TL;DR
• Evidence layers: population signals + small human trials + a 2025 Harvard Nature study.
• Mechanisms: circadian/GSK-3β, autophagy, mitochondria, inflammation, plasticity.
• Dosing: microdose 0.06 mg Li; very low 0.3–0.5 mg Li; consistency > sheer dose.
• High “psychiatric” doses can work but bring more side effects.
• Author’s practice: 0.5 mg Li/day (lithium orotate). Educational, not medical advice.

This article is for educational purposes only and does not constitute medical advice. Lithium can interact with medications and is not appropriate for everyone. Do not start, stop, or change any treatment without talking to your healthcare professional.

***

If this helped you, collect this post on Paragraph to support my work. Thank you!

***

Lithium has been on my “supplement radar” for a few years now. I started paying attention when the first trials appeared, after it was suspected that it could slow—or even reverse—cognitive decline, and that a deficiency of it might be involved in neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

As with many health-related compounds, the evidence is sparse at the beginning: there are few studies or they’re not well designed; follow-up periods are very short; work is done only in animals or, in humans, with very small samples.

Even though social media, at the drop of a hat, fills up with people touting the use of such molecules—people need something to talk about online and, if possible, to grab attention—I believe the precautionary principle should always apply. Without serious evidence of efficacy and safety, no supplement should be recommended for use.

That’s one reason I’ve never written about lithium. But the situation has changed following a recent study (August 2025) from Harvard University on the relationship between lithium deficiency and neurodegenerative diseases.

It’s time to write about it and, as always, let’s start at the beginning.

Lithium (Li) is an alkali metal found in the Earth’s crust. In the human body it circulates as the Li⁺ ion, and we obtain it mainly from water and from foods that are grown (vegetables and grains).

It isn’t an essential nutrient, and therefore authorities have not established reference intakes. However, as we’ll see, because of its biological actions in the body, some researchers have proposed a minimum daily intake.

In very small amounts, lithium acts as a “fine-tuner” of several cellular functions and “touches” pathways that influence the brain, biological rhythms, cellular metabolism, and immunity. Let’s look at them.

1. Tunes the internal clock (sleep, daytime rhythms).
Lithium slows a switch-like protein, GSK-3β, that takes part in the biological clock. In doing so, it can modulate the amplitude and period of circadian rhythms—a basic piece for sleeping better and keeping the brain “in sync.” The evidence comes from cell studies and from people treated with lithium for bipolar disorder (study, study, study).

2. Activates the cell’s “clean-up and recycling” service (autophagy).
Cells need to recycle old or damaged parts. Lithium promotes autophagy through a specific route—reducing inositol/IP3—distinct from the well-known mTOR pathway. This helps clear accumulated proteins and aged mitochondria in various cell types, especially neurons, which aids in treating neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease (study, study, study).

3. Protects, improves, and increases mitochondria (energy).

In sum: cleaning/autophagy (fewer “traffic jams” inside the cell) + energy/mitochondria (more “battery” and more resilient neurons) + less inflammation (a less hostile environment for neurons) + better brain function (more neurons, better connected, with more memory and cognition) + a tuned biological clock (cells better synchronized for repair and performance) + fewer harmful proteins (fewer chemical signals that drive deterioration).

A whole “toolbox” that helps explain why lithium could protect the brain and help prevent or improve Alzheimer’s and Parkinson’s.

When it comes to Alzheimer’s, every clue counts. With lithium, there are two layers of evidence that together sketch an interesting story: what we observe in populations and what clinical trials in people show.

In 2017, in Denmark, after earlier evidence from cells and animals, researchers asked: Is a higher level of lithium in drinking water associated with a lower incidence of dementia? To answer this, they designed a study: over 18 years they analyzed data from about 75,000 patients with dementia and 700,000 healthy controls, estimating their lithium exposure based on the amount present in the water of their home municipality.

Result: areas with more natural lithium in drinking water tended to register fewer new cases over time.

That said, observational studies don’t prove cause and effect (correlation does not imply causation). The fact that two things coincide doesn’t mean one causes the other. To move forward, we need one more step: clinical trials in humans.

When lithium was tested at low doses and for long enough, results were better than in very short trials. In older adults with mild cognitive impairment, a 12-month randomized trial observed less cognitive worsening and a significant decrease in tau protein in the cerebrospinal fluid compared with placebo (study).

