dr yasko has a webinar on it here:
http://www.dramyyasko.com/resources/webisodes/lithium-connection-webisode/
The other ones are good, but as often, the audio can be poor.
Lithium orotate, methylation and thyroid
- Thread starter Beyond
- Start date
http://www.dramyyasko.com/resources/webisodes/lithium-connection-webisode/
The other ones are good, but as often, the audio can be poor.
triffid113
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Thanks. I didn't know that. I am supposed to take lithium according to Yasko but I don't. My hair analysis says I'm not low yet so I don't plan to worry about it until then. had o motivation to try it as the only thing I knew it to be needed for is bipolar.
Little Bluestem
All Good Things Must Come to an End
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The lithium used for bipolar is a different form available by prescription only.
juniemarie
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L.O. turns me into a drugged zombie I wonder if my reaction is tied into something to do with my thyroid
juniemarie. Did you recover when you stopped taking it? I get worried about thyroid type reactions and not recovering.
stridor
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I used to take 1000 mg of lithium a day for bipolar and now take 10 mg/day. Lithium orotate is often found in preparations that contain 5 mg per pill. I suspect that there is well water in parts of North America that may contain that much. I looked before and I could not find anything that suggested the doses we take here will lead to problems. Any studies demonstrating problems deal with doses like I took for Bipolar.
Many people here will have accumulated enough heavy metal to have disrupted mineral transport and will have low lithium.
Lithium is one of the element/medications that has been shown to be neuroprotective and even more than this, it increases BDNF = brain-derived-neurotrophic factor = increase number and connections between neurons. I have no clue whether I have low lithium but I do know that I am low in glutathione and that I need all the neuroprotection that I can get. That said, I shut my thyroid off with meds and therefore have nothing on the line.
FWIW - T4 to T3 conversion problems and high reverse T3 are common with mercury toxicity.
Many people here will have accumulated enough heavy metal to have disrupted mineral transport and will have low lithium.
Lithium is one of the element/medications that has been shown to be neuroprotective and even more than this, it increases BDNF = brain-derived-neurotrophic factor = increase number and connections between neurons. I have no clue whether I have low lithium but I do know that I am low in glutathione and that I need all the neuroprotection that I can get. That said, I shut my thyroid off with meds and therefore have nothing on the line.
FWIW - T4 to T3 conversion problems and high reverse T3 are common with mercury toxicity.
Little Bluestem
All Good Things Must Come to an End
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Was the 1000 mg of lithium you took lithium orotate or another form?
stridor
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This is one of the better reviews on this topic. brad
MTHFR+ and Lithium
MTHFR+ and Lithium
For a comprehensive review of this subject, click on this link:
http://www.dramyyasko.com/resources/webisodes/lithium-connection-webisode/
These are your Cliff Notes:
Lithium has been known for years to be useful for bipolar disorder. Despite all that is known about lithium and its impact on biochemical pathways, no one has defined the mechanism by which lithium has its impact on bipolar disorder. It is likely to be an effect on multiple pathways. There are a number of enzymes in the body that are known to be impacted and inhibited by lithium.
Lithium comes together with methylation at COMT, the enzyme catechol-o-methyl-transferase. COMT breaks down dopamine and nor epinephrine. Dopamine is a critical neurotransmitter for motivation, focus and attention, among other functions. Nor epinephrine is involved with modulating the impact of stressors. Both are central to nervous system function.
COMT uses methyl groups to accomplish this deactivation. COMT - - breaks down dopamine at a steady even rate and uses significant numbers of methyl groups. COMT ++ breaks down these neurotransmitters more slowly and uses fewer methyl groups.
We know that giving a patient more methyl groups than they can use produces symptoms. They get mood swings and start to look bipolar. Children will become hyperactive, stimmy or get other symptoms when they are put on methyl B12 if it is too much for them.
Lithium may inhibit the production of a central enzyme in the sulfur system, thioredoxin reductase. The detail and complexity surrounding this issue is explained in the presentation you can access at Dr Amy’s webinar link posted above.
It appears that lithium may be increasing the production of COMT and inhibiting the production of thioredoxin reductase. COMT and thioredoxin reductase have genes that are on opposite strands of chromosome 22. Their promoter regions overlap which implies some mutual regulation. Having a shared promoter means that at any given time you can make either the COMT transcript or you can make thioredoxin, but you cannot make both.
This circumstance is analogous to a roadway being closed down to one lane. The line of traffic can move only in one direction at a time. One lane is stopped while the other one can go. A shared promoter generates the same situation in gene transcription. You can make either COMT or thioredoxin , but not both at the same time.
Dr Amy emphasizes that this is her hypothesis, it is not scientific fact. But based on this hypothesis, she started looking carefully at lithium levels and opened up a whole new area in her program. Using this hypothesis makes a difference for patients. She noticed that certain SNPs are associated with excess lithium excretion. They are MTR+, SHMT+, and MTHFR C677T +. An out of balance methylation cycle will also cause increased lithium excretion.
