The Efficacy of Lithium in the Treatment of Spikeopathy (Long-COVID and Post-Vac)

General Considerations in the Light of the first Clinical Trial Results

In a recent post on his Substack, American cardiologist Dr. Peter McCullough remarked that he is not aware of any

“mechanism for the psychiatric drug [Lithium] to influence the Spike protein, which is the underlying cause of the [Long-COVID] syndrome.”

First, to clarify: lithium is not just used as a psychiatric drug in very high doses, but it is a natural element and essential element in trace amounts for humans, animals, and plants alike – a topic I explore in detail in my forthcoming book on this topic. Also, I would like to address the mechanism by which lithium can effectively alleviate symptoms of Long-COVID, which are triggered by the spike protein or components thereof, the S1-subunit.

Spikeopathy and Its Cause

The long-lasting neurological symptoms after severe SARS-CoV-2 infection, called Long-COVID, as well as after spike-mRNA injection, called Post-Vac – commonly referred to as "spikeopathy" (see) – are symptoms of a SARS-CoV-2 spike protein furin-cleaved S1 subunit, entering the brain and inducing long-term neuroinflammation (see).

The "spike" receptor TLR4 of brain immune cells was shown to trigger the neuroinflammatory response (see), causing symptomatic spikeopathy (see).

TLR4 induces the neuroinflammatory response upon S1 subunit binding via activation of the intracellular signal transducer GSK-3 (see), making GSK-3 (besides TLR4 itself) a key target against spikeopathy.

Lithium to the Rescue: Understanding the Mechanism

GSK-3 is naturally downregulated by lithium (see). Based on the findings of Spuch C et al, published under the title "Efficacy and Safety of Lithium Treatment in SARS-CoV-2 Infected Patients" (see), lithium was suggested as a possible first-line treatment not only for severe COVID-19 but also for spikeopathy:

“Lithium, through its immunomodulatory action, reduces inflammatory cytokine levels by preventing cytokine storms, thus reducing the severity of the infection and the risk of death. In fact, lithium can also be studied for earlier use, such as at the time of diagnosis, in order to avoid hospitalization altogether, as well as in the treatment of ‘Long Covid’ syndromes.”

This was studied by Thomas J. Guttuso, Jr., MD, Professor of neurology at the Jacobs School of Medicine and Biomedical Sciences, University of Buffalo, as he revealed in a press release in January 2023 (see):

“I was shocked when the patient saw improvement within a matter of days.”

The press release goes on to say that he has treated 10 other Long-COVID patients with low-dose lithium; nine saw improvements with lithium. None experienced side effects.

“I just kept hearing the same story: that within days they were noticing satisfactory benefit,”

says Guttuso.

Pharmacodynamics Hurdles for Lithium Aspartate in Long-COVID

Guttuso et al. published on 2 October 2024 the results of a follow-on small controlled trial in which 26 patients with Long-COVID were treated with 10-15 mg lithium aspartate (LiAs) for three weeks, in which no improvement was seen at these doses (see).

Of course, it is difficult to draw reliable conclusions from such a small, open-label study, the authors admit, especially as an effect was seen at higher doses but only in very small number of patients:

"40 to 45 mg/d [of lithium aspartate, LiAs] was associated with numerically greater reductions in fatigue and cognitive dysfunction scores than 15 mg/d."

Patients who reached serum lithium levels of 0.18-0.49 mEq/l (mmol/l) reported significant symptomatic improvements, indicating that such serum levels may be necessary.

The pharmacodynamics of LiAs are not well understood, particularly regarding lithium levels reached in the brain, the main target organ regarding spikeopathy. Hence the fact that the clinical trial by Guttuso et al. in treating brain fog after COVID-19 showed no improvement with low doses of lithium as LiAs and required relatively high concentrations of LiAs to be effective may simply be a problem with its pharmacodynamics.

