The Mystery of Declining Tooth Decay

Abstract

Large temporal reductions in tooth decay, which cannot be attributed to fluoridation, have been observed in both unfluoridated and fluoridated areas of at least eight developed countries over the past thirty years. It is now time for a scientific re-examination of the alleged enormous benefits of fluoridation.

Full text

NATURE
VOL.
322
IO
JULY
1986
I25
mystery
of
declining
tsot~.
decay
from
Mark
Diesendorf
Large temporal reductions in tooth decay, which cannot be attributed tofluoridation, have been observed
in
both unfluoridated andfluoridated areas
of
at
least eight developed countries over the
past
thirty
years. It is now time for a scientlfic re-examination
of
the alleged enormous benefits
of
jluoridation.
FLUORIDATION
consists of raising the
concentration of the fluoride ion
F-
in
water supplies
to
about
1
part per million
(p.p.m.) with the aim of reducing dental
caries (tooth decay) in children.
In
fluori-
dated areas, there are now many longi-
tudinal (temporal) studies which record
large reductions
in
the incidence ofcaries‘.
The results of these and
of
fixed time
sur-
veys have led
to
the ‘fluoridation
hypothesis’, namely that the principal
cause of these reductions
is
fluoridation.
Until the early
1980s,
there had been
comparatively few longitudinal studies
of
caries in unfluoridated communities. Only
a
small minority of the studies in fluori-
dated areas had regularly examined con-
trol populations, and there seemed to be
little motivation to study other unfluori-
dated communities. But during the period
1970-81,
especially in western Europe
where there is little fluoridation,
a
number
of
dental examinations were made and
compared with surveys carried out a
decade
or
so
before. It
soon
became clear
that large reductions in caries had been
occurring in unfluoridated areas (see
below). The magnitudes
of
these reduc-
tions are generally comparable with those
observed in fluoridated areas over similar
periods of time.
In
this article, these reductions are
reviewed and attention
is
also
drawn
to
a
second category of canes reduction which
cannot be explained by fluoridation. This
category
is
observed in children described
by proponents
of
fluoridation
as
having
been ‘optimally exposed’, that
is,
children
who have received water fluoridated at
about
1
p.p.m. from birth. The observation
is
that caries
is
declining with time in
‘optimally exposed’ children of
a
given
age.
In
some cases, the magnitudes
of
these reductions are much greater in per-
centage
terms
than the earlier reductions
in the same area which had been attributed
to fluoridation.
The problem of explaining the two
categories
of
reduction goes well beyond
the field
of
dentistry: contributions from
nutritionists, immunologists, bacteriol-
ogists, epidemiologists and mathematical
Table
1
Studies reporting large reductions
in
dental caries
in
unfluoridated areas
Location Years surveyed
iustralia
Denmark
Holland
New
Zealand
Norway
Sweden
United
Kingdom
United States
Brisbane
Sydney
Various towns
The Hague
Various towns
Auckland (parts)
Various towns
Various towns
North Sweden
Bristol
Bristol
Devon
Gloucestershire
Isle
of
Wight
North- West England
Scotland
Shropshire
Somerset
Somerset
Dedham, Mass.
Nonvood, Mass.
Massachusetts: sample
of
schools
Ohio
1954, ’77
1961,
’63,
‘67
1972, ‘79
1969, ‘72, ‘75, ’78
1966, ‘743 ‘81
1970,
’80
1973. ’78, ’81
1967, ’77
1970, ‘79
1973, ‘79
1971, ‘81
Annually
from
1964
1971, ‘80
1969, ’80
1970, ’80
1970, ‘80
1975-79
annually
1963-19
1955.
’74
1958, ’72, ’78
1951,
’51
1972, ’78
1965, ’80
References
2,
3
4
53
38
11
12
54
39
55
56
56
37
37*
57
58
59
10
60
61
40
40
41
62
*
Unpublished communication
from
i.
Tee
(1950).
Area
Dental Officer, Gloucestershire,
to
R.
J.
Anderson
er
a[.)’
statisticians, amongst others, may be
required.
Caries in unfluoridated areas
Table
1
lists over
20
studies which report
substantial temporal reductions in caries
in children’s permanent teeth in
unfluori-
dated areas of the developed world.
In
many
of
these cases, the magnitudes
of
these reductions are comparable with
those observed in fluoridated areas and
attributed
to
fluoridation.
