Saturday, September 22, 2012

More Research by Dr. Mark Millar: On Alzheimer's

Is Lithium a Breakthrough Preventative for Alzheimer’s?

Lithium study reveals about a 90% reduction of

Alzheimer’s in the elderly!

America’s elderly population is anxiously waiting for a breakthrough cure for Alzheimer’s disease, hoping that the pharmaceutical industry will develop a novel drug to end the nightmare of this devastating degenerative illness. From the research I have seen on the complexity of all the various chemical pathways involved in this degenerative process it looks to me like it will be decades, if ever, before the pharmaceutical industry will develop the silver bullet for Alzheimer’s disease. The best we can hope for from the pharmaceutical industry will be the development of many different drugs treating various groups of symptoms for those stricken with this illness.

Fortunately, Lithium magnificently prevents the degenerative process of Alzheimer’s disease and does so by actively neutralizing most of the major neuro-toxic chemical pathways involved in this illness. The breadth and depth of Lithium’s ability to mitigate, neutralize and suppress the neurotoxicity of Alzheimer’s disease (AD) is truly breath taking.

The understanding of lithium’s preventative abilities in AD was first discovered in animal studies, and finally in 2007 it was discovered that lithium prevents AD in humans.

The following study was conducted at the University of Sao Paulo, Brazil, in the Laboratory of Neuroscience. Paula Nunes MD, PhD and her colleagues studied the effect of long-term lithium treatment in an elderly patient group who had Bipolar Disorder (BD) and had been using lithium on a long-term basis. They then compared the rate of AD to elderly bipolar patients who were not taking lithium for the disorder. (1) The results were astounding!

The highest rates of Alzheimer’s disease are found in the elderly over 80 years of age and in the elderly with mood disorders. In both of these groups the incidence rate of AD is as high as 1 in 3 individuals.

In the study conducted by Nunes et. al., in 2007, the group of bipolar patients not taking lithium was found to have a rate of Alzheimer’s at 1 in 3 individuals, while the lithium treated bipolar patients rate of AD was only 1 in 22 individuals! Both treatment groups were of the same age.

These findings robustly suggest that lithium is a preventative cure for Alzheimer’s.

Additionally the group of BD patients that were on long-term lithium treatment was found to have a rate of AD that was 35% lower than the general population and approximately 90% less than the non-lithium group! The following statistics are the incidence rates of AD for each group, again of the same approximate age. (1)

Lithium treated BD patients 1 in 22 (4.5%)
Non-lithium treated BD patients 1 in 3 (33.3%)
General population AD rate 1 in 14 (7%)

Follow this link to the study: Lithium and risk for Alzheimer's disease in elderly patients with bipolar disorder. (Nunes et. al., 2007) >(1)<- Don't miss reviewing this source

Is it theoretically possible that lithium may completely eliminate the incidence of AD if the optimal amount of lithium is ingested?

Because of the differences between how high doses of pharmaceutical lithium and lithium orotate are tolerated, it is my belief that the elderly may not have been taking enough lithium to completely protect them from AD. That may be why we see a 4.5% incidence rate in those elderly patients who had taken lithium

The good news is that with Lithium Orotate, the elderly population can increase the intra-cellular concentration of lithium without any adverse side effects or adverse drug interactions. This I believe will allow the optimal lithium dosage to reduce the rate of AD to 1% or less within the general population. Recommended Lithium Orotate supplementation for the prevention of Alzheimer’s is 2-6 tablets per day.

While the primary cause of Alzheimer’s disease (AD) remains controversial, a preponderance of evidence strongly suggests that Aluminum toxicity is at least one of the primary causal factors in the pathogenesis (cause) of AD. The following studies show that when aluminum is administered to animals, they develop all the classic chemical and physical signs of neurotoxicity associated aluminum toxicity as seen in AD. Furthermore, I believe that the co-administration of lithium with aluminum in these animal studies demonstrates, beyond a reasonable doubt, that lithium is the supreme neuro-protector of the central nervous system against aluminum neurotoxicity.