In patients with established Alzheimer’s, a small trial with microdoses (0.3 mg of elemental lithium) over 15 months showed stabilization versus the decline in the control group, especially from the third month onward (study).

When we talk about Parkinson’s, we think of dopaminergic neurons that are gradually lost and of protein build-up (such as alpha-synuclein) that clogs the cell. As early as 2012 it was shown that lithium can prevent both alpha-synuclein accumulation (study) and neurodegeneration, protecting against cell death in an animal model (study).

In humans, the evidence isn’t “overwhelming” yet, but there are interesting trials highlighting its inhibitory effects on oxidative stress, inflammation, and the glutamatergic pathway, with few adverse effects at low doses (study).

In 2023, 16 people with Parkinson’s received, daily for 6 months, one of three possible regimens: high dose (150 mg lithium carbonate = 28 mg of elemental lithium), medium dose (45 mg lithium aspartate = 2.25 mg lithium), or low dose (15 mg lithium aspartate = 0.75 mg lithium).

What happened? The medium dose was the most effective: there was greater expression of Nurr1 and SOD1 (two neuroprotection targets) and a reduction in neurofilament light chain (NfL), a marker of neuronal damage. The catch was tolerance: at that dose, 33% of participants withdrew from the study due to side effects (study, study).

It is now well known how crucial mitochondria are to health and aging, and how neurodegenerative diseases—such as Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis (ALS)—are closely linked to mitochondrial alterations (study).

The relationship between lithium and mitochondria is a classic case in which a molecule proves clinically effective, but the mechanisms of action are not known with certainty. We know that lithium affects mitochondrial biology, increasing the number of mitochondria (study) and protecting them from damage (study); what isn’t clear is how it does so.

Given the energetic role of mitochondria in neuronal processes—neurotransmitter release and reuptake, neuronal electrical activity, neuron–glia communication—it is highly plausible that lithium acts through mitochondria, and that part of its efficacy in these diseases stems from modulating mitochondrial processes. In other words, it’s quite possible that mitochondria are lithium’s target and that lithium works in these cases precisely because of its mitochondrial effect.

Alzheimer’s isn’t just one of the saddest and most disabling diseases of our time; it’s also the one where we’ve made the least progress in understanding its causes and in developing drug treatments (very expensive and not very effective). Still, we should never lose hope: fortunately, science doesn’t stop.

Less than a month ago (August 2025), a study on Alzheimer’s was published in Nature—in my view, one of the most interesting in recent years. The Harvard team and collaborators wanted to know whether, long before symptoms appear, the brain loses any key “micronutrient.”

They analyzed 27 metals in human brain samples from three groups of people (no impairment, mild cognitive impairment, and Alzheimer’s) and traced the brain’s “natural” lithium.

Findings:

1. Less lithium in the brain already in early stages.
In people with mild cognitive impairment (a frequent prelude to Alzheimer’s), brain lithium was lower; in Alzheimer’s it dropped even further.

2. Amyloid “holds on to” lithium.
Part of the lithium gets trapped in amyloid plaques (one of Alzheimer’s hallmarks), which reduces its availability to healthy cells. In plaque-free regions, free lithium was lower, and this was associated with poorer memory.

3. If you lower dietary lithium in mice, the brain worsens.
In Alzheimer’s models and in healthy older mice, halving brain lithium increased amyloid and abnormally tagged tau, activated brain inflammation, led to loss of synapses and myelin, and worsened memory. Replenishing with microdoses of lithium orotate reversed pathology and restored memory. Blocking GSK-3β (one of the things lithium does, as we saw) also corrected several effects.

4. Replacing lithium in “microdoses” worked in mice—but not with just any salt.
They tested two salts: lithium carbonate (the one used in psychiatry for bipolar disorder) and lithium orotate. At very low doses (meant to mimic “physiological,” not drug, levels), orotate reduced plaques and tau, calmed inflammation, improved synapses, and restored memory. With carbonate, at that low dose, the same effect wasn’t seen. Why? Because carbonate binds more to amyloid and gets “lost” in the plaques; orotate binds less and reaches healthy tissue better.

5. Safety in animals (at that low dose).
At those microdoses, mice showed no kidney or thyroid abnormalities (basic parameters).