Several of these studies give clues as to
factors which are unlikely
io
be
the main
causes of the reductions. A comparison of
the
1954
and
1977
dental health surveys
in Brisbane’,’ indicates to
a
reduction of
about
50%
in caries, as measured by the
number of decayed, missing and filled per-
manent teeth
(DMFT)
per child and
averaged over the age groups, in the
23-
year period. The
1977
survey distinguished
between children who took fluoride tablets
regularly, irregularly
or
not at all.
Although there were differences in canes
incidences between the three categories
(which could reflect factors unrelated to
fluoride levels), even the
“no
tablet” group
had
on
average
40%
less caries experience
than that recorded in
1954.
So
fluoride
tablets were
not
the principal cause
of
the
reductions observed in Brisbane.
The first Sydney study‘ showed that
children with “naturally sound” teeth
increased from
3.8%
in
1961
to
20.2%
in
1967
and
28%
in
1972.
The paper, which
was titled enthusiastically “The Dental
Health Revolution”, was originally used
widely to promote fluoridation
in
Aus-
tralia. The authors stated that: “Almost
certainly, the availability
of
fluoride both
in tablet form and delivered through town
water supplies has been the predominant
factor.
. .
.
These very large reductions rep-
resent
a
modern triumph
of
preventive
health care’’4. Yet the major proportion
of
the reported improvement had already
occurred before Sydney was fluoridated
in
1968.
Moreover,
no
evidence was pres-
ented that fluoride tablets were widely
used in the
1960s.
Fluoride toothpaste
was
only introduced into Australia in
1967’.
Although the index “naturally sound”
teeth
is
unsuitable for more detailed

126
COMMENTARY
..l
3
v~ar
4
1963
69
71
72
79
Year
Fig.
1
Decline in caries, as measured by
DMFT,
in Tamworth, Australia, for children in age
groups 6 years to 13 years. Data compiled from refs
14,
15. The vertical line cutting graph for
each age group denotes year at which maximum possible benefit from fluoridation was reached.
Tamworth
was fluoridated in 1963.
studies which disringuish decayed, miss-
ing and filled teeth, the populations
examined were very large (over 9,000
children at each examination) and the
results clear-cut.
Asecond Sydney study’ used the DMFT
index, but was irrelevant for establishing
any link with fluoridation, since it reported
only
on
examinations in 1963 and 1982,
but not around 1968 when Sydney was
fluoridated. As in several other fluorida-
tion studies, the key data were either not
collected
or
not reported6. Although the
two Sydney papers have an author in com-
mon (James
S.
Lawson, a senior officer
of
the New South Wales Health Com-
mission), the second paper does not even
cite the first. This suggests that, once it
became clear that the first Sydney study
contained evidence unfavourable to fluori-
dation, it was
a
source of embarrassment
to some fluoridation proponents who are
apparently trying to denigrate it.
However, independent confirmation of
the large reductions in caries before
fluori-
dation reported in the first Sydney study4
is readily obtained by comparing the
results
of
two separated by 20
years by Barnard. These surveys showed
that the mean
DIMF
index
(‘1’
denotes a
permanent tooth which cannot be
resto_red)-for school children aged
13
and
14
declined from
11.0
in
1954-55
to
6.0
in
1972. The four years from 1968, when
fluoridation commenced in Sydney, to
I
1972, would not have contributed sig-
nificantly to the decline in caries preva-
lence in this age group’.
The authors of one of the British
studies” cited in Table
1
point
out
that
sales of fluoride toothpaste in the United
Kingdom were less than
5%
of total sales
in
1970,
but rose to more than 95%
of
sales in 1977. They quote unpublished
annual data from unfluoridated parts
of
Gloucestershire, collected from 1964
onwards, which show substantial
improvements in children’s teeth before
the use
of
fluoride toothpaste became
significant.
Many of the studies in the Netherlands
reviewed by Kalsbeek“, were carried
OUI
to evaluate the effectiveness
of
the schoo
NATURE
VOL.
322
10
JULY
1986
iental health programme. Temporal
:eductions in
DMFT
of about
50%
occur-
red between 1970 and 1980, whether
or
not
the
children had taken part in the
dental health education
program.
Kalsbeek
also
reviewed the use
of
fluoride
tablets and toothpaste and concluded
from the data that “factors other than the
effects
of
different fluoride programmes
must play
a
role.”