Dr Amy suggests only low dose lithium support because lithium also inhibits ribonucleotide reductase. Ribonucleotide reductase takes ribonucleotides, ie, RNAs, and breaks them down into building blocks for DNA and other RNAs. So one of the toxic impacts of high dose lithium is its impact on RNA breakdown. You need to support with DNA building blocks, for example using Nucleotide Immune Support. The RNA formulas also supply these building blocks.
Lithium is an essential trace element. You must get it from your diet. The average intake of lithium from the diet should be up to 3100 mcg, or 3.1 mg. Dr Amy wants to supplement with very low level lithium, around 2.5 mg. She wants to do it consistently and she does not want to get near biologic doses. What it takes to actually increase a patient’s lithium levels can be significantly more, especially with sicker patients.
You have to keep watching the lithium and cobalt levels on a UEE. High lithium levels on a UEE may indicate excess excretion, but when cobalt, the oxidized form of B12, starts to show, you know the lithium level is coming into balance and you can start to push the long route instead of just the short route as I discussed last week. The replay link to my discussion last week will be available on my blog at http://chronicdiseaserecovery.wordpress.com/
if it is not there already. All of the replays will ultimately be cataloged there.
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. We suggest getting around this problem by painting a 2’’ square of iodine on your skin and watching how long it takes for your body to absorb it.
If it is gone in 1 hour, you need iodine. Keep painting it on daily for transdermal supplementation.
If it stays on for 24 hours, you have enough iodine in your system. You can extrapolate the times between those two limits. Given all that has been said about the positives of using lithium if you are low in it, it is best not to just toss it aside because someone told you it was bad for thyroid. You may need both lithium and iodine. You can get both in the way just described.
http://www.dramyyasko.com/resources/webisodes/lithium-connection-webisode/
These are your Cliff Notes:
Lithium has been known for years to be useful for bipolar disorder. Despite all that is known about lithium and its impact on biochemical pathways, no one has defined the mechanism by which lithium has its impact on bipolar disorder. It is likely to be an effect on multiple pathways. There are a number of enzymes in the body that are known to be impacted and inhibited by lithium.
Lithium comes together with methylation at COMT, the enzyme catechol-o-methyl-transferase. COMT breaks down dopamine and nor epinephrine. Dopamine is a critical neurotransmitter for motivation, focus and attention, among other functions. Nor epinephrine is involved with modulating the impact of stressors. Both are central to nervous system function.
COMT uses methyl groups to accomplish this deactivation. COMT - - breaks down dopamine at a steady even rate and uses significant numbers of methyl groups. COMT ++ breaks down these neurotransmitters more slowly and uses fewer methyl groups.
We know that giving a patient more methyl groups than they can use produces symptoms. They get mood swings and start to look bipolar. Children will become hyperactive, stimmy or get other symptoms when they are put on methyl B12 if it is too much for them.
Lithium may inhibit the production of a central enzyme in the sulfur system, thioredoxin reductase. The detail and complexity surrounding this issue is explained in the presentation you can access at Dr Amy’s webinar link posted above.
It appears that lithium may be increasing the production of COMT and inhibiting the production of thioredoxin reductase. COMT and thioredoxin reductase have genes that are on opposite strands of chromosome 22. Their promoter regions overlap which implies some mutual regulation. Having a shared promoter means that at any given time you can make either the COMT transcript or you can make thioredoxin, but you cannot make both.
This circumstance is analogous to a roadway being closed down to one lane. The line of traffic can move only in one direction at a time. One lane is stopped while the other one can go. A shared promoter generates the same situation in gene transcription. You can make either COMT or thioredoxin , but not both at the same time.
Dr Amy emphasizes that this is her hypothesis, it is not scientific fact. But based on this hypothesis, she started looking carefully at lithium levels and opened up a whole new area in her program. Using this hypothesis makes a difference for patients. She noticed that certain SNPs are associated with excess lithium excretion. They are MTR+, SHMT+, and MTHFR C677T +. An out of balance methylation cycle will also cause increased lithium excretion.
Dr Amy suggests only low dose lithium support because lithium also inhibits ribonucleotide reductase. Ribonucleotide reductase takes ribonucleotides, ie, RNAs, and breaks them down into building blocks for DNA and other RNAs. So one of the toxic impacts of high dose lithium is its impact on RNA breakdown. You need to support with DNA building blocks, for example using Nucleotide Immune Support. The RNA formulas also supply these building blocks.
Lithium is an essential trace element. You must get it from your diet. The average intake of lithium from the diet should be up to 3100 mcg, or 3.1 mg. Dr Amy wants to supplement with very low level lithium, around 2.5 mg. She wants to do it consistently and she does not want to get near biologic doses. What it takes to actually increase a patient’s lithium levels can be significantly more, especially with sicker patients.