Lithium Orotate: A Superior Form of Lithium for Enhanced Brain Delivery

Lithium in the form of lithium orotate (LiOr) has been shown to reach the brain more efficiently than another form, e.g. lithium carbonate (LiCO), because it is a very stable compound that is thought to be actively transported across the blood-brain barrier (see). For example, a 10-fold lower serum concentration of lithium in the form of LiOr than in the form of LiCO has the same clinical effect in a mouse model of mania (see):

“LiCO maintained a partial block of AIH at doses of 15 mg/kg or greater in males and 20 mg/kg or greater in females. In contrast, LiOr elicited a near complete blockade at concentrations of just 1.5 mg/kg in both sexes, indicating improved efficacy and potency.”

LiOr has also been shown to be three times more concentrated in the brain than LiCO at equimolar treatment in an experimental rat model, which may explain the difference in clinical efficacy shown above: (see).

The superiority of LiOr over other lithium salts has already been extensively discussed in an article entitled "Lithium orotate: A superior option for lithium therapy?" (see), as well as the ability to more efficiently cross the blood-brain barrier:

“LiOr is proposed to cross the blood-brain barrier and enter cells more readily than Li₂CO₃ [LiCO], which will theoretically allow for reduced dosage requirements and ameliorated toxicity concerns.”

Therefore, I continue to recommend 5 mg of elemental lithium (once or twice daily, depending on the clinical severity of the spikeopathy) in the form of LiOr, as much lower serum lithium concentrations may be required to achieve beneficial results. Assuming that LiAs behaves pharmacodynamically similarly to LiCO, 5 to 10 mg of elemental lithium in the form of LiOr could be as effective as 45 (positively tested by Guttuso et al) and even 90 mg of lithium in the form of LiAs, as it would achieve similar brain lithium concentrations.

Premature Dismissal of Lithium's Potential in Long-COVID

But despite the seen improvement at the higher LiAs concentrations (45 mg) by Guttuso et al, McCullough posted only a few days after the publication of Guttuso et al findings that lithium

"has joined the long-list of various drugs and supplements that have failed to improve long-COVID syndrome caused by the SARS-CoV-2 Spike protein."

First of all, this statement is factually inaccurate, as improvements were seen with LiAs, but not at the low concentrations as originally hoped. Therefore, Guttuso notes (see) that

"it is possible the randomized controlled trial was ineffective because the dose of lithium aspartate used was too low."

McCullough's dismissive "verdict" on a natural treatment option appears both premature and highly counterproductive, given the severity of the spikeopathy epidemic following the genetic assault on humanity – first through a released bioweapon, followed by a global initiative to inject the bioweapon's payload (the mRNA encoding the furin-cleavable spike protein) into much of the world's population. In fact, based on the observations and the results of Guttuso et al, I continue to recommend LiOr as the first choice for treating brain fog after COVID-19 (and spike-mRNA injections), at the doses mentioned above (5-10 mg elemental Li in the form of LiOr).

Secondly, as it is known that long-lasting COVID is more likely to develop after severe COVID-19, which is driven by cytokine storms – that is more likely to occur with micronutrient deficiencies, e.g., vitamin D (see) and many others – effective treatment of spikeopathy demands more than just lithium (although it did improve symptoms at higher brain concentrations by itself).

Thirdly and finally, I would caution against considering lithium as a miracle drug. While it can be effective against a broad range of symptoms as well as diseases, in case the latter are caused by lithium deficiency, there is a risk of ignoring the additional causes of diseases and their symptoms in spikeopathy and others, such as other micronutrient deficiencies. While Lithium is one such essential trace element, it is not the only one that may be lacking. In fact, prevention and treatment of most common diseases requires a systemic approach to be effective.

Conclusion

Encouraged by the study by Guttuso et al, I propose to switch from LiAs to LiOr at comparatively lower lithium doses, while addressing additional deficiencies as part of a systemic approach to the treatment of spikeopathy.