The study in the partly fluoridated city
of Auckland, New Zealand’*, examined
the influence of social class (which reflects
environmental and lifestyle factors, such
as diet) as well as fluoridation
on
dental
health as measured by the levels of dental
treatment received by children. The paper
showed that treatment levels have con-
tinued to decline
in
both fluoridated and
unfluoridated parts of the city and that
these reductions are related strongly to
social class, there being less caries in the
“above average social rank” group than
in other children.
Thus
the main ethical
argument for fluoridation, that it should
assist the disadvantaged, is not borne out
by this study.
Fluoridation’s
benefits
On
15
December 1980, the Dental Health
Education and Research Foundation, one
of
the main fluoridation promoting bodies
in New South Wales (NSW), issued a
press release entitled, “Fluoridation
dramatically cuts tooth decay in Tam-
~orth”’~. This document, which highlight-
ed results of a study conducted by the
Department of Preventive Dentistry,
Sydney University, and the Health
Corn-
mission
of
NSW,
stated in part:
Tarnworth’s water supply was fluoridated in
1963, and the last survey
in
the area
was
conducted in August 1979. It shows decay
reductions ranging
from
71%
in 15-year-olds
to 95% in 6-year-olds..
. .
All
those surveyed
were continuous residents using town water.
The
“95%
”
reduction actually correspon-
ded
to
a reduction in DMFT from
1.3
in
1963 to 0.1 in 197914, which is 92%. The
press release implied incorrectly that all
this reduction was due to fluoridation.
However,
it
has been claimed ever since
Table
2
Extent of fluoridation in Australia, 1977 and 1983
%
Of
state
%
Of
state
Year city fluoridated? fluoridatedi
State
or
territory Capital city fluoridated*
in
1977 in 1983
Canberra
1964
100
100
Tasmania Hobart 1964 74
77
ACT
NSW Sydney 1968
61
81
WA
Penh
1968 83 83
SA
Adelaide 197 1 71
70
Victoria Melbourne 1977
0.7
then
73
71
Queensland Brisbane
Not
10
5
fluoridated
*
Each capital city has the majority of the population
of
its state
or
territory.
t
That is, the percentage
of
population of state/territory which drinks fluoridated water. Data
from Annual Reports of Director-General
of
Health,
for
example ref. 17.
r
t
r
t
>
\
t
r
6
1
t
L
a
F
e
1
fl
fl
C
\1
C
tc
c
fc
b
b
a
0
U
IT
0
tc
W
)I
P
Ir
51
T
Ct
PI
Ct
e>
ss
dc
ar
0:
rii
of
re
P‘
MI
FI
te
fit
(7
SC
Iai
19
flu
u
i
0:
thl
\?
h.i
ap
is
ez.

I%6
_-
)oral
:cur-
:r
.ram.
,ride
uded
n
the
nmes
I\
i
city
lined
,fleets
such
lental
lental
paper
con-
d and
i
that
in the
than
:thical
;hould
ne out
glY
to
Health
m,
one
bodies
sued
a
id
;blight-
by the
ntistry,
I
Com-
dated
in
:
rea
was
;
1s
decay
:
ear-olds
’
I
u
rv
e
y
e
d
n
water.
respon-
n
1.3 in
Yo.
The
that all
idation.
er since
state
iated?
983
0
1
1
3
0
1
5
ater. Data
COMMENTARY
NATURE
VOL.
322
IO
JULY
1986
the commencement of fluoridation that the
maximum possible benefits from fluorida-
tion are obtained in children who have
drunk fluoridated water from birth.
Six-
year-olds would have done this by 1969,
when, according to the published data”,
they had
a
DMM index of 0.6. The further
reduction in caries in optimally exposed
6-year-olds, observed in years following
1969, cannot be due to fluoridation.
Thus,
one can say that at best fluorida-
tion could have approximately halved the
DMFT
rate in 6-year-olds between 1963
and 1969. (Since there was
no
control
population, one could also say that at
worst fluoridation might have had
no
effect in that period.) But from 1969 to
1979, caries in 6-year-olds was reduced a
further 83%, by some other factor(s) than
fluoridation.
Figure
1
shows that the unknown factors
caused in children of each age from
6
years
to 9 years similar large reductions in caries.