Does Aluminum cause Alzheimer’s?


Alzheimer’s in mice, rabbits, and rats manifests symptomatically with considerable similarity to humans and these animals are a suitable source of research data because of the close relationship with humans in the chemical reactions they possess. As well, they exhibit very similar physical impairments to humans with Alzheimer’s. Furthermore, because both animals and humans appear to be inflicted with Alzheimer’s induced by aluminum neurotoxicity, we will examine (below) the effects of aluminum (AL) toxicity upon the central nervous system of these animals.

I have listed below 35 degenerative, Neuro-toxic, cell death inducing, neuro-degenerative changes or symptoms within the brains of these animals; all of them negative and due directly to Aluminum Neuro-toxicity. It is not important that you read each negative effect, just notice how many negative changes there are and see the studies below to read how lithium positively affected each of these degenerative changes caused by aluminum.

The first thought on this is how overwhelmingly toxic aluminum is to the brain.

The second thought: Is there anything that can reduce or prevent this aluminum-induced damage from occurring within the brain?

The preventative for every single one of these degenerative, Neuro-toxic, reactions caused by aluminum is lithium!

In every one of the following 35 Neuro-degenerative changes lithium, either partially or completely, neutralized the negative reaction. In each test case lithium had a significant effect on every physical change within the animals.

In most cases lithium returned the bio-chemical levels to near normal; proving once again (I believe) that…

Lithium is the unchallenged, #1, supreme Neuro-protector of the brain!

Following is the complete list of how human patients initially expressed the negative effects of aluminum-induced neurotoxicity that had been counteracted in the animals supplemented with lithium. Be sure to read the researchers quotes below.

Neuro-Physical changes

Diminished locomotion activity: I don’t feel like getting up off the couch. (2)
Diminished muscular function: “I can’t run on the tread-mill”. (2)

Neuro-Cognitive changes

Spatial Memory impairment: Experienced as, “where am I, or where am I going?” (1)
Short-term Memory impairment: “Where did I put my car keys?” (2)
Decreased Cognitive function: “I can’t figure this out, I’m confused!” (2)
Increased anxiety. “I feel frightened.” (2)

Loss of brain cells

Aluminum caused - Structural damage and disorganization to the layers of brain/cerebrum.(3)

Aluminum caused - Loss of brain cells. (3-5)

Aluminum caused - Loss of Purkinje cells within the cerebellum. (3)

Aluminum caused - Loss of neurons (brain cells) within the hippocampus. (4)

Aluminum caused - Structural damage and disorganization of vacuolar spaces. (3)

Neuro-Chemical changes

Dopamine and Serotonin levels are lowered significantly by AL: “I feel so depressed.” (2)

Free radical/oxidative damage, significantly increased in both Cerebrum and Cerebellum. (2)

Decreased acetylcholinesterase activity. (2)

Decreased monoamine oxidase activity. (2)

Increased lipid peroxidation. (3)

Increased catalase activity. (3)

Increased superoxide dismutase activity. (3)

Increased glutathione reductase activity. (3)

Decreased glutathione-s-tranferase. (3)

Decreased total oxidized glutathione. (3)

Increased Nitric Oxide Synthase. (3)

Induces cytochrome C release. (4,5)

Decreases levels of Neuro-protective protein Bcl-2. (4)

Decreases levels of Neuro-protective protein Bcl-X. (4)

Increases levels of the pro-apoptotic Bax. (4)

Activates Caspase-3. (4)

Causes damage, fragmentation/mutation of DNA. (4,6)

Produces degenerative changes within the cell-mitochondria. (4)

Produces degenerative changes within the endoplasmic reticulum. (4)

Increased Nitric oxide synthase. (6)

Increased L-citrulline. (6)

Causes chromatin condensation in the nuclear membrane, in both the Cerebrum and Cerebellum and induces mitochondrial swelling. (6)

In every one of these animal studies Lithium was supplemented in the diet to determine what benefit was noted. (2-6)

Here are a few quotes regarding some of the protective effects the researchers found when lithium (Li) was given to the animals along with the aluminum (Al).

