Posted by Larry Hoover on January 13, 2009, at 9:48:24
In reply to Re: What's the deal with silver amalgams? » Larry Hoover, posted by yxibow on January 12, 2009, at 23:09:49
Amalgam dental restorations have not been proven safe, certainly not by the ADA, or any other dental organization. They have remained in use not because they have been approved by e.g. the FDA, but because their use precedes scientific inquiry into their safety. They have been grand-fathered in.
I don't want to sound like Bill Clinton, but we have to consider the meaning of the word safe. In the old way of thinking, exposure was considered safe until proven toxic (think tobacco). Modern scientific thought seeks to apply the precautionary principle, where the plausibility of risk is sufficient to prevent exposure to a risk, with the burden falling on the proponent of the risk-taking. Under current thinking, there is no way on Earth that mercury would be permitted as a permanent implant in the mouth.
About a decade ago, I was a contract researcher for the World Wildlife Fund, charged with determining human exposure and risk assessment to a number of chemicals, including bisphenol-A, which was recently restricted in Canada, due to its hormone disruptive potential. Anyway, there are a number of dental restoratives that contain bisphenol-A within a group sometimes called "white fillings", and as a sealant, so I spent some weeks in a university library dedicated to dental literature, reading and copying many hundreds of articles. My curiosity, and my risk analysis, had me simultaneously studying mercury amalgam. There has never been a time when the dental community was satisfied that there was no risk from mercury exposure arising from amalgams. I believe that legal liability concerns drive the public declarations of amalgam safety, not scientific evidence thereof.
One of the primary failings of virtually all studies of amalgam risk and reports of adverse effects arising therefrom is that they standardize on mercury exposure. If you were looking at Prozac safety, and standardized on dose, you could dismiss those people with rarer side effects just because most people don't react that way at that dose. But that's what's happening to people who are sensitive to mercury exposure. And unlike Prozac, which you can simply stop taking, you can't stop the release of mercury from amalgams in your mouth.
Mercury is a cumulative toxin. There is no safe exposure.....not as I define safe, anyway. There is a cumulative threshold beyond which symptoms become apparent. But each of us has our own threshold, determined by both genetic and environmental variables. When examined from the perspective of identified risk factors, amalgam illness does rise above the dismissive level of "not statistically different from matched controls". The devil has been in determining what those factors might be.
I just did a quick sampling of the literature this morning to show that there are known factors influencing mercury sensitivity (and surely others not yet identified).
Norway has banned mercury amalgam altogether. Health Canada has strongly recommended against amalgam installations in pregnant women, or in the deciduous teeth of children. At last count, four U.S. states require informed consent disclosure of the risks of mercury exposure via amalgam restorations. The FDA was recently sued to force it to declare a risk of that exposure. I think the pendulum is swinging.
The following four abstracts demonstrate statistically significant consequences of amalgam mercury exposure, in the context of specific risk factors. These include serotonin transporter gene polymorphism, Apo-lipoprotein gene polymorphism (the same gene associated with Alzheimer's), selenium status/metabolism, and thyroid antibodies. The latter may be entirely due to a selenium-dependent process, as the antibodies to TPO are negatively correlated with selenium status (as indicated by glutathione peroxidase levels).
It just makes sense to avoid mercury exposure, in any way that is practical.
Lar
J Toxicol Environ Health A. 2008;71(19):1318-26.
The association between serotonin transporter gene promoter polymorphism (5-HTTLPR), self-reported symptoms, and dental mercury exposure.Heyer NJ, Echeverria D, Farin FM, Woods JS.
Battelle Centers for Public Health Research and Evaluation, Seattle, Washington 98109-3598, USA. heyern@battelle.orgThe associations between a polymorphism of the serotonin transporter gene (5-HTTLPR), dental mercury exposure, and self-reported symptoms were evaluated among 157 male dentists and 84 female dental assistants. Self-reported symptoms and detailed work histories were obtained by computerized questionnaire. Spot urine samples were collected and analyzed for mercury concentrations to evaluate recent exposures, whereas a chronic mercury exposure index was created from the work histories. 5-HTTLPR polymorphism status was determined using a polymerase chain reaction (PCR)-based assay. Scores for current, recent, and chronic self-reported symptom groups were evaluated with respect to recent and chronic mercury exposure and 5-HTTLPR polymorphism status. Multiple regression analysis controlled for age, socioeconomic status, tobacco and alcohol use, self-reported health problems, and medications. Analyses were restricted to Caucasian subjects due to the highly skewed distribution of the 5-HTTLPR polymorphism. Separate evaluations were conducted for dentists and dental assistants. In contrast to previous reports, no consistent associations were found between either urinary mercury concentration or the chronic index of mercury exposure and any category of symptoms. However, both significant and consistent associations were observed between increased symptoms and the 5-HTTLPR polymorphism involving two copies of the short or "s" allele (full mutation), but not with the polymorphism involving only one copy (heterozygous), demonstrating a gene-dose relationship for symptom reporting. These findings suggest that within this restricted population increased symptoms of depression, anxiety, and memory are associated with the 5-HTTLPR polymorphism among both males and females.