Unfortunately, there are
no
published data
for Tamworth beyond 1979
or
in the years
between 1972 and 1979, and
so
it cannot
be confirmed whether the large reductions
obser~edl~.~~ from 1972 to 1979 in children
aged
IO
to
15
were also due to these
unknown factors.
A similar reduction beyond the
maximum possible for fluoridation is
observed for children of each age from 6
to 9 in the published data from CanberraI6,
which cover the period from 1964, the
stated year of fluoridation, to 1974. In
particular,
DMFT
rates declined by 50%
in 6-year-olds from 1970 to 1974 and by
54%
in 7-year-olds from 1971 to 1974.
These reductions in optimally exposed
children cannot be due to fluoridation.
Published post-1974 data are needed to
check
on
further reductions in optimally
exposed children aged over
9
years.
From 1977 onwards, data have been
systematically collected from the school
dental services in each Australian state
and territoryg*”. Table 2 shows the degree
of fluoridation in each of these states/ter-
ritories in 1977 and 1983 and
also
the dates
of
fluoridation
of
the capital cities
of
these
regions. Each of these cities dominates the
population of the state
or
territory in
which it lies. The evidence presented in
Fig. 2 and Table 2 suggests that states and
territories which had been extensively
fluoridated for
at
least 9 years before 1977
(Tasmania, Western Australia and New
South Wales) had qualitatively similar
large reductions
in
caries
from
1977
to
1983 as a state which was only extensively
fluoridated in 1977 (Victoria) and a state
which had a small and declining fraction
of fluoridation (Queensland). Although
the results of the school dental health sur-
vey are recorded by age and state, the data
have only been publi~hed~~~~*~*
so
far for
ages 6-13 averaged in each state, or for
each age for the whole
of
Australia. There
is
evidence that the use of fluoride tooth-
m
u
c
m
=
3-
a
x
al
v)
?
;
2-
U
IIIII
1977
78
79
80
GI
82
83
Year
Fig.
2
Decline
in
the average
number
of
(per-
manent)
teeth
per
child with caries
experience
in
each
Australian
state and
the
Australian
Capiral Territory
as
observed
in
school
dental
services‘7.
‘Caries
experience’
can
be
one
or
more
decayed,
missing
or
filled teeth, and
con-
sists
of
an
average
for
children
aged
6-13
years.
See
Table
2
for
information
on
the
extent
of
fluoridation
in
each
stare/territory
in
1977
and
1983
and the
year
when
the
main
population
centre
of
each
state/territory
was
fluoridated.
x,
Victoria;
0,
Tasmania;
0,
Queensland;
-
-
-
ACT.
---
SA;
-,
NSW;
--,
WA;
.--.--.,
paste in Australia reached
a
high plateau
around 1975,
so
these observed reductions
in caries can be due neither to fluoride
toothpaste’
nor
to fluoridated water.
It is to be hoped that similar data
on
caries reductions in “optimally exposed”
children will be sought in other fluoridated
countries.
In
a
region of Gloucestershire,
United Kingdom where the main water
supply was naturally fluoridated with
0.9 p.p.m. fluoride until 1972, reductions
in canes of
5
1% were observed in 12-year-
old children between 1964 and 197919.
Factors other than fluoridated water must
have caused these reductions. After 1972,
the main water supply was drawn from a
bore with less than 0.2 p.p.m. fluoride,
so
a recent survey of caries there would be
of great interest.
Benefits overestimated?
In some fluoridated areas (for example
Tamworth, Australia), temporal reduc-
tions in caries have been wrongly credited
to fluoridation. The magnitude of these
reductions is similar in both fluoridated
and unfluoridated areas, and is also gen-
erally comparable with that traditionally
attributed
to
fluoridation. Can it be
con-
cluded that communities which prefer not
to fluoridate, either because of concern
about potential health
or
for
ethical reasons (for example compulsory
medication; medication with an uncon-
trolled dose), do not necessarily face
higher levels of tooth decay than fluori-
dated communities?
In
other words, is it
reasonable to ask whether it could be gen-
erally true that a major part of the benefits
121
currently attributed to fluoridation is
really due to other causes’?
Such a hypothesis would seem
to
be
possible in principle because
it
is
well
known that fluoridation is neither
‘necessary‘
nor
‘sufficient’ (the words
between inverted commas being used in
the formal logic sense) for sound teeth;
that
is, some children can have sound teeth
without fluoridation, and some children
can have
very
decayed teeth even though
they consume fluoridated water-’.
