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The following letter is in response to the recently
released York Review.
The writer, Paul Connett, was a peer reviewer of the study. A synopsis
of the York Review can be accessed on the web at http://www.bmj.com/cgi/content/full/321/7265/855
October 11, 2000
Letters-to-the-Editor,
British Medical Journal
Dear Editor,
As an invited peer reviewer of the York Review of fluoridation,
please permit me to add a few concerns about this report and the
spin it has been given in the press. While a number of people have
correctly pointed out that this York Review deals a very serious
blow to water fluoridation based upon the findings of a much lower
benefit for caries reduction than claimed by promoters, and a much
higher level of dental fluorosis than is acceptable, I am very disturbed
that the authors are not making it clear that dental fluorosis is
in fact an indication of a toxic effect of fluoride, in a similar
fashion that the blue line on gums was an early indicator of lead
poisoning. The fact that neither tooth mottling nor the blue line
causes any obvious pain is beside the point. Tooth mottling indicates
that fluoride has poisoned the enzyme involved in removing protein
from between the mineral prisms prior to enamel formation (DenBesten,
1999). It raises - or should raise -the obvious question of what
other enzymes might have been poisoned by fluoride which have no
visible effects. British researcher Jennifer Luke (1998) may have
answered this question in her Ph.D thesis. It would appear that
fluoride accumulates in the human pineal gland and experiments in
animals indicate that fluoride lowers melatonin levels. Unfortunately,
the York reviewers didn't consider Luke's work, nor others' work
on the thyroid gland or many animal experiments conducted over the
last 10 years which wave very large red flags of concern about fluoride's
potential health effects. I have reviewed many of these concerns
elsewhere (see www.fluoridealert.org).
Turning to an issue that the York team did examine, the authors
claim that there is no evidence of a relationship between increased
hip fracture in the elderly and exposure to fluoride in drinking
water. I feel that properly interpreted the current literature provides
considerable evidence of such harm.
Paul Wilson of the York team is quoted in an Associated Press report
(Oct 5, 2000) as saying that "the studies he examined tracked
the effects of up to 4 mg per liter in drinking water". This
is not accurate. In their review of hip fracture the York team included
an unpublished study by Li et al (1999) which they indicated showed
no association between fluoride and hip fracture. The York team
was only able to draw this conclusion because they limited their
comparison to hip fractures in the village with low fluoride levels
with the hip fractures at 1 ppm (i.e. 1 mg per liter). When I reviewed
this study, as part of my invited review, I found Li et al examined
the hip fracture rates in six Chinese villages with different water
fluoride concentrations: 0.25 - 0.34 ppm; 0.58 - 0.73 ppm; 1.00
- 1.06 ppm; 1.45 - 2.19 ppm; 2.62 - 3.56 ppm, and 4.32 - 7.97 ppm.
The authors chose the village with 1 - 1.06 ppm fluoride for their
baseline for comparison. Their reported odds ratios for hip fracture
were 0.99; 1.12; 1.00 (control); 2.13; 1.75 and 3.26. In other words
they found an approximate doubling of the hip fracture rate for
fluoridation levels over 1.5 ppm and tripling for water levels over
4 ppm.
In my view, the York team did a disservice by confining themselves
to hip fractures in villages with fluoride concentrations at 1 ppm
or below. Paul Wilson compounds this disservice by claiming that
they actually considered studies which looked at effects up to 4
ppm (4 mg per liter), when in this critical case they clearly did
not.
Paul Wilson further distorts the scientific record when he claims
in the same AP report that, the fear of osteoporosis has never been
based on strong evidence. In actual fact, since 1990 there have
been 18 studies (4 unpublished, including one abstract) which have
examined a possible association with hip fracture in the elderly
and fluoride in the drinking water. 10 of these found a positive
association (increased hip fracture rates) and 8 did not. Moreover,
these studies were prompted by the fact that when fluoride (50 -
80 mg per day) was used to treat patients with osteoporosis in an
effort to harden their bones and reduce fracture, it was found that
the treatment increased not decreased hip fracture rates (Hedlund
and Gallagher, 1989 and Riggs et al, 1990). The fact that 50% of
all the fluoride that we swallow accumulates in our bones should
give us pause. Increased hip fracture in the elderly is not a minor
problem. One in four of those suffering a hip fracture in the U.S.are
dead within a year of their treatment and one in two never regain
an independent existence.
It is unfortunate that the York team has managed to convey the message
that there is "no evidence of harm" when in actual fact
there is "mixed evidence of harm". A critical difference.
They also beg the question of how one should resolve mixed epidemiological
findings when one is giving advice to a government which is considering
putting a toxic substance into the drinking water of every man,
woman and child in the population. The precautionary principle says
"If in doubt, leave it out". As far as hip fractures are
concerned, the York Team says, based upon meta-analysis of a mixed
bag of poor studies, we find no evidence of harm. Not very reassuring
and not very helpful when they themselves avoided the key piece
of dose-response evidence presented by Li and co-workers.
Dr. Paul Connett,
Professor of Chemistry,
St. Lawrence University, Canton, NY 13617.
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