Lithium

[Swarfmaker]

I've noticed that the times my mother seems to have had improvements
was when she had been taking lithium orotate. I had been giving her
about 120mg per day (about 1/2 the recommended dose on the bottle)
just prior to switching over to cinnamon in April, 2008. I didn't
think the lithium was working. But now I'm beginning to think that
maybe the lithium and cinnamon have a synergistic effect. So, I
started giving her 60mg of lithium orotate per day. I'm still not sold
on lithium orotate, but I think it's worth a try. Prescription lithium
carbonate, citrate, or chloride would probably be better, along with a
physician's supervision... if you can get one to go along with the
experiment.

Here is some info I dug up about lithium:

Lithium at 50: have the neuroprotective effects of this unique cation
been overlooked?
Biological Psychiatry. 1999 Oct 1;46(7):929-40. PMID: 10509176
[PubMed]

Manji HK, Moore GJ, Chen G.

Department of Psychiatry and Behavioral Neurosciences,
Wayne State University School of Medicine, Detroit, Michigan
48201,USA.

"Recent advances in cellular and molecular biology have resulted in
the identification of two novel, hitherto completely unexpected
targets of lithium's actions, discoveries that may have a major impact
on the future use of this unique cation in biology and medicine.
Chronic lithium treatment has been demonstrated to markedly increase
the levels of the major neuroprotective protein, bcl-2 in rat frontal
cortex, hippocampus, and striatum. Similar lithium- induced increases
in bcl-2 are also observed in cells of human neuronal origin, and are
observed in rat frontal cortex at lithium levels as low as
approximately 0.3 mmol/L. Bcl-2 is widely regarded as a major
neuroprotective protein, and genetic strategies that increase bcl-2
levels have demonstrated not only robust protection of neurons against
diverse insults, but have also demonstrated an increase the
regeneration of mammalian CNS axons. Lithium has also been
demonstrated to inhibit glycogen synthase kinase 3 beta (GSK-3 beta),
an enzyme known to regulate the levels of phosphorylated tau and beta-
catenin (both of which may play a role in the neurodegeneration
observed in Alzheimer's disease). Consistent with the increases in
bcl-2 levels and inhibition of GSK-3 beta, lithium has been
demonstrated to exert robust protective effects against diverse
insults both in vitro and in vivo. These findings suggest that lithium
may exert some of its long term beneficial effects in the treatment of
mood disorders via underappreciated neuroprotective effects. To date,
lithium remains the only medication demonstrated to markedly increase
bcl-2 levels in several brain areas; in the absence of other adequate
treatments, the potential efficacy of lithium in the long term
treatment of certain neurodegenerative disorders may be warranted."


Inhibition of glycogen synthase kinase-3 by lithium correlates with
reduced tauopathy and degeneration in vivo
Proceedings of the National Academy of Sciences of the United States
of America
PNAS | May 10, 2005 | vol. 102 | no. 19 | 6990-6995
http://www.pnas.org/cgi/content/abstract/102/19/6990?ck=nck

"Neurofibrillary tangles composed of hyperphosphorylated, aggregated
tau are a common pathological feature of tauopathies, including
Alzheimer's disease. Abnormal phosphorylation of tau by kinases or
phosphatases has been proposed as a pathogenic mechanism in tangle
formation. To investigate whether kinase inhibition can reduce
tauopathy and the degeneration associated with it in vivo, transgenic
mice overexpressing mutant human tau were treated with the glycogen
synthase kinase-3 (GSK-3) inhibitor lithium chloride. Treatment
resulted in significant inhibition of GSK-3 activity. Lithium
administration also resulted in significantly lower levels of
phosphorylation at several epitopes of tau known to be
hyperphosphorylated in Alzheimer's disease and significantly reduced
levels of aggregated, insoluble tau. Administration of a second GSK-3
inhibitor also correlated with reduced insoluble tau levels,
supporting the idea that lithium exerts its effect through GSK-3
inhibition. Levels of aggregated tau correlated strongly with degree
of axonal degeneration, and lithium-chloride-treated mice showed less
degeneration if administration was started during early stages of
tangle development. These results support the idea that kinases are
involved in tauopathy progression and that kinase inhibitors may be
effective therapeutically."


Lithium delays progression of amyotrophic lateral sclerosis.
http://www.pnas.org/cgi/reprint/105/6/2052

"ALS is a devastating neurodegenerative disorder with no effective
treatment. In the present study, we found that daily doses of lithium,
leading to plasma levels ranging from 0.4 to 0.8 mEq/liter, delay
disease progression in human patients affected by ALS. None of the
patients treated with lithium died during the 15 months of the follow-
up, and disease progression was markedly attenuated when compared with
age-, disease duration-, and sex-matched control patients treated with
riluzole for the same amount of time. In a parallel study on a genetic
ALS animal model, the G93A mouse, we found a marked neuroprotection by
lithium, which delayed disease onset and duration and augmented the
life span. These effects were concomitant with activation of autophagy
and an increase in the number of the mitochondria in motor neurons and
suppressed reactive astrogliosis. Again, lithium reduced the slow
necrosis characterized by mitochondrial vacuolization and increased
the number of neurons in lamina VII that were severely affected in
saline-treated G93A mice. After lithium administration in G93A mice,
the number of these neurons was higher even when compared with saline-
treated WT. All these mechanisms may contribute to the effects of
lithium, and these results offer a promising perspective for the
treatment of human patients affected by ALS."