To confirm
or
refute the hypothesis,
it
is necessary (but not ‘sufficient’) to
examine the absolute values of caries
prevalence in fluoridated and unfluori-
dated areas.
If
it is true that the absolute
values of caries prevalence in some
unfluoridated areas are comparable with
those in some unfluoridated areas of the
same country, then the hypothesis is sup-
ported (but not proven), and there would
be
a
strong case for the scientific re-
examination of the epidemiological
studies which appear to demonstrate large
benefits from fluoridation.
The earliest set
of
studies comparing
caries
in
fluoridated and unfluoridated
areas were time-independent surveys of
caries prevalence in areas with ’high’
natural levels of fluoride in water supplies,
conducted by
H.
T.
Dean and others in
the United States’6. The surveys purported
to show that there is
an
“inverse relation-
ship” between caries and fluoride con-
centration. From the viewpoint of modern
epidemiology, these early studies were
rather primitive. They could be criticized
for the virtual absence of quantitative,
statistical methods, their nonrandom
method of selecting data and the high
sensitivity of the results to the way in
which the study populations were
grouped”.
Results running counter to the alleged
inverse relationship have been reported
from time-independent surveys
in
naturally fluoridated locations
in
India”,
Sweden”, Japan2g, the United States” and
New Zealand31.63. The Japanese survey’9
found
a
minimum in caries prevalence in
communities with water F-concentrations
in the range 0.3-0.4 p.p.m.; above and
below this range, caries prevalence
increased rapidly.
These
survey^^'-^^
also
selected their
study regions nonrandomly. But recently
Ziegelbecker3’ attempted to make
a
selec-
tion close
to
a
random sample by consider-
ing
‘all’
available published data
on
caries
prevalence
in
naturally fluoridated areas.
His
large
data set, which includes Dean’s
as
a sub-set, comprises 48,000 children
aged 12-14 years drawn from 136 com-
munity water supplies in seven countries.
He found essentially
no
correlation
between caries and
log
of fluoride con-
centration. The are generally
omitted from lists‘ of studies
on
the role
of fluoridation in caries prevention.

NATURE
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322
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JULY
1986
COMMENTARY
128
E
9
10
11
12 13
14
Age
in
years
Further evidence can be drawn from
Fig.
2.
In
1983, the absolute value of caries
prevalence in the Australian state of
Queensland (which is only
5%
fluori-
dated) was approximately equal to that in
the states of Western Australia (83%
fluoridated) and South Australia
(70%
fluoridated).
The classical British fluoridation trials
at Watford and Gwalchmai were longi-
tudinal controlled studies.
In
this regard
they were better designed than the major-
ity
of other studies which have been con-
ducted around the world. However, as in
the case of almost
all
other surveys, the
examinations were not ‘blind’. The review
of the British trials by the
UK
Department
of Health after
11
years of fluoridation
showed that children in fluoridated towns
had approximately one less DMFT (that
is,
essentially one less cavity) than children
of the same age in unfluoridated towns
(see Fig. 3). The rate of increase in caries
with age was the same in both popula-
tion~~~.
Thus
there are a number of counter-
examples to the widely-held belief that
“All
studies show that communities where
water contains about 1 p.p.m. fluoride
have about
50%
lower caries prevalence
than communities where water has much
less than
1
p.p.m. fluoride”.
At this point the empirical data presen-
ted here may be summarized as follows.
In
the developed world:
(1)
there have been large temporal reduc-
tions in caries in unfiuoridated areas of at
least eight countries;
(2)
there have been large temporal reduc-
tions
in
several fluoridated areas which
cannot be attributed
to
fluoridation;
(3) the absolute values
of
caries preva-
lence in several fluoridated areas are com-
parable with those in several unfluoridated
regions of the same country.
Hence there is a case for scientific re-
examination
of
the experimental design
Fig.
3
The
variation
with
age
of
decayed,
miss-
ing
and
filled
permanent
teeth
(DMFT)
in
fluoridated
test
towns
(x)
and unfluoridated
control
towns
(0)
in
Britain,
graphed
from
data
published
by
the
UK
Department
of
Health3’.