The lead investigator, Bruce A. Yankner, compares the Alzheimer’s brain to a battlefield because of the destruction present, and explains that “lithium deficiency is the communication breakdown that leads to war. … Lithium deficiency is a possible common mechanism for the multisystem degeneration of the brain that gives rise to dementia. … The idea that lithium deficiency could be a cause of Alzheimer’s disease is new and suggests a different therapeutic approach. … Our analysis of brain genes suggests that all the major neuron types are affected by lithium.”

In psychiatry, lithium has long been used as a mood stabilizer. It’s employed to treat mania and, above all, to prevent relapse in bipolar disorder. It also has evidence for reducing suicide risk.

The salt used is lithium carbonate, at approximately 300–1200 mg/day (56–188 mg of elemental lithium). However, as a medication it isn’t prescribed strictly in mg/day; instead, it’s titrated to serum levels (around 0.6–1.2 mmol/L). It has a narrow therapeutic window—little difference between what works and what can cause problems. At these higher doses there are side effects to keep in mind:

1. Thyroid: lithium can dampen thyroid function and raise antibody levels; hypothyroidism or goiter is relatively common, so TSH is monitored regularly.

2. Kidney: it can cause excessive thirst and urination due to nephrogenic diabetes insipidus; over the years it’s associated with a higher risk of chronic kidney disease, especially with long treatments and higher levels.

3. Calcium/parathyroid: in a minority, calcium rises and hyperparathyroidism appears.

Over the years, studies have used a wide range of doses, from high (emulating those used in psychiatry) to very low. All have shown benefits, but two important points are worth keeping in mind:

1. Consistency and regularity in supplementation matter more than the dose itself.

2. Very high doses carry many more side effects.

In brief:

• High (“psychiatric”) doses short-term (< 3 months): do not work (study).

• High doses long-term (> 12 months): work, but with side effects (study, study).

• Very low doses (0.3 mg of elemental lithium) long term (> 15 months): work with no adverse effects; moreover, improvements are noticeable from the third month onward (study, study).

In terms of dosing, what this new study reveals is that it’s enough to maintain physiological levels of endogenous lithium through microdoses of lithium orotate to restore memory and slow or reverse several disease features (reduction of amyloid plaques and tau tangles, and improved microglial clearance).

Microdoses were tested in mice. Those “physiological” doses in humans would correspond to 0.06 mg of lithium (1.4 mg of lithium orotate).

It’s a good starting point for further research to see whether this benefit could be greater by increasing the dose—as seen in prior studies—moving from microdoses to low or very low doses.

First, three things:

1. I have a family history of Alzheimer’s and a confirmed genetic predisposition (APOE3/4 variant).

2. I’ve been taking lithium daily since August 2025, when I read the Harvard study.

3. I don’t take lithium alone: I also take care of diet, exercise, and sleep.

Second, let’s break doses into four groups:

1. High doses: > 40 mg of elemental lithium per day. Those used in psychiatry.

2. Low doses: 5 mg of elemental lithium per day. Used in capsules in some over-the-counter supplements.

3. Very low doses: 0.3–0.5 mg lithium per day. Shown to work.

4. Microdoses: 0.06 mg lithium per day. Physiological level used in the 2025 Harvard study.

My current regimen: I use a very low dose: 13 mg lithium orotate (0.5 mg of elemental lithium) per day.

For two reasons:

1. That physiological dose has been shown to work, but it’s the minimal effective dose; it doesn’t mean slightly higher doses couldn’t be more effective.

2. Doses below 5 mg of elemental lithium per day are considered safe and free of side effects (study, review); with my dose I’m still well below what’s been verified as safe (ten times lower).

In other words, the potential benefit-to-risk ratio I use to set supplement doses is very high.

The first thing we need to know is that you don’t supplement with elemental lithium, but in salt form (orotate, carbonate, sulfate…). Depending on the salt, the amount of elemental lithium varies, which is what really matters to us.

Over-the-counter supplements usually come as lithium orotate (4.28% of elemental lithium) and, according to the latest Harvard study, it’s the most effective salt for reaching the brain at low doses.

On the market, orotate comes in two main forms:

1. Capsules of about 117 mg of orotate (5 mg of elemental lithium). The upper limit of what’s safe.

2. Solution (0.5 mg of elemental lithium—500 ppm—per 1 mL in the bottle). This is the one I use because, with the dropper, I can adjust the dose to whatever I want. With 20 drops I reach my desired dose (0.5 mg of elemental lithium).

***

Enjoyed this? Collect this post on Paragraph to support more research like this.

