Fluoride Action Network

Fluoride & the Pineal Gland: Study Published in Caries Research

By Paul Connett, PhD | March 27, 2001

The wheels of science grind very slowly. Finally, the first half of the work that was the subject of Jennifer Luke’s Ph.D. thesis; presentation in Bellingham, Washington (ISFR conference) in 1998 and a videotaped interview I had with her, has been published in Caries Research.

In my view this work is of enormous importance and could be (or should be) the scientific straw that breaks the camel’s back of fluoridation. Many of our subscribers are familiar with the details but let me repeat them here.

When Luke found out that the pineal gland – a little gland in the center of the brain, responsible for a very large range of regulating activities (it produces serotonin and melatonin) -was also a calcifying tissue, like the teeth and the bones, she hypothesized it would concentrate fluoride to very high levels. The gland is not protected by the blood brain barrier and has a very high perfusion rate of blood, second only to the kidney.

Luke had 11 cadavers analyzed in the UK. As she predicted she found astronomically high levels of fluoride in the calcium hydroxy apatite crystals produced by the gland. The average was 9000 ppm and went as high as 21,000 in one case. These levels are at, or higher, than fluoride levels in the bones of people suffering from skeletal fluorosis. It is these findings which have just been published.

It is the ramifications of these findings which have yet to be published. In the second half of her work she treated animals (Mongolian gerbils) with fluoride at a crack pineal gland research unit at the University of Surrey, UK (so there is no question about the quality of this work). She found that melatonin production (as measured by the concentration of a melatonin metabolite in the urine) was lower in the animals treated with high fluoride levels compared with those treated with low levels.

Luke hypothesizes that one of the four enzymes needed to convert the amino acid tryptophan (from the diet) into melatonin is being inhibited by fluoride. It could be one of the two enzymes which convert tryptophan to serotonin or one of the two which convert serotonin to melatonin.

Significance? Huge. Melatonin is reponsible for regulating all kinds of activities and there is a vast amount of work investigating its possible roles in aging, cancer and many other life processes. The one activity that Luke is particularly interested in is the onset of puberty. The highest levels of melatonin ( produced only at night) is generated in young children. It is thought that it is the fall of these melatonin levels which acts like a biological clock and triggers the onset of puberty. In her gerbil study she found that the high fluoride treated animals were reaching puberty earlier than the low fluoride ones.

We know from recent studies – and considerable press coverage – that young girls are reaching puberty earlier and earlier in the US. Luke is not saying that fluoride (or fluoridation) is the cause but her work waves a very worrying red flag. Fluoride’s role in earlier puberty needs more thorough investigation. Of an interesting historical note, in the Newburgh versus Kingston fluoridation trial (1945-1955), it was found that the girls in fluoridated Newburgh were reaching menstruation, on average, five months earlier than the girls in unfluoridated Kingston, but the result was not thought to be significant at the time (Schlessinger et al, 1956).

When one considers the seriousness of a possible interference by fluoride on a growing child’s pineal gland (and for that matter, elderly pineal glands) it underlines the recklessness of fluoridation. The precautionary principle would say, as would basic common sense, that you don’t take these kind of risks with our children for a benefit which, at best, amounts to 0.6 tooth surfaces out of 128 tooth surfaces in a child’s mouth (Brunelle and Carlos, 1990, Table 6).

To read Luke’s PhD thesis, click here.

Paul Connett