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Have MCI, sharing new intel re Lithium Orotate
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-doseThe 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.”
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I have read that with interest. The neuropsychologist told me that my cognitive impairment as revealed in her 3 hour test batteries was barely “mild” impairment . And yet my blood markers as described in ATN test and newer pTau217 test suggests a large amount of amyloid and Tau proteins on board and suggest a diagnostic indication of Alzheimer’s.
I am going off LiO until we see the dosage Yankner et al target for their trial. Not because I think 10mg is dangerous but because i am experiencing sleep disruption and want to try and identify what may be contributing to it. I need to have my slow wave non-REM sleep reach at least 15% of total sleep for the Glymphatic process clean up any debris overnight.
Anyone have suggestions about taking Lithium Orotate (aka LiO) with, during, or just after meals? A 1975 NIH study (PMID:1096537) says, "... Lithium should therefore preferably be administered after meals. ..." They found that helped the few subjects who had mild gastric discomfort taking LiO on an empty stomach, and aided absorption in some subjects and situations.
Has anyone here received specific instructions, or have related experiences to share?
@plus "... we've backed off to 5.8mg - 1mg Pure... brand + 4.8mg of the other. After a day or two of the 21mg combo my wife seemed a bit worse ..."
Followup: The 5.8mg didn't help, and in fact she kept getting worse. Now suspicious of the 4.8mg brand, I switched her to the 1mg "Pure..." brand and 5mg KAL 2xDay. Immediate slight and now continuing improvement. Hoping even more that our upcoming new neurologist with more Alzheimer's experience will prescribe LiO, so we might actually know what's in it.
@plus I realize we are all wandering through the desert of resources hoping to find a productive path. But now that you and your LO seem to be in a positive place, I strongly encourage you to hold steady on dosage.
I cannot imagine that (a) there is a prescription that could be written for LiO. As far as I am aware the OTC mineral supplement Form is all there is. My guess is that best case you may get a ”let me know how that works out” from your Doc- and More likely you will get “let’s Wait For human trials” - which are seeking philanthropic funding since no pharmaceutical entity can monetize it - so-big pharma is out. Plus they are already in the game with the two approved drugs in trial now.
I encourage you to dive into understanding how LiO affects available lithium getting to the brain by avoiding sequestration within the amyloid plaques. And then how the trash amyloid plaque and tau must be removed - flushed out - and that Glymphatic process only occurs during slow wave non-REM sleep.
So there are a lot of moving parts in this process. LiO seems to facilitate some but not all of them. So i personally am working daily to achieve 12-15% slow wave sleep (SWS) that is not REM by using an apple watch and an app that is pretty consistent in how it classifies sleep stages.
My point is rather than trying to find the optimal dosage early, find one that isn't problematic - recognizing that less is more - and work on the other requisites to rid the brain of amyloid and tau proteins. It is all necessary to produce results.
@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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1 Reaction@nb14 "... *after a meal* would probably let more LiO travel to the brain."
Thanks! Today's our first trial of that, and we're slightly worse w/in daily variation so we'll continue and monitor for a few days. We've also been on morning & night Famotidine for reflux for years, and today we stopped taking it with the LiO so maybe it had been helping.
Plenty of variables to consider!
@pb50 "...encourage you to hold steady on dosage." Thanks for that and all your contributions on this topic - including starting it!
"...amyloid plaque and tau must be removed - flushed out - and that Glymphatic process..." Yes! I keep thinking each day will be the one with enough easing of chaos to delve into that whole topic further. Maybe tomorrow...
"...a lot of moving parts in this process." Absolutely!! "...working daily to achieve 12-15% slow wave sleep..." Hope you can scrape together the cash for the ring to help with that, and report back on if/how it helps.
"...rather than trying to find the optimal dosage early, find one that isn't problematic" None have been, so far. Sometimes high dose has worked notably better, other times (eg. 4.8mg) worse. This is one of the reasons I'm favoring high dose at this few weeks into the LiO. As for "...less is more" I'm not sure that's the case, given we're not modified mice w/all the other biological differences - plus the unregulated nature of OTC supplements. My impression is you're saying too much LiO if effective, could poison the brain with uncollected debris. My hope is that our efforts to reduce nocturia while increasing daytime hydration can help. Sleep monitoring probably wouldn't hurt, but we already know better sleep is probably good and we're working at it.
Again, thank you for your kind and helpful contributions here, taking the time to offer your informed perspective, and your patience with my slow experimental learning curve.
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1 Reaction@pb50
You sound discouraged.
You should be encouraged.
My understanding is that the ptau-217 tests show results decades before the symptoms occur. It, and amyloid beta, build very slowly. The best time to address it is before you have symptoms.
Shielding the Brain From Alzheimer’s | Psychology Today
https://www.psychologytoday.com/us/blog/the-breakthrough-depression-solution/202602/shielding-the-brain-from-alzheimers
The author has written several books on lithium and recommends lithium for his patients and in paid seminars. He is highly biased, but maybe his bias is justified.
My overly simplistic understanding of the brain cleaning process is that microglia, which need lithium, bag up the trash (autophagy) and the glymphatic system takes it out. So both are needed.
@nb14 many thanks for that encouragement. I am accepting that regardless of measurement method, i have a wad of amyloid parked on my brain, that it didnt get there quickly and won’t evaporate quickly. So my beat effort will be to try and maximize the trash removal by learning how to increase my slow wave, mon-REM sleep. So that is my mission. I will of course maintain my 10-12mg of lithium/day…
Thanks to the helpful acid/LiO post by @pb50 I'm now keen to take our LiO at lowest stomach acid level, so I found this on NIH via Gemini summary:
Stomach acid follows a natural circadian rhythm, meaning its levels fluctuate in predictable patterns every 24 hours. Acid levels are typically lowest in the morning, gradually rise throughout the day, and peak in the late evening and middle of the night.The normal pH of the human stomach is extremely acidic, ranging between 1.5 and 3.5. Here is how the levels break down throughout the day:
Morning (Lowest): Upon waking, acid levels are at their lowest because the body rests and doesn't eat overnight.
Daytime (Active): When you eat, the hormone gastrin triggers a significant release of hydrochloric acid to break down food, especially proteins. In between meals, the pH remains moderately low to maintain a sterile gut environment.Late
Evening & Night (Highest): Due to circadian rhythms, un-stimulated acid production surges late in the day and peaks in the middle of the night.
So my new strategy:
Famotadine (Pepsid) upon waking to reduce acid level, and take the day's LiO dose. After our MD's original prescription for 30 minutes after Famotadine: begin light breakfast.
Comments and suggestions welcome as always. 🙂