You have to keep watching the lithium and cobalt levels on a UEE. High lithium levels on a UEE may indicate excess excretion, but when cobalt, the oxidized form of B12, starts to show, you know the lithium level is coming into balance and you can start to push the long route instead of just the short route as I discussed last week. The replay link to my discussion last week will be available on my blog at http://chronicdiseaserecovery.wordpress.com/
if it is not there already. All of the replays will ultimately be cataloged there.
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. We suggest getting around this problem by painting a 2’’ square of iodine on your skin and watching how long it takes for your body to absorb it.
If it is gone in 1 hour, you need iodine. Keep painting it on daily for transdermal supplementation.
If it stays on for 24 hours, you have enough iodine in your system. You can extrapolate the times between those two limits. Given all that has been said about the positives of using lithium if you are low in it, it is best not to just toss it aside because someone told you it was bad for thyroid. You may need both lithium and iodine. You can get both in the way just described.
Beyond
Juice Me Up, Scotty!!!
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I want to add that taking orally liquid Iodine blasts mosts of intestinal pathogens so is something to consider. I plan to experiment with Lugol´s in the future.
I've got lithium orotate on order. I take between 10-45mg of methyl b12 and the effect of it has decreased over time. I'll report if anything comes of trying LO out.
I painted the iodine onto the back of my hand. Does it disapear down to an iodine stain from being a blob or am I supposed to only paint on an amount that looks like an iodine stain and then see if it disapears to invisible. I painted a blob on and then smeared it out into a few smaller blobs. Not looking forward to trying to hold my hand right side up and not let the iodine stain anything else for more than an hour.
I painted the iodine onto the back of my hand. Does it disapear down to an iodine stain from being a blob or am I supposed to only paint on an amount that looks like an iodine stain and then see if it disapears to invisible. I painted a blob on and then smeared it out into a few smaller blobs. Not looking forward to trying to hold my hand right side up and not let the iodine stain anything else for more than an hour.
- Messages
- 79
l engle what brank of mthylb12 you use?for so high dose?enzy?
Hi,
Here's what's interesting: I was needing very high doses of either AOR or Enzymatic therapy Mb12 to see any benefit to cognitive functioning. This was in the first year of taking methylb12. After the first year, methylb12 stopped working for any of my brain symptoms though continued to help with physical energy somewhat.
I started lithium orotate a few days ago and am now getting a cognitive benefit from just 1mg of enzymatic therapy's methyl b12. It's early to start recommending this course of action to anyone else but it's what I'm currently experiencing. I'll be delighted if this allows me to take a much smaller amount of methyl b12, as it is expensive and inconvenient to take large amounts.
For the lithium orotate I took 5mg for the first couple of days but felt that it had a negative thyroid effect (uncomfortable throat sensations, lowered body temperature). I reduced to 2.5 mg, which lessened the throat sensations and didn't lower my body temperature. Just today I tried lowering to around 1mg of lithium orotate, to see if I could get the cognitive benefits without any thyroid effects.
For me the methyl b12 and lithium orotate don't seem to work very well on their own but taking the lithium orotate just before starting to dissolve the methylb12 enables them to work together.
I get an improvement in brain fog, a minor improvement in mental and physical stamina, and an improved mood from this combination. I hope the thyroid effects will not be too detrimental as I don't want to stop taking these supplements.
- Messages
- 79
thanks for the answer man.i will try lithium too.but i will take lithium at night for insomnia and methylb12 in morning with methylfolate.and i will see what happens.
for thyroid try iodoral(slowly go up) with selenium.and a bit zinc too
for thyroid try iodoral(slowly go up) with selenium.and a bit zinc too
if you have autoimmune thyroid issues then iodine can be problematic. Just something to watch out for.
- Messages
- 79
so 1mg was enough with b12?
With the lithium orotate for me, yes. Without it, no, not nearly enough. It's different for every person. There's no etsablished amount of B12 needed by each individual, you have to try for yourself. And I haven't been taking lithium orotate long enough to know if the benefits will last, or if side effects will come up.
- Messages
- 79
sorry i meant lithium.1mg of lithium was enough for b12 to get absorbed and see changes?or you answered that?
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@Dreambirdie
What happened when you took iodine? How much did you take, for how long, what was the reaction and what happened when you stopped taking it? Thanks
Dreambirdie
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Sorry, but I am not in the mood to go over all that again. I posted about it on this thread back in 2010. You can read it here: http://forums.phoenixrising.me/index.php?threads/in-depths-of-iodine-despair.2150/
Weirdly, @Dreambirdie, I have the same averse reactions to Iodine and HC (never again!) but lithium orotate has been a very friendly thing in the past. I just started taking it again two days ago, so we'll see how it goes.
I'm distressed to read about the thyroid/lithium bit though, bc I already had low thyroid for years, and then a recent series of xrays thrashed it. My morning oral temp is now 95.2!! Brr!
I don't remember the differences in lithium forms, just that orotate is supposed to be more gentle and beneficial than whatever is the one they give in Rx for bipolar people. I almost wonder of *that* is the one that messes with the thyroid? And maybe the orotate one doesn't? Just thinking aloud here I have absolutely no idea.