Have MCI, sharing new intel re Lithium Orotate

Posted by pb50 @pb50, Dec 31, 2025

I have discussed previously that I have mild cognitive dysfunction and after two rounds of neuropsych testing over two years and Lab & imaging testing confirming my clinical profile, I am taking Lithium Orotate as a nutritional supplement. But I consume professional intel on studies religiously. Like this one.

https://www.psychiatrictimes.com/view/lecanemab-or-lithium-compare-benefits-risks-and-dose

The key question that stood out to me which the physician author (Dr Phelps) asks in his review of studies is below. I highly emcourage reading this. You have to follow some links and jump back and forth a bit but make the effort. For those of you fond of calculating elemental lithium there is a section on calculating equivalent dosing to the mice study.

“Brain lithium prevents amyloid plaque formation and phosphorylation of tau proteins. In the process of AD dementia, lithium is sequestered in plaques, creating a positive feedback loop: more plaque, less lithium, leading to more plaque, and so on. Giving lithium orotate to young adult mice almost completely prevented plaque formation and tau phosphorylation. Starting lithium orotate after plaques and phosphorylated tau have already formed almost completely reversed the expected cognitive impairment. Lithium carbonate is far less effective. If all this were true in humans, lithium orotate would be an obvious treatment both to prevent AD dementia and to treat it once detected.

Of course, skeptics’ first response has been “these are mouse data.” Aron et al point out that lithium levels in human and mouse brains are comparable, supporting the relevance of mouse models for studying the biological effects of lithium. Skeptics, including a prominent neurologist following a national presentation on AD treatment, have said that we should wait for a randomized trial of lithium orotate in humans (personal communication, August 2025). But the recent lithium carbonate randomized trial took 8 years to mount and complete. What shall we suggest to patients and families for the next 8 years?

A healthy lifestyle—including a Mediterranean-like diet, regular physical activity, and avoidance of smoking, excessive alcohol, social isolation, sleep disorders, and hearing loss—is an important means of preserving cognitive function in people at risk of developing dementia.

The subsequent article will compare lecanemab and lithium’s benefits, risks, and costs. With ApoE genotyping and the new pTau/amyloid blood test, patients and families need help now deciding between treatment alternatives.”

Interested in more discussions like this? Go to the Early Dementia & Mild Cognitive Impairment (MCI) Support Group.

pb50 | @pb50 | Aug 9 7:53pm

One more thing. Just to be clear, am I wrong that the study phenomena you describe in terms of amyloid sequestration of lithium and the way in which LiO eliminates that sequestration is absolutely wasn’t found on people - just mice to date.
…….your post….
The Harvard study, using human brain tissue, found that people with mild cognitive impairment had a large deficit of Li in their brain due to this sequestration. People with Alzheimer’s Disease had a much greater deficit. They found that Li from Lithium orotate (LiO) was sequestered much less. They proposed to replace the sequestered Li, from LiC, with Li from LiO, to maintain the same natural concentration of Li in the brain, homeostasis, and restore the brain’s natural functioning.

pb50 | @pb50 | Aug 9 8:17pm

This is my last comment on this. I am taking 5mg lithium from lithium orotate. So i am taking 5mg elemental lithium - maybe 20 times the mouse equivalent dose - as you would expect.
Good night.
Photo attached.

nb14 | @nb14 | Aug 10 8:34pm

In reply to @pb50 "One more thing. Just to be clear, am I wrong that the study phenomena you describe..." + (show)

@pb50
The Harvard team did amazing work using samples of human brain tissue.

In addition to finding the Li deficit in MCI and AD brain tissue, they were able to separate the brain tissue from the Amyloidβ plaque and do measurements:
“A highly significant concentration of Li in Aβ plaques was detected in every case of MCI and AD, which increased from MCI to AD.”

In the lab, they tested human amyloid-beta plaque samples in solutions of LiC and LiO to determine whether the Li would bind to the plaque.
“Notably, LiC exhibited higher binding affinity than LiO for both Aβ42 fibrils and oligomers across a broad Li concentration range.”

In both of these cases, they then confirmed these findings with tests in mice. Their tests in mice also identified the wide ranging negative effects of low lithium in the brain.