***

Get Evolutionary Nutrition on Amazon

TL;DR
• Evidence layers: population signals + small human trials + a 2025 Harvard Nature study.
• Mechanisms: circadian/GSK-3β, autophagy, mitochondria, inflammation, plasticity.
• Dosing: microdose 0.06 mg Li; very low 0.3–0.5 mg Li; consistency > sheer dose.
• High “psychiatric” doses can work but bring more side effects.
• Author’s practice: 0.5 mg Li/day (lithium orotate). Educational, not medical advice.

This article is for educational purposes only and does not constitute medical advice. Lithium can interact with medications and is not appropriate for everyone. Do not start, stop, or change any treatment without talking to your healthcare professional.

***

If this helped you, collect this post on Paragraph to support my work. Thank you!

***

Lithium has been on my “supplement radar” for a few years now. I started paying attention when the first trials appeared, after it was suspected that it could slow—or even reverse—cognitive decline, and that a deficiency of it might be involved in neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

As with many health-related compounds, the evidence is sparse at the beginning: there are few studies or they’re not well designed; follow-up periods are very short; work is done only in animals or, in humans, with very small samples.

Even though social media, at the drop of a hat, fills up with people touting the use of such molecules—people need something to talk about online and, if possible, to grab attention—I believe the precautionary principle should always apply. Without serious evidence of efficacy and safety, no supplement should be recommended for use.

That’s one reason I’ve never written about lithium. But the situation has changed following a recent study (August 2025) from Harvard University on the relationship between lithium deficiency and neurodegenerative diseases.

It’s time to write about it and, as always, let’s start at the beginning.

Lithium (Li) is an alkali metal found in the Earth’s crust. In the human body it circulates as the Li⁺ ion, and we obtain it mainly from water and from foods that are grown (vegetables and grains).

It isn’t an essential nutrient, and therefore authorities have not established reference intakes. However, as we’ll see, because of its biological actions in the body, some researchers have proposed a minimum daily intake.

In very small amounts, lithium acts as a “fine-tuner” of several cellular functions and “touches” pathways that influence the brain, biological rhythms, cellular metabolism, and immunity. Let’s look at them.

1. Tunes the internal clock (sleep, daytime rhythms).
Lithium slows a switch-like protein, GSK-3β, that takes part in the biological clock. In doing so, it can modulate the amplitude and period of circadian rhythms—a basic piece for sleeping better and keeping the brain “in sync.” The evidence comes from cell studies and from people treated with lithium for bipolar disorder (study, study, study).

2. Activates the cell’s “clean-up and recycling” service (autophagy).
Cells need to recycle old or damaged parts. Lithium promotes autophagy through a specific route—reducing inositol/IP3—distinct from the well-known mTOR pathway. This helps clear accumulated proteins and aged mitochondria in various cell types, especially neurons, which aids in treating neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease (study, study, study).

3. Protects, improves, and increases mitochondria (energy).

In sum: cleaning/autophagy (fewer “traffic jams” inside the cell) + energy/mitochondria (more “battery” and more resilient neurons) + less inflammation (a less hostile environment for neurons) + better brain function (more neurons, better connected, with more memory and cognition) + a tuned biological clock (cells better synchronized for repair and performance) + fewer harmful proteins (fewer chemical signals that drive deterioration).

A whole “toolbox” that helps explain why lithium could protect the brain and help prevent or improve Alzheimer’s and Parkinson’s.

When it comes to Alzheimer’s, every clue counts. With lithium, there are two layers of evidence that together sketch an interesting story: what we observe in populations and what clinical trials in people show.

In 2017, in Denmark, after earlier evidence from cells and animals, researchers asked: Is a higher level of lithium in drinking water associated with a lower incidence of dementia? To answer this, they designed a study: over 18 years they analyzed data from about 75,000 patients with dementia and 700,000 healthy controls, estimating their lithium exposure based on the amount present in the water of their home municipality.

Result: areas with more natural lithium in drinking water tended to register fewer new cases over time.

That said, observational studies don’t prove cause and effect (correlation does not imply causation). The fact that two things coincide doesn’t mean one causes the other. To move forward, we need one more step: clinical trials in humans.

When lithium was tested at low doses and for long enough, results were better than in very short trials. In older adults with mild cognitive impairment, a 12-month randomized trial observed less cognitive worsening and a significant decrease in tau protein in the cerebrospinal fluid compared with placebo (study).

