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.
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.
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.
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
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.
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.
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.
