In my previous post, I asked the question "what's wrong with my thymus?" and got the answer "you have a hollow heart and the I'm trying to fill up the gap that has been created". Last night, I thought I'd try again with another question, namely "what happened to my gall bladder?" I was lying in bed preparing for sleep and the question was only asked half-heartedly but an answer came back as quick as a flash: "manganese".
This came as something of a shock because this single word clearly didn't emerge from my unconscious because I've never really thought about manganese or even read anything much about it. It occurred to me that there might have been some sort of interaction between the manganese compounds in my body and the fluoridated water that I was drinking in Brisbane at the time my gall bladder problem arose (late July of 2016). I resolved to investigate the matter further in the morning.
And I did. It turns out that:
- gallstones are often found in people with “lower levels of Vitamin E, manganese, and the amino acid methionine.”
- manganese “reacts with fluorine to give manganese(II) fluoride (MnF2) and manganese(III) fluoride (MnF3)”
https://www.britannica.com/science/manganese - “Manganese levels were determined in liver, kidney and bone (femur) of mice subjected for 16 weeks to 0 ppm (control), 10 ppm, 25 ppm, 50 ppm, 100 ppm and 200 ppm of fluoride in drinking water. Following fluoride ingestion, manganese levels were significantly reduced in liver (in 50, 100 and 200 ppm groups) and kidney (in 100 and 200 ppm groups). On the other hand, bone manganese levels were significantly elevated following ingestion of 25 ppm or more fluoride. The results suggest that excessive fluoride ingestion disturbs manganese metabolism.”https://www.sciencedirect.com/science/article/abs/pii/0048969782900717
Manganese does react with fluoride very readily and this information confirms what I'd already suspected: after twenty years in Asia, my body was not used to fluoridated water and reacted badly after a year of exposure to it. The lowered levels of manganese probably encouraged the growth of gallstones and eventually one obstructed the blood flow to my gall bladder, leading to the demise of that organ.
It's too late for my gall bladder but this ability to ask a question about a physical ailment and get an answer is intriguing. I've really only tried it two times now and I wondered if I can ask questions for other people and receive answers. I asked a question for a friend of mine who has small fibre neuropathy but who is also on antidepressants. I asked what would help his peripheral neuropathy and the answer came back "iodine" with an image of mixing bowl filled with a yellow powder. I did a little research as came back with:
- Peripheral Neuropathy: Iodine Deficiency can also damage the body's peripheral nerves. In this condition, one can face several issues, such as tingling in the hands or feet, sharp, stabbing pains, numbness in the hands or feet, thinning of the skin, drop in blood pressure and others. Source: https://www.news18.com/news/lifestyle/world-iodine-deficiency-day-some-common-consequences-of-hypothyroidism-2355177.html
- Some widely used psychoactive drugs, such as tricyclic antidepressants and antipsychotic phenothiazines exhibit iatrogenic effects on the thyroid. These side effects may arise from interactions at different steps of thyroid hormone biosynthesis. These drugs can induce a change in iodine capture by thyroid cells or can complex iodine, making it unavailable for thyroid hormone synthesis and thus decreasing thyroid hormone blood levels; they can also inhibit thyroid peroxidase activity and thus T3 and T4 synthesis or enhance deiodination of T4 to T3 or to Rt3 by stimulation of deiodinase activity. Moreover, tricyclic antidepressants interfere with the hypothalamic-pituitary-thyroid axis via the noradrenergic or serotonergic systems and might therefore decrease T4 or T3 blood levels, respectively. Phenothiazines can induce autoimmune hypothyroidism, as shown by an increase in the expression of the major histocompatibility complex antigen and by a production of antithyroglobulin or antithyroperoxidase antibodies. However, all these mechanisms are only speculative in humans, as they have only been demonstrated in vitro or in animal experiments. Clinically, thyroid function and affective disorders are closely linked. On one hand, the therapeutic response to antidepressants could be influenced by the thyroid status; on the other hand, the larger the thyroxin decrease induced by antidepressants, the better the therapeutic effect might be. Moreover, cotreatment with thyroid hormones and antidepressant drugs could allow either a decrease in the rate of treatment failure or a faster recovery from depression. As antipsychotic or antidepressant treatments are administered over long periods in humans, their thyroid toxic effects must be taken seriously. Source: https://pubmed.ncbi.nlm.nih.gov/9571980/
Figure 1
I'll continue experimenting with this (perhaps) new found ability and see what comes of it.