In patients with established Alzheimer’s, a small trial with microdoses (0.3 mg of elemental lithium) over 15 months showed stabilization versus the decline in the control group, especially from the third month onward (study).

When we talk about Parkinson’s, we think of dopaminergic neurons that are gradually lost and of protein build-up (such as alpha-synuclein) that clogs the cell. As early as 2012 it was shown that lithium can prevent both alpha-synuclein accumulation (study) and neurodegeneration, protecting against cell death in an animal model (study).

In humans, the evidence isn’t “overwhelming” yet, but there are interesting trials highlighting its inhibitory effects on oxidative stress, inflammation, and the glutamatergic pathway, with few adverse effects at low doses (study).

In 2023, 16 people with Parkinson’s received, daily for 6 months, one of three possible regimens: high dose (150 mg lithium carbonate = 28 mg of elemental lithium), medium dose (45 mg lithium aspartate = 2.25 mg lithium), or low dose (15 mg lithium aspartate = 0.75 mg lithium).

What happened? The medium dose was the most effective: there was greater expression of Nurr1 and SOD1 (two neuroprotection targets) and a reduction in neurofilament light chain (NfL), a marker of neuronal damage. The catch was tolerance: at that dose, 33% of participants withdrew from the study due to side effects (study, study).

It is now well known how crucial mitochondria are to health and aging, and how neurodegenerative diseases—such as Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis (ALS)—are closely linked to mitochondrial alterations (study).

The relationship between lithium and mitochondria is a classic case in which a molecule proves clinically effective, but the mechanisms of action are not known with certainty. We know that lithium affects mitochondrial biology, increasing the number of mitochondria (study) and protecting them from damage (study); what isn’t clear is how it does so.

Given the energetic role of mitochondria in neuronal processes—neurotransmitter release and reuptake, neuronal electrical activity, neuron–glia communication—it is highly plausible that lithium acts through mitochondria, and that part of its efficacy in these diseases stems from modulating mitochondrial processes. In other words, it’s quite possible that mitochondria are lithium’s target and that lithium works in these cases precisely because of its mitochondrial effect.

Alzheimer’s isn’t just one of the saddest and most disabling diseases of our time; it’s also the one where we’ve made the least progress in understanding its causes and in developing drug treatments (very expensive and not very effective). Still, we should never lose hope: fortunately, science doesn’t stop.

Less than a month ago (August 2025), a study on Alzheimer’s was published in Nature—in my view, one of the most interesting in recent years. The Harvard team and collaborators wanted to know whether, long before symptoms appear, the brain loses any key “micronutrient.”

They analyzed 27 metals in human brain samples from three groups of people (no impairment, mild cognitive impairment, and Alzheimer’s) and traced the brain’s “natural” lithium.

Findings:

1. Less lithium in the brain already in early stages.
In people with mild cognitive impairment (a frequent prelude to Alzheimer’s), brain lithium was lower; in Alzheimer’s it dropped even further.

2. Amyloid “holds on to” lithium.
Part of the lithium gets trapped in amyloid plaques (one of Alzheimer’s hallmarks), which reduces its availability to healthy cells. In plaque-free regions, free lithium was lower, and this was associated with poorer memory.

3. If you lower dietary lithium in mice, the brain worsens.
In Alzheimer’s models and in healthy older mice, halving brain lithium increased amyloid and abnormally tagged tau, activated brain inflammation, led to loss of synapses and myelin, and worsened memory. Replenishing with microdoses of lithium orotate reversed pathology and restored memory. Blocking GSK-3β (one of the things lithium does, as we saw) also corrected several effects.

4. Replacing lithium in “microdoses” worked in mice—but not with just any salt.
They tested two salts: lithium carbonate (the one used in psychiatry for bipolar disorder) and lithium orotate. At very low doses (meant to mimic “physiological,” not drug, levels), orotate reduced plaques and tau, calmed inflammation, improved synapses, and restored memory. With carbonate, at that low dose, the same effect wasn’t seen. Why? Because carbonate binds more to amyloid and gets “lost” in the plaques; orotate binds less and reaches healthy tissue better.

5. Safety in animals (at that low dose).
At those microdoses, mice showed no kidney or thyroid abnormalities (basic parameters).

