The following excerpt is boring, so move along now. It’s from a recent review article on all the potential causes and therapeutic options for Alzheimer’s Disease (AD). I post it here so I can find it later. Click the link at bottom to RTWT.
“Lithium is not yet generally recognized as a trace element but several lines of evidence make it a strong candidate. For instance, long-term low-dose exposure to lithium exerts anti-aging capabilities and unambiguously decreases mortality in animal models. In humans, epidemiological studies indicate an inverse correlation between lithium concentration in drinking water and mood, depression and suicide rates, amongst other psychiatric conditions. In a study that compared elderly bipolar patients (who exhibit a higher risk for dementia) who had received chronic lithium treatment, with bipolar patients who had not received lithium, it was shown that the prevalence of the treated group was equivalent to the general, age-comparable population, whereas the non-lithium-treated patients had an incidence of dementia that was six times greater, i.e. 5 % vs. 33 %, respectively. In another study it was shown that lithium treatment resulted in an increase in volumes of the hippocampi in both hemispheres compared to an unmedicated group, an effect that was apparent even after a brief treatment period of about 4 weeks on average. Importantly, intake of lithium not only in standard therapeutic but also in trace doses reduces the risk for dementia, suicide, and other behavioural outcomes, suggesting an pharmacological interference with key regulators of these pathological processes. So, lithium naturally regulates critical cell signalling pathways and a lack of lithium in the diet can therefore cause increased disease risk.It has been shown that lithium modulates negatively the activity of the two kinases GSK-3α and GSK-3β, which might explain both the relative specificity and sensitivity of the effects of low-dose lithium treatment (see below). Since GSK-3β-activation by oligomeric Aβ promotes neuroinflammation, phosphorylation of tau and disturbance of AHN [adult hippocampal neurogenesis], all key mechanisms in the AD process, in inhibition of GSK-3 by lithium results in reduced tauopathy and neurodegeneration in vivo. Likewise, lithium treatment was shown to improve AHN, neuropathology and cognitive functions in a mouse model of AD. Furthermore, such “AD-mice” treated from two months of age had decreased numbers of senile plaques, no neuronal loss in cortex and hippocampus and increased BDNF levels when compared to non-treated transgenic mice. In order to achieve this effect, it was sufficient to give lithium at about one per mill of the high standard-dose therapy in bipolar disorder, a dose which can cause some significant side effects. Hence the authors of the study believe that their data support the use of (virtually side-effect free) microdose lithium in the prevention and treatment of Alzheimer’s disease.Indeed, long-term lithium treatment already provided preliminary evidence of its disease-modifying properties for amnestic MCI [mild cognitive impairment] in a randomised controlled trial, where the lithium-treated group had fewer conversions from MCI to AD. Lithium treatment was associated with a significant decrease in cerebrospinal fluid concentrations of hyperphosphorylated tau and better performance on the cognitive subscale of the Alzheimer’s Disease Assessment Scale and in attention tasks. At a more advanced stage of AD, microdose treatment with only 300 μg lithium administered once daily stabilized the AD patients during the complete evaluation phase of 15 months. For instance, whereas the treated group showed no decreased performance in the mini-mental state examination (MMSE), lower scores were observed for the control group during the same period, with significant differences occurring after three months, and increasing progressively.Importantly, lithium, besides being required for efficient AHN and blocking AD-specific pathological processes, also impacts on cell-rejuvenating autophagy. Lithium was found to inhibit the activity of inositol monophosphatase (IMPase), which leads to a decrease of myo-1, 4, 5-triphosphate (IP3). This reduction of IP3-activity induces autophagy, independent of mTOR. In this context it is important to note that lithium chloride extends the lifespan of the nematode Caenorhabditis elegans, possibly by means of mitochondrial rejuvenation, which suggests that lithium exerts its effects on evolutionary highly conserved mechanisms. Intake of drinking water with comparable low lithium concentrations were found to be inversely correlated with all-cause mortality in a large epidemiological study in Japan. Hence a lack of lithium is linking aging and frailty (all increasing mortality) to disturbed autophagy, and AD to impaired AHN, and, thus, might represent another important and modifiable risk factor in this neurodegenerative disease. Traces of lithium can be ingested in some geographic areas by drinking local tap water or otherwise by consuming commercially available, mineral-rich spring waters, containing suitable concentrations of around 1 mg lithium per litre. Hence microdose lithium intake by means of one or two glasses of such water a day is not only of potential therapeutic value (see below) but also a safe preventive measure, by means of simply reducing an intake-deficit of an important novel trace element.”
“Taken together, besides the importance of IMF and physical exercise, also dietary MCTGs [medium-chain trigylcerides] can be an attractive (indirect) source of ketone bodies during the non-fasting state. The intake of coconut oil as a healthy source of MCTGs has additional positive effects on neuronal insulin resistance, neuroinflammation as well as Aβ-toxicity, improves the LDL/HDL-cholesterol quotient by increasing HDL, and ameliorates several others key progression factors of AD. Hence the use of virgin coconut oil is highly recommended as a safe and healthy alternative for polyunsaturated oils for frying and baking and butter and an important part of a comprehensive strategy for the prevention and treatment of AD.”