This led them to believe that LiO was a candidate for further testing in mice.

As I read it, the testing of human brain tissue samples found:
The problem: low lithium
The cause: lithium sequestration
A candidate solution: LiO

BTW, as they were doing their mouse tests of LiO, they often compared the brain RNA and proteins between the mice and humans at the same stage and found a very high consistency between them. They didn’t simply feed their mice LiO and then run them through a maze.

pb50 | @pb50 | Aug 11 2:49pm

thanks for clarifying for us!

plus | @plus | 3 days ago

In reply to @nb14 "Today is the 1 year anniversary of the publication of the Harvard study relating Alzheimer’s Disease..." + (show)

@nb14

Today is the 1 year anniversary of the publication of the Harvard study relating Alzheimer’s Disease and Lithium. I’ve taken the liberty of summarizing some of the “intel regarding lithium orotate” we have discussed in this group. Please feel free to add or correct.

1. We get about 1 mg of lithium(Li) from lithium carbonate(LiC) in our food and water every day. More in some geographical areas, less in others.

2. This supports our brain functioning for much of our life, perhaps 50 years, until, for some reason, amyloid beta plaque accumulates and sequesters the Li from LiC. [The first part is my own personal opinion]

3. The Harvard study, using human brain tissue, found that people with mild cognitive impairment had a large deficit of Li in their brain due to this sequestration. People with Alzheimer’s Disease had a much greater deficit. They found that Li from Lithium orotate (LiO) was sequestered much less. They proposed to replace the sequestered Li, from LiC, with Li from LiO, to maintain the same natural concentration of Li in the brain, homeostasis, and restore the brain’s natural functioning.

4. Lithium orotate is a nutritional supplement that has been on the market for 30 or 40 years. Common capsule sizes are 1, 5, 10 and 20 mg. It does not occur in nature.

5. These amounts are for the amount of Lithium, not the total weight of the LiO . Supplements typically give their “serving size” in terms of Lithium from lithium orotate. For instance, a 5 mg supplement provides 5 mg of lithium from about 130 mg of LiO.

6. Harvard tested the LiO replacement idea using normal mice and in mice genetically modified to get Alzheimer’s symptoms with excellent results. The results of the LiO research in mice, however, have *not* been validated in human clinical trials. These studies are being developed.

7. There are various calculations, using different assumptions, of the human equivalent of the LiO dose used in the Harvard mouse research. The ones I’ve seen for a 154 lb person are: .76 mg, .54 mg and .3 mg (Dr. Yankner of Harvard), all less than 1 mg. These do not account for possible differences between mice and humans.

8. The common nutritional supplement levels of LiO are too low to show up in the standard lithium blood test which is intended for people taking massive amounts of LiC for bipolar disorder.

9. At Harvard, they also did some experiments with 10 times and 100 times the basic lithium dosage with no toxicity observed in mice, but also no increase in effectiveness.

10. One scientist has suggested that LiO effectiveness could be affected by the high acid levels in the human stomach and it might be best to take it with food.

11. Some doctors recommend not taking LiO until clinical studies are complete in 6-8 years. Other doctors feel that the LiO supplement dosages are low enough that they should not cause a problem. Always consult your own doctor.

12. Dosages of LiO mentioned by online doctors — but to be clear not recommended or given as medical advice — include: 1-10 mg(for depression patients), 1-5 mg(“probably not a problem"), 5 mg.

Again, always consult your doctor.

Jump to this post

@nb14 "...I’ve taken the liberty of summarizing..."

Wow, Thank You! Having been mostly "offline" from this forum for much longer than realized, it was a very pleasant surprise to find your summary.

I'd just posted an AI Summary in a new Topic here, followed by several comments of my own. I'd gotten that AI summary after we chatted last night with close long-term friends who'd asked me to summarize. Today I wanted to know if I'd made grievous mistakes or missed important elements, thus the AI consultation.

After making that post in between taking care of issues in yet another busy (exciting, as I reported there) day, finding your summary I took the liberty of cross-posting it there. Apologies if you'd rather I hadn't (if so, maybe I could get it deleted).

Anyway, thank you! 😀

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