Note
that
the
rate
of
increase
of
DMFT
is
essentially the same
in
both groups. Children
in
the
fluoridated areas
have
an
average
only
one
less
cavity
than
children
of
the
same
age
in
the
unfluoridated areas
md statistical analysis of those studies
which appear to prove or “demonstrate”
:hat fluoridation causes large reductions
in
caries. Indeed the few re-examinations
which have already been done confirm
that there are grounds for concern.
The original justification for fluorida-
tion
in the United States, Britain, Canada,
Australia, New Zealand and several other
English-speaking countries was based
almost entirely
on
the North American
studies, which were of two kinds. The limi-
tations of the first set, the time-indepen-
dent surveys conducted in naturally
fluori-
dated areas of the United States’6, have
been referred
to
above.
The second set of North American
studies consists of five longitudinal
studies-carried out at Newburgh, Grand
Rapids, Evanston and Brantford (two
studies)-which commenced
in
the mid-
1940s. Only three of them had controls for
the
full
period
of
the study. These studies
were criticized rigorously in a detailed
monograph by S~tton~~,
on
the grounds
of inadequate experimental design (for
example,
no
‘blind’ examinations and
inadequate baseline measurement), poor
or
negligible statistical analysis and,
in
particular, failure to take account of large
variations in caries prevalence observed
in the control towns. The second edition
of Sutton’s monograph contains reprints
of replies by authors of three of the North
American studies and another author
together with Sutton’s comments
on
thesr
replies.
It
is difficult to avoid the
con.
clusion that Sutton’s critique still stands
Indeed, this was even the view of the pro.
fluoridation Tasmanian Royal Com
mission35. Yet, in major, recent review!
of fluoridation, such as that by tht
British Royal College of
physician^'^
these North American studies are stil
referred to as providing the foundation!
for fluoridation, and Sutton’s
i:
not cited.
An examination has just been comp-
eted of the experimental design of all of
he eight published fluoridation studies
:onducted in Australia. One (Tasmania)
s
a time-independent survey.
Four
Townsville, Perth, Kalgoorlie and the
iecond Sydney study) are longitudinal
itudies with only two examinations of the
est group and either
no
control
or
only a
;ingle examination of a comparison group.
The remaining three studies (Tamworth,
Zanberra and the first Sydney study) have
ieveral examinations of the test group, but
IO
comparison group at all. Thus there
ias not been a single controlled longi-
.udinal study in Australia. (M.D., to be
ublished). Moreover, it has been shown
ibove that three of the Australian studies
:the first Sydney4, Tamw~rth’~”~ and
Can-
)erra16) inadvertently provide evidence
:hat some other factor(s) than fluoridation
ls/are playing an important role in the
jecline of caries prevalence.
Hence the hypothesis that fluoridation
has very large benefits requires re-
examination by epidemiologists, mathe-
matical statisticians and others outside of
the dental profession. The danger of fail-
ing to perform scientific research
on
the
mechanisms underlying the large reduc-
tions in caries discussed in this paper is
that the strong emphasis
on
fluoridation
and fluorides may be distracting attention
away from the real major factors. These
factors could actually be driving a cyclical
variation of caries with time3’. It is poss-
ible that the condition
of
children’s teeth
could return
to
the
poor
state observed in
the
1950s.
even in the presence of a wide
battery
of
F-treatments.
Causes
of
caries
reductions
Many of the authors who reported the
reductions in unfluoridated areas ac-
knowledged that the explanation has
not
yet been determined scientifi~ally’’~~~-~’.
It is after all much easier to perform a
study which measures temporal changes
in the prevalence of a multifactorial dis-
ease than to identify the causes of such
changes.
Nevertheless, the authors of some
of
these studies have speculated that impor-
tant causes of the reductions which they
observe might be topical fl~orides~~.’~
(such as in toothpastes, rinses and gels),
fluoride
tablet^^.^',
school dental health
programmes9, a lower
frequency
of
sugar
intake39, the widespread use of antibiotics
which may be suppressing
Srreprococcus
muruns
bacteria in the mouth“, the
increase in total fluoride intake from the
environment9.“?,
or
a cyclical variation in
time resulting from as yet unknown
causes’’.
The present overview has revealed that
several
of
the studies contain evidence
against some of these proposed factors.
We have seen that the Brisbane study3 and

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md
IZY
COMMENTARY
NATURE
VOL.