“Lithium supplementation to Al treated animals caused a significant improvement in the activities of enzymes… Further, lithium when given along with Al was also able to regulate the levels of dopamine, serotonin and reactive oxygen species in both the regions and the values were found close to the normal controls.” (Bhalla et. al., 2010)(2)

“Pretreatment for 14 days with 7 mm of lithium carbonate in drinking water prevents aluminum-induced … and reduces DNA damage.” (Ghribi et. al., 2002)(4)

“Al treatment also revealed an increase in DNA fragmentation… Interestingly, Li supplementation to Al treated rats reduced the damage inflicted on DNA by Al.” (Bhalla et. al., 2010)(6)

“Agents such as lithium … have the ability to prevent aluminum-induced neuronal death by interfering with the mitochondrial and/or the endoplasmic reticulum-mediated apoptosis cascade.” (Savory et. al., 2003)(5)

“Therefore, the study shows that Li has a potential to exhibit neuroprotective role in conditions of Al-induced oxidative stress…” (Bhalla et. al., 2009)(3)

To reemphasize, in each of the 35 previous Neuro-degenerative changes, lithium either partially or completely neutralized the negative reactions. In every case lithium had a significant effect on every cognitive and physical change within the animals.

Perhaps most exciting is the immediate benefit that Alzheimer’s patients are achieving with Lithium Orotate supplementation. Lithium is a natural anti-depressant, boosting serotonin levels.

The individuals taking Lithium Orotate are far less irritable, depressed and show far fewer emotional outbursts (according to family reports). A medical doctor recently informed me that his father was showing significant improvement of AD related symptoms. The doctor reported that his father was now sleeping through the night.

1. Nunes PV, Forlenza OV, Gattaz WF. Lithium and risk for Alzheimer's disease in elderly patients with bipolar disorder. Br J Psychiatry. 2007 Apr;190:359-60. PubMed PMID: 17401045.

1. Ribes D, Colomina MT, Vicens P, Domingo JL. Impaired spatial learning and unaltered neurogenesis in a transgenic model of Alzheimer's disease after oral aluminum exposure. Curr Alzheimer Res. 2010 Aug;7(5):401-8. PubMed PMID: 19939225.

2. Bhalla P, Garg ML, Dhawan DK. Protective role of lithium duringaluminium-induced neurotoxicity. Neurochem Int. 2010 Jan;56(2):256-62. Epub 2009 Nov 4. PubMed PMID: 19895864.

3. Bhalla P, Dhawan DK. Protective role of lithium in ameliorating the
aluminium-induced oxidative stress and histological changes in rat brain. Cell Mol Neurobiol. 2009 Jun;29(4):513-21. Epub 2009 Jan 29. PubMed PMID: 19184412.

4. Ghribi O, Herman MM, Spaulding NK, Savory J. Lithium inhibits aluminum-induced apoptosis in rabbit hippocampus, by preventing cytochrome c translocation, Bcl-2 decrease, Bax elevation and caspase-3 activation. J Neurochem. 2002Jul;82(1):137-45. PubMed PMID: 12091474. Pretreatment for 14 days with 7 mm of lithium carbonate in drinking water prevents aluminum-induced translocation of cytochrome c,… and reduces DNA damage.(4)

5. Savory J, Herman MM, Ghribi O. Intracellular mechanisms underlying aluminum-induced apoptosis in rabbit brain. J Inorg Biochem. 2003 Sep 15;97(1):151-4. Review. PubMed PMID: 14507471.

6. Bhalla P, Singla N, Dhawan DK. Potential of lithium to reduce aluminium-induced cytotoxic effects in rat brain. Biometals. 2010 Apr;23(2):197-206. PubMed PMID: 19936942.

“Al treatment also revealed an increase in DNA fragmentation… Interestingly, Li supplementation to Al treated rats reduced the damage inflicted on DNA by Al.”(6)