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.

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@plus
As for timing of the dosage, there is a recent editorial by Tomas Hajek.
https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/lithium-orotate-distinct-compound-or-simply-li-after-administration/52E4CFC3727F480DF94FBE4E93BFA7BD
He states that because the human stomach is much more acidic than a mouse stomach, LiO would be separated in the human stomach and so the special properties of LiO would not reach the brain, only the Lithium ion. It would be no different than taking LiC. He does say that taking it *after a meal* would probably let more LiO travel to the brain.
Of course, more experiments are needed.

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@nb14
I see it as a low-cost, no-risk adjustment. If there’s any chance that a less acidic gastric environment preserves more intact LiO and allows the orotate carrier to do whatever it does in terms of amyloid evasion, taking it after a meal is worth doing. I already take it in the morning because i take Magnesium L-Threonate in the evening and those two compete. So I just need to be sure i eat my yogurt first before my normal morning meds.

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Well, whether logical or not,
I am gonna do my collagen & warm almond milk shooter, have a double espresso, eat yogurt, then take my meds - which always include Pepcid

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