Lo and behold, shortly after sending out yesterday’s bulletin on fluoride & oxidative stress, I received the latest issue of the excellent quarterly journal FLUORIDE (2004; volume 37, issue 2). In this latest issue, there are a number of new studies (1-4) very relevant to the discussion of fluoride and oxidative stress.
Of particular interest was a study by Dr NJ Chinoy and colleagues from India, looking at fluoride and arsenic’s impact on the brain of mice (1).
As with Dr. Guan’s team at the Karolinska Institute (5, 6), and other researchers (7-12), Chinoy’s team found that fluoride increased the level of oxidative stress in brains of the fluoride-treated animals (1). The three main findings of the study were:
- Fluoride treatment decreased the level of anti-oxidant enzymes in the brain (e.g. catalase, GSH-PX and SOD). Anti-oxidant enzymes provide the body a natural defense against oxidative stress.
- Fluoride treatment increased the level of lipid peroxidation in the brain. Lipid peroxidation is an indicator of oxidative stress.
- These toxic effects were reduced by simultaneous treatment with antioxidant vitamins (vitamins C and E).
A possible connection with fluoride’s impact on Pineal Gland?
While not discussed by Chinoy (1), nor the other research teams investigating this issue (5-12), it is conceivable that some of the increased oxidative stress observed in fluoride-treated animals is related to fluoride’s impact on the pineal gland.
As was brought to light by a 1997 PhD dissertation from Jennifer Luke (from the University of Surrey in England) the pineal gland is a major magnet for fluoride accumulation within the body (13, 14). The heightened vulnerability of the pineal gland lies in the fact that it contains small crystals of a substance known as hydroxyapatite (the same substance found in bone and well known to accumulate fluoride). This is significant because the pineal gland, which is not protected by the blood brain barrier, has a very high perfusion rate of blood – hence the hydroxyapatite crystals within the pineal gland are continually exposed to fluoride circulating in the bloodstream.
Based on these factors, Luke hypothesized in the mid-1990s that the pineal gland would in fact be a target for fluoride accumulation. To test this hypothesis she analyzed the fluoride content of pineal glands taken from 11 human cadavers in England. Sure enough, when she conducted the analysis, she found very high – an average of 9000 parts per million (ppm) and up to 21,000 ppm! – levels of fluoride in the crystals of the gland (13, 14). Luke’s work was a breakthrough because prior to her analysis this fact had never before been known, if even considered.
But that’s only half the story. The other half involves the animal research that Luke conducted after finding the high levels in humans. Naturally, Luke was interested to find out what this high level of accumulation within the pineal gland may be doing to the functioning of this tiny, yet important, gland. In research Luke later conducted on mongolian gerbils (13), she found that fluoride exposure reduced the levels of melatonin in the gerbils (as measured by the metabolites of melatonin in the gerbils’ urine).
Melatonin, a hormone that regulates many activities within the body, including potentially the onset of puberty (15), is regulated in part by the pineal gland. Hence, Luke’s animal findings suggested that the fluoride accumulation within the gland, may in fact be interfering with the gland’s function – in particular its regulation of melatonin.
So, how does this potentially relate to the issue of oxidative stress in the brain?
Of melatonin’s many functions, one of it’s most important may be it’s role as a powerful anti-oxidant for the brain and other tissues – to help ward off and reduce oxidative stress (16-19). Thus, anything which can reduce the melatonin level in the body, would – by logical deduction – be expected to reduce the body’s defense against oxidative stress in the brain.
The potential significance of this can be glimpsed in the following statement from a recent review (18) concerning melatonin’s anti-oxidant’s properties:
“Since melatonin, the hormone secreted from the pineal gland has a remarkable anti-oxidant property and whose rate of production declines with increase in age, has prompted many to suggest that this hormone plays a crucial role in the genesis of neurodegenerative diseases.”
Of course, I am engaging in conjecture here, but the fluoride/pineal/oxidative stress connection may well be worth examining in future research. Can fluoride indeed reduce melatonin levels (13), and if so, is this related to a subsequent increase in oxidative stress? If yes, to what extent has this factor been involved in the repeatedly observed relationship (1, 4, 6, 7-12, 20-33) between fluoride and oxidative stress, both in animals and in humans?
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2) Jhala DD, et al. (2004). Reversible toxicity of fluoride and arsenic in ovary of mice. Fluoride 37: 71-79.
3) Nair SB, et al. (2004). Beneficial effects of certain antidotes in mitigating fluoride and/or arsenic induced hepatoxicity in mice. Fluoride 37: 60-70.
4) Wang A, et al. (2004). Antagonistic effect of selenium on oxidative stress, DNA damage, and apoptosis induced by fluoride in human hepatocytes. Fluoride 37: 107-116.
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