My initial interest is largely attributed to a
recent
Swedish book [1]. Although I remain skeptical to many suggestions given
there (and in many other "saved patient's books"), I am not so certain
that this aspect can be regarded unimportant. The mercury load may not
be so impressive in most cases - and may indeed be so in singular ones.
Amalgam is widely dissepated among people and can only
be considered one among several factors which worsens MS in predisposed
persons but not strictly a causative factor. It has been used in
dentristy
since its invention in 1833 (mercury already since 1819 in other
combinations),
was forbidden the first time in New York in 1839 but returned in 1855.
In 1898, a case of mercury neurosis caused by amalgam fillings was
published.
In Germany, 1928, Alfred Stock tried to get amalgam fillings prohibited
- as we know in vain [1]. In 1966, Baasch suggested a connection
between
amalgam and MS and thereby opened an emotional discussion
pro-&-contra
[2,3]; for discussion is referred to some review articles [4,5]. In a
Swedish
publication, Ahlot-Westerlund found an 8-fold increase in the mercury
levels
in MS. Firnhaber et al. [6] found that 51 MS patients suffered more
recently
from carious teeth than a "control group" of 51 epileptics. Ingalls [7]
suggests the amalgam causality and makes aware that a second heavy
metal,
lead, may operate almost interchangeable with mercury. Siblerud et
al.
[8] found a depressed red blood cell picture, decreased thyroxine and
se-IgG
levels, increased blood urea nitrogen level and fewer T-lymphocytes and
T-8 (CD8) suppressor cells in MS patients with amalgam fillings
preserved
compared to MS patients who had their amalgam removed. Hair mercury was
higher in the amalgam group. In the amalgam group there were 33.7% more
exacerbations during the last 12 months.
Huggins and Levy [9] found dramatic changes of
photolabelling
of cerebrospinal fluid proteins following these dental interventions.
They
gave an exellant explanation of mercurys neural toxicology which is
reproduced
in the following:
" ... mercury is released from dental amalgam in the
form of Hg0 ... [this] is more likely than Hg2+
to
concentrate in the CNS after it has passed the blood-brain barrier ...
Once in the brain, it is oxidized by the intracellular hydrogen
peroxide-catalase
system to its divalent cation, Hg2+. Since the Hg2+
form cannot diffuse out of the different nerve cells after this
transformation,
mercury gradually accumulates in the brain.
"Mercury has a number of mechanisms leading to toxicity
in biological systems. These include the following:
"Mercury is unevenly distributed in the brain and
spinal chord, with the heaviest deposits found within the motor nuclei
of the rhomboencephalon ...".
In contrast, in a recent publication, Brieger et al.
[10] warned against the error performed by MS patients in seing their
disease
as a result of mercury poisoning. Fung et al. [11] found that
the
concentrations of mercury and the mercury/selenium molar ratios in
autopsy
brain preparations were significantly lower in the hippocampi of
multiple
sclerosis patients as compared to age-matched controls. No
statistically
significant differences were detected for the concentrations of mercury
and the mercury/selenium molar ratios for the remaining six brain
regions
among these groups. In a similar study, Clausen [12] found no
significant
differences between the deceased patients with and without MS
concerning
total mercury. However, the lipid-soluble mercury (preferably
methyl-mercury)
expressed per cell unit (DNA) was found significantly decreased in MS.
These data may be explained either by a wash-out of lipid soluble
mercury
due to break-down of the blood-brain barrier in MS or to abnormalities
in methylation processes probably related to the vitamin B12-metabolism
in MS. In some contrast to these observations, McGrother et al. [19]
found
excess dental caries among MS cases as compared to controls in a
case-control
study. (Unknown position: [13]).
In conclusion, this question (as most other
clinical
ones) cannot be solved in the contradictory literature, unless these
are
selected according to the bias of the seacher. Small studies on a
limited
amount of patients are as little impressive as enthusiastic claims of
success
with amalgam removal. Although the toxicity of mercury is out of
question,
its pathological role in MS remains speculative. Even if it plays a
role
in some patients (accepting MS as a group of diseases rather than a
single
entity), it is still not proved that removal of ancient amalgam
fillings
causes any improvement. As almost usual in medical reasoning, also the
opposite remains unproved.
Various measures have been suggested in order to avoid
too large serum-mercury levels exactly in connection to the removal of
dental amalgam. They may include the ingestion of various antioxidants
and penicillamine both before and after this measure. More important
are
especially "physical measures" to be taken by the dentist, in order to
avoid swallowing off amalgam particles - aparently not an easy topic.
d-Penicillamine
As a scavenging agent of various heavy-metal
poisonings,
including mercury and lead, the drug d-penicillamine has gained a
prominent
position. Indeed, some studies suggest a positive effect of
d-penicillamine
in MS [14,15,16], including a recent experimental study [17], whereas
one
turned out negatively [18]. This is, however, no proof that heavy
metals
are ethiologically important in MS: penicillamine has been found
effective
in rheumatoid arthritis and other autoimmune diseases, and quite
possibly
for different reasons. Both the tissue-type plasminogen activator
(t-PA)
and the metalloproteinase gelatinase B (MMP-9) are interconnected in an
enzyme cascade which contributes to destruction of the blood brain
barrier
and demyelination, and both enzymes are inhibited by d-penicillamine
[16].
Moreover, additional antiviral properties have been attributed to this
drug, thus providing similarity to interferon-beta (IFB) which was
first
used in MS due to the infectious theory and later preferred for its
modulation
of the immune system, including inhibition of MMP-9. However, the
adverse
effects of penicillamine are much more pronounced than those of IFB and
will probably not allow a prolonged therapy. For "pulsation therapy" of
a few weeks duration in response to relapses of the disease, it remains
an interesting, though currently insufficiently studied alternative.
Update 2009:
Finally, the American FDA admitted what was long a
fact in other nations (e.g. Sweden, Canada and France) where the use of
amalgam is forbidden or restricted: "The mercury
contained in silver dental fillings may pose neurological risks to
children and pregnant women" [20]. The first step on a strangely
neglected way of who are else exposed to the risk of amalgam.
Revised Jan. 6, 2009