312
IO
JULY
19x6
the Dutch review" suggest that fluoride
tablets may not be important; the Sydney
study', one of the British studies'' and the
Dutch review" each provides evidence
against fluoride toothpaste; and the Dutch
review" found
no
benefit in their school
dental health education programmes.
Although there is evidence that fluoride
toothpaste cannot be
an
important
mechanism of caries reduction in some
of
the studies reported here, it must be stated
that, unlike the case
of
fluoridation, there
are also
a
few well-designed randomised
controlled trials which demonstrate sub-
stantial reductions in caries
from
fluoride
to~thpaste~~. Hence, the hypothesis can
be made that topical fluorides sometimes
improve children's teeth, although they
are not necessary.
So
topical fluorides may
comprise one
of
several factors contribut-
ing to the solution of the scientific problem
of
explaining the reduction in tooth decay.
Leverett4* has speculated that the caries
reductions in his smaller set of unfluori-
dated locations may be due to
"an
increase
in fluoride in the food chain, especially
from the use
of
fluoridated water in food
processing, increased use
of
infant for-
mulas with measurable fluoride content,
and
even unintentional ingestion of
fluoride dentifrices." This hypothesis can-
not explain the reductions in prefluorida-
tion Sydney4,
or
those in unfluoridated
parts
of
Gloucestershire which started in
the late
1960~'~.
The ingestion
of
fluoride
toothpastes (and gels) by young children
is well documented and could account
for
an intake of about
0.5
mg
F-
per day in
the
very
young-. But the food processing
-
pathway is unlikely to be significant in
western Europe where there is hardly any
fluoridation, and infant formulas which
are made up with unfloridated water will
give only small contributions. Thus
it
appears that Leverett's hypothesis may at
best be relevant to
a
minority
of
the studies
listed in Table
1.
Here, the working hypothesis is presen-
ted that fluoridation and other systemic
uses of fluoride, such
as
fluoride tablets,
have at best
a
minor effect in reducing
caries; that the main causes of the
observed reductions in caries are changes
in dietary patterns, possible changes in the
immune status of populations and, under
some circumstances, the use
of
topical
fluorides. Indeed,
a
promising explanation
is
that the apparent benefit from fluorides
is derived from their topical action. Then,
since fluoridated water has
a
fluoride ion
concentration
lo-'
times that
of
fluoride
toothpaste, its action in reducing caries is
likely to be much weaker.
It is known that immunity plays
a
role
in the development of caries,
as
it
does
with other diseases. Research is currently
in progress to try to develop
a
vaccine
against ~aries'~-~~. None
of
the data pres-
ented in the present paper provides
evidence against immunity
as
a
factor.
Dentists often argue against changes in
dietary patterns
as
a
major factor,
on
the
grounds that sugar consumption has
remained approximately constant in most
developed countries over the past few
decades. However, this
is
a
simplistic argu-
ment. First, crude industry figures
on
total
sales of sugar
in
developed countries
con-
tain
no
information
on
the distribution of
sugar consumption with age and time of
day. The form
of
sugar ingested-for
example in canned food, soft drinks
or
processed cereals-may
also
be important.
Second, tooth decay is increasing together
with increases in sugar and other ferment-
able carbohydrates in the diet
in
several
developing co~ntries~~.~~. This was also
the case with Australian aborigines, even
when their water supplies consisted of
bores containing fluoride at close to the
"optimal" concentration for the local cli-
mate50.51
Third, there is more
to
diet than
sugar.
For
instance, there is some
evidence, even conceded occasionally by
pro-fluoride bodiess2, that certain foods
which do not contain fluorides
(for
example wholegrain cereals, nuts and
dairy products) may protect against tooth
decay.
So
the whole question
of
the
relationship between total diet and tooth
decay needs much greater input from
nutritionists and dietitians.
Perhaps the real mystery
of
declining
tooth decay is why
so
much effort has gone
into poor quality research
on
fluoridation,
instead of
on
the more fundamental ques-
tions of diet and immunity.
The main body
of
this research was
performed while the author was
a
prin-
cipal research scientist in the CSIRO
Division
of
Mathematics and Statistics,
Canberra.
0
Mark Diesendorf is ai the
Humon
Sciences
Pro-
gram,
Atrsrralian
National University,
GPO
Box
4,
Canberra
ACT
2601,
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'
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