The lead investigator, Bruce A. Yankner, compares the Alzheimer’s brain to a battlefield because of the destruction present, and explains that “lithium deficiency is the communication breakdown that leads to war. … Lithium deficiency is a possible common mechanism for the multisystem degeneration of the brain that gives rise to dementia. … The idea that lithium deficiency could be a cause of Alzheimer’s disease is new and suggests a different therapeutic approach. … Our analysis of brain genes suggests that all the major neuron types are affected by lithium.”

In psychiatry, lithium has long been used as a mood stabilizer. It’s employed to treat mania and, above all, to prevent relapse in bipolar disorder. It also has evidence for reducing suicide risk.

The salt used is lithium carbonate, at approximately 300–1200 mg/day (56–188 mg of elemental lithium). However, as a medication it isn’t prescribed strictly in mg/day; instead, it’s titrated to serum levels (around 0.6–1.2 mmol/L). It has a narrow therapeutic window—little difference between what works and what can cause problems. At these higher doses there are side effects to keep in mind:

1. Thyroid: lithium can dampen thyroid function and raise antibody levels; hypothyroidism or goiter is relatively common, so TSH is monitored regularly.

2. Kidney: it can cause excessive thirst and urination due to nephrogenic diabetes insipidus; over the years it’s associated with a higher risk of chronic kidney disease, especially with long treatments and higher levels.

3. Calcium/parathyroid: in a minority, calcium rises and hyperparathyroidism appears.

Over the years, studies have used a wide range of doses, from high (emulating those used in psychiatry) to very low. All have shown benefits, but two important points are worth keeping in mind:

1. Consistency and regularity in supplementation matter more than the dose itself.

2. Very high doses carry many more side effects.

In brief:

• High (“psychiatric”) doses short-term (< 3 months): do not work (study).

• High doses long-term (> 12 months): work, but with side effects (study, study).

• Very low doses (0.3 mg of elemental lithium) long term (> 15 months): work with no adverse effects; moreover, improvements are noticeable from the third month onward (study, study).

In terms of dosing, what this new study reveals is that it’s enough to maintain physiological levels of endogenous lithium through microdoses of lithium orotate to restore memory and slow or reverse several disease features (reduction of amyloid plaques and tau tangles, and improved microglial clearance).

Microdoses were tested in mice. Those “physiological” doses in humans would correspond to 0.06 mg of lithium (1.4 mg of lithium orotate).

It’s a good starting point for further research to see whether this benefit could be greater by increasing the dose—as seen in prior studies—moving from microdoses to low or very low doses.

First, three things:

1. I have a family history of Alzheimer’s and a confirmed genetic predisposition (APOE3/4 variant).

2. I’ve been taking lithium daily since August 2025, when I read the Harvard study.

3. I don’t take lithium alone: I also take care of diet, exercise, and sleep.

Second, let’s break doses into four groups:

1. High doses: > 40 mg of elemental lithium per day. Those used in psychiatry.

2. Low doses: 5 mg of elemental lithium per day. Used in capsules in some over-the-counter supplements.

3. Very low doses: 0.3–0.5 mg lithium per day. Shown to work.

4. Microdoses: 0.06 mg lithium per day. Physiological level used in the 2025 Harvard study.

My current regimen: I use a very low dose: 13 mg lithium orotate (0.5 mg of elemental lithium) per day.

For two reasons:

1. That physiological dose has been shown to work, but it’s the minimal effective dose; it doesn’t mean slightly higher doses couldn’t be more effective.

2. Doses below 5 mg of elemental lithium per day are considered safe and free of side effects (study, review); with my dose I’m still well below what’s been verified as safe (ten times lower).

In other words, the potential benefit-to-risk ratio I use to set supplement doses is very high.

The first thing we need to know is that you don’t supplement with elemental lithium, but in salt form (orotate, carbonate, sulfate…). Depending on the salt, the amount of elemental lithium varies, which is what really matters to us.

Over-the-counter supplements usually come as lithium orotate (4.28% of elemental lithium) and, according to the latest Harvard study, it’s the most effective salt for reaching the brain at low doses.

On the market, orotate comes in two main forms:

1. Capsules of about 117 mg of orotate (5 mg of elemental lithium). The upper limit of what’s safe.

2. Solution (0.5 mg of elemental lithium—500 ppm—per 1 mL in the bottle). This is the one I use because, with the dropper, I can adjust the dose to whatever I want. With 20 drops I reach my desired dose (0.5 mg of elemental lithium).

***

Enjoyed this? Collect this post on Paragraph to support more research like this.

***

Get Evolutionary Nutrition on Amazon