A new paper from Harvard Medical School has rekindled scientific interest in one of the simplest elements in the universe: lithium. Once best known as a frontline treatment for bipolar disorder, lithium is now being studied for a very different role — potentially preventing, or even reversing, the brain changes associated with Alzheimer’s disease.
Harvard’s Bruce Yankner and his colleagues examined 27 common and trace metals in the brains and blood of people with normal cognition, mild cognitive impairment (MCI), and Alzheimer’s disease. Only one element stood out: lithium. The researchers found significantly lower lithium levels in the brains of people with MCI and Alzheimer’s, and, strikingly, the lithium that remained was often sequestered inside amyloid plaques — the sticky protein clumps that characterize the disease.
The Plaque “Trap” Problem
This discovery highlights a vicious cycle: lithium normally inhibits an enzyme called GSK3β, which promotes both amyloid plaques and tau tangles, the two pathological hallmarks of Alzheimer’s. But as plaques accumulate, they appear to “trap” lithium, reducing its availability and weakening the brain’s defenses. Less lithium means more plaques and tangles, which in turn further deplete lithium — a self-perpetuating downward spiral.
To test whether lithium depletion actively drives disease, Harvard researchers turned to Alzheimer’s-model mice — genetically engineered animals that develop plaques, tangles, and memory decline much like human patients. Mice on a lithium-deficient diet developed earlier and more severe Alzheimer’s-like pathology. They had more plaques, more tau tangles, increased inflammation, and accelerated memory decline compared to controls. In short, lithium deficiency appeared to mimic and worsen the disease.
Why Lithium Orotate?
The team then compared 16 different lithium salts to see which form could best evade plaque sequestration and remain bioavailable in the brain. One salt — lithium orotate — stood out. When the afflicted mice were treated with lithium orotate, the results were remarkable. Not only did the compound prevent further plaque and tangle formation, it even reversed existing pathology. Memory performance rebounded to near-normal levels.
By contrast, lithium carbonate, the prescription form used in psychiatry, failed to produce these effects. It appeared to be hoovered up by plaques, leaving too little lithium to nourish neurons.
From the Lab to YouTube
Nick Norwitz, an Oxford- and Harvard-trained Ph.D. and physician-in-training, recently broke down the Harvard findings in a YouTube video that has already attracted wide attention. In the 10-minute presentation, Norwitz explained how lithium, long known as a psychiatric drug, may also function as a “neuroprotective nutrient” at extremely low doses. He noted epidemiological studies showing that communities with higher natural lithium in drinking water often have lower dementia rates.
What captured the imagination of many viewers was his personal decision: Norwitz announced he has started taking 5 milligrams of lithium orotate daily, and has recommended the same to his parents. He framed it as a safe middle ground — far below the 600-plus milligrams of lithium carbonate used for bipolar disorder, but above trivial dietary exposure. For him, the motivation is especially personal: he carries two copies of the APOE-ε4 gene, which increases Alzheimer’s risk fifteenfold.
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Anecdotes and Caution
Not everyone’s experience has been positive. In the comment section beneath Norwitz’s video, one viewer wrote that taking 5 mg of lithium orotate initially boosted mood, but within two weeks produced anhedonia, or loss of pleasure. That individual later restarted supplementation at just 1 mg per day, reporting better results.
These anecdotes underline an important reality: lithium is biologically potent even at microdoses, and individual tolerance may vary. Unlike vitamin D or zinc, lithium has no official Recommended Dietary Allowance. In fact, there are no USDA, FDA, CDC, or NIH guidelines on its use for Alzheimer’s prevention, nor any approved medical indications outside of psychiatric disorders.
Where the Science Stands
It is crucial to note that Harvard’s dramatic results were in mice, not people. Human data are much more limited. A Brazilian clinical trial in 2019 tested very low doses of lithium carbonate (providing about 300 micrograms of elemental lithium daily) in patients with mild cognitive impairment. That study suggested slower cognitive decline over 15 months, but it did not demonstrate reversal of disease, nor did it use lithium orotate.
Today, no large human trials have confirmed that lithium orotate is safe or effective for Alzheimer’s. Supplement brands vary in quality and labeling, and lithium orotate is sold in the United States as a dietary supplement, not as a regulated pharmaceutical.
The Road Ahead
The excitement around Harvard’s study and Norwitz’s commentary reflects a growing appetite for novel approaches to a disease with few effective treatments. But the gap between animal studies and human application is wide. Experts caution that while microdose lithium looks promising, it remains theoretical until rigorously tested in clinical trials.
If lithium orotate proves safe and effective in humans, it could represent a paradigm shift: an inexpensive, low-dose intervention that restores brain resilience rather than simply slowing decline. Until then, it remains a compelling hypothesis — one that has sparked both scientific curiosity and public debate.
Dave Soulia | FYIVT
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