Here is another take on the use of lithium:

[From "The Misunderstood Mineral Part 1" By Jonathan V. Wright, M.D.]
http://www.tahoma-clinic.com/lithium1.shtml

I suggest reading the whole article, but here is an excerpt...

Taking (grey) matters into your own hands

"Hercule Poirot, Agatha Christie's famous fictional detective, had an
amusing quirk in his incessant concern for his "little grey cells." I
thought of Hercule several years ago when I saw the following headline
in an issue of the Lancet: "Lithium-induced increase in human brain
grey matter."

"That may not sound like an earth-shattering piece of news, but it
actually was quite a major discovery. To that point, medical experts
believed that once our brains matured, it was all downhill from then
on. Decades of autopsies, x-rays, and, more recently, brain scans have
repeatedly shown that brains shrink measurably with aging. But
according to their report in the Lancet, Wayne State University
(Detroit) researchers found that lithium has the ability to both
protect and renew brain cells.1 Eight of 10 individuals who took
lithium showed an average 3 percent increase in brain grey matter in
just four weeks.

"Lithium may help to generate entirely new cells too: Another group of
researchers recently reported that lithium also enhances nerve cell
DNA replication.2 DNA replication is a first step in the formation of
a new cell of any type.

"The Wayne State study used high-dose lithium, but I'm certainly not
using that amount myself, nor do I recommend it. Prescription
quantities of lithium just aren't necessary for "everyday" brain cell
protection and re-growth. Studies done years ago have shown that very
low amounts of lithium can also measurably influence brain function
for the better."

[From "The Misunderstood Mineral Part 2" By Jonathan V. Wright, M.D.]
http://www.tahoma-clinic.com/lithium2.shtml

Lithium fights crime and some of your most nagging health concerns

"Turns out it's not only the strict use of the death penalty lowering
crime rates in some areas of Texas. And while I'm sure "Dubya" would
be quick to take credit, it's not stricter laws or changes in
sentencing guidelines either. Using 10 years of data accumulated from
27 Texas counties, researchers found that the incidence of homicide,
rape, burglary, and suicide, as well as other crimes and drug use,
were significantly lower in counties whose drinking water supplies
contained 70-170 micrograms of lithium per liter than those with
little or no lithium in their water.

"The researchers wrote: "These results suggest that lithium at low
dosage levels has a generally beneficial effect on human
behavior...increasing the human lithium intakes by supplementation, or
the lithiation [adding lithium] of drinking water is suggested as a
possible means of crime, suicide, and drug-dependency reduction at the
individual and community level."

"And that's not to mention all of the lithium health benefits we went
over in Part 1: It may be useful in treating Alzheimer's disease,
senile dementia, and possibly Parkinson's disease. Lithium not only
protects brain cells against normal wear and tear, but also offers
additional protection against a whole variety of toxic molecules,
including patent medications. It can also promote brain cell
regeneration and increase brain cell mass. In essence, the research
suggests that lithium is a brain anti-aging nutrient.

"All of these results are every bit as good as (if not better than)
the data that led to dumping toxic waste (fluoride) into so many
public water supplies. So why haven't public health and safety
"authorities" been pushing for further intensive research on water-
borne lithium and criminal behavior?"

Uncovering Lithium's Mode of Action

ScienceDaily (May 21, 2010) — Though it has been prescribed for over
50 years to treat bipolar disorder, there are still many questions
regarding exactly how lithium works. However, in a study appearing in
this month's Journal of Lipid Research, researchers have provided
solid evidence that lithium reduces brain inflammation by adjusting
the metabolism of the health-protective omega-3-fatty acid called
DHA... they also demonstrated that lithium treatment increased levels
of a metabolite called 17-OH-DHA in response to inflammation. 17-OH-
DHA is formed from the omega-3 fatty acid DHA (docosahexaenoic acid)
and is the precursor to a wide range of anti-inflammatory compounds
known as docosanoids. Other anti-inflammatory drugs, like aspirin, are
known to also enhance docosanoids in their mode of action... the
concentration of DHA did not increase, which suggests that lithium may
increase 17-OH-DHA levels by affecting the enzyme that converts DHA to
17-OH-DHA...
http://www.sciencedaily.com/releases/2010/05/100521191440.htm

Unfortunately, in clinical trials of lithium for treating patients
with PSP, the participants had to drop out due to side effects.