Neuro Endocrinol Lett. 2006 Aug;27(4):415-23.
Mercury toxicity presenting as chronic fatigue, memory impairment and depression: diagnosis, treatment, susceptibility, and outcomes in a New Zealand general practice setting (1994-2006).Wojcik DP, Godfrey ME, Christie D, Haley BE.
Northland Environmental Health Clinic, 2 Dip Rd, Kamo, Whangarei, Northland, New Zealand. wojcik@wave.co.nzIn a group of 465 patients diagnosed as having chronic mercury toxicity (CMT), 32.3% had severe fatigue, 88.8% had memory loss, and 27.5% had depression. A significant correlation was found between CMT and the Apo-lipoprotein E4 genotype (p=0.001). An investigation into an additional 864 consecutively seen general practice patients, resulted in 30.3% having evidence consistent with CMT, and once again a significant correlation was found with the APO-E4 genotype (p=0.001). Removal of amalgam mercury fillings when combined with appropriate treatment resulted in a significant symptom reduction (p<0.001) to levels reported by healthy subjects.
Environ Res. 2001 Dec;87(3):141-6.
Dental amalgam and selenium in blood.Høl PJ, Vamnes JS, Gjerdet NR, Eide R, Isrenn R.
Department of Odontology-Dental Biomaterials, University of Bergen, Aarstadveien 17, Bergen, N-5009, Norway.It has been suggested that selenium (Se) exhibits protective effects against mercury (Hg) toxicity in humans due to formation of a Hg-Se complex bound to selenoprotein P in blood. The aim of the present study was to investigate Se concentrations in persons who had been examined with respect to general health problems associated with dental amalgam fillings. The Se concentrations were determined in whole-blood samples of 80 individuals by hydride generation atomic absorption spectrometry. The subjects comprised two main groups: 21 healthy controls with amalgam fillings and 20 patients who claimed symptoms from existing amalgam fillings. The median concentration of Se in blood (119.2 microg/L) was statistically significantly lower in subjects who claimed symptoms of mercury amalgam illness than in healthy subjects with amalgam (130.3 microg/L). The difference was more evident in individuals with more than 35 amalgam surfaces (P=0.003). Additional control groups without amalgam fillings comprised 19 healthy controls without amalgam experience and 20 subjects who have had amalgam fillings removed due to suspected symptoms associated with amalgam. The Se concentrations in these groups were not different from those with amalgam. It is indicated that persons with ill health self-related to dental amalgam might have a Se metabolism different from that of healthy people.
Neuro Endocrinol Lett. 2006 Dec;27 Suppl 1:25-30.
Erratum in:
Neuro Endocrinol Lett. 2007 Oct;28(5):iii.
Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis.Sterzl I, Prochazkova J, Hrda P, Matucha P, Bartova J, Stejskal V.
Institute of Immunology and Microbiology, 1st Medical Faculty, Charles University, General Faculty Hospital, Prague, Czech Republic. ister@lf1.cuni.czOBJECTIVES: The impact of dental amalgam removal on the levels of anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies was studied in patients with autoimmune thyroiditis (AT) with and without mercury allergy. METHODS: Thirty-nine patients with AT were tested by an optimized lymphocyte proliferation test MELISA for allergy (hypersensitivity) to inorganic mercury. Patients were divided into two groups: Group I (n = 12) with no hypersensitivity to mercury and Group II (n = 27) with hypersensitivity to mercury. Amalgam fillings were removed from the oral cavities of 15 patients with hypersensitivity to mercury (Group IIA) and left in place in the remaining 12 patients (Group IIB). The laboratory markers of AT, anti-TPO and anti-Tg autoantibodies, were determined in all groups at the beginning of the study and six months later. RESULTS: Compared to levels at the beginning of the study, only patients with mercury hypersensitivity who underwent amalgam replacement (Group IIA) showed a significant decrease in the levels of both anti-Tg (p=0.001) and anti-TPO (p=0.0007) autoantibodies. The levels of autoantibodies in patients with or without mercury hypersensitivity (Group I and Group IIB) who did not replace amalgam did not change. CONCLUSION: Removal of mercury-containing dental amalgam in patients with mercury hypersensitivity may contribute to successful treatment of autoimmune thyroiditis.
poster:Larry Hoover
thread:873639
URL: http://www.dr-bob.org/babble/20090104/msgs/873732.html