marginal deficiencies of B12 and folic acid, the transport of this latter vitamin also being modulated by lithium.
Lithium has a direct effect on nor epinephrine pathways. Lithium indirectly inhibits thioredoxin reductase. There is an inverse relationship between thioredoxin reductase and COMT, so it may be that lithium increases COMT leading to decreased nor-epinephrine.
Other positives of lithium:
Lithium stimulates tyrosine hydroxylase which is a secondary pathway to dopamine production.
Lithium has neuroprotective actions against a variety of insults. It increases GABA activity. It helps to protect against glutamate excitotoxicity by inhibiting the NMDA receptor induced calcium influx.
Lithium plays a role with sodium and potassium balance.
Lithium may help to repair neurons and reduce some of the trauma after injury.
It induces enhancement of mitochondrial oxidative phosphorylation in human brain tissue.
It plays a role with respect to myelination by enhancing the expression of brain derived neurotrophic factor.
And finally, lithium has been shown to be protective in Alzheimer’s disease.
Lithium and thyroid.
Lithium has an impact on thyroid hormone production because it competes with iodine for uptake from the GI tract.[..]
The only source I've managed to find of the link between lithium and increased B12 transport into cells is here: http://www.scribd.com/doc/125176090/Lithium-Induced-Perturbations-of-Vitamin-B12-Folic-Acid-and-DNA-Metabolism (Lithium Induced Perturbations of Vitamin B12, Folic Acid, and DNA Metabolism)
I can't copy/paste anything from it though, but Dr Yasko has highlighted portions of the text.
The most relevant bits being:
- Lithium was associated with elevated levels of serum unsaturated B12 binding capacity
- In the cell model tested, lithium increased uptake of B12 and folate
- Psychiatric patients taking lithium had an average increase in their serum B12 levels over controls not ingesting lithium
So someone could have good serum B12 levels, and not be able to get any into their cells (where it's needed) without lithium. For reference, here are what low B12 symptoms look like:
What are symptoms of low B12?
Symptoms can vary from person to person, and you can have some, but not all, and yours can be different from someone else’s. But they can include:
• numbness/tingling/pins and needles in your hands, arms, legs or feet
• leg pain
• difficulty walking with balance
• weakness in muscles
• tremors
• poor reflexes
• tongue soreness
• pale in complexion
• headaches
• feeling of dizziness
• vision problems (blurriness, spots in eyes, etc)
• breathlessness
• memory problems/forgetfulness (giving you a wrong diagnosis of dementia or Alzheimers!)
• irritability
• confusion or brain fog
• fatigue
• depression
• difficulty getting pregnant
From a personal perspective I got a bunch of these from taking lithium orotate without B12. Standard B12 supplements make those symptoms worse, and the only thing that reversed them was the active form of B12 - dibencozide.
Further reading on MTHFR and lithium here: http://www.scribd.com/doc/298739352/Chapter-13-14-Excerpt-from-Feel-Good-Nutrigenomics-Your-Roadmap-to-Health