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Life Extension Magazine

LE Magazine April 2001

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Silver concentrations in human tissues. Their dependence on dental amalgam and other factors.

Human tissue samples (liver, kidney cortex, 5 brain regions: grey matter of cerebrum, white matter of cerebrum, nucleus lentiformis, cerebellum, brain stem) from 173 decreased persons were analysed for silver (Ag) by GF-AAS (Graphite Furnace Atomic Absorption Spectrometry) and the results compared with the number of teeth with amalgam fillings and the concentration of inorganic mercury (Hg), which had been determined in the same tissue samples in a previous study. It was found that the mean Ag concentrations in liver and brain of adult females are approximately twice that of males. Moreover, the Ag concentrations, especially in the brain, depend possibly on age. To exclude these confounding factors as far as possible, the influence of dental amalgam and the correlation of Ag and Hg were evaluated only in a sub-group of 93 males, aged 11-50 years. In this sub-group statistically significant correlations were found between the number of teeth with dental amalgam and the Ag concentrations in the cerebral cortex and the liver. No such correlation was found for the kidney. Ag and inorg. Hg correlate well in this sub-group in the liver, but not in the cerebral cortex or the kidney. Individuals from this sub-group with (i) 0-2 and with (ii) more than 9 teeth with amalgam fillings show mean Ag concentrations (micrograms/kg in tissue wet weight, geom. mean) of 1.59 and 5.41 in the grey matter of cerebrum, 1.42 and 4.25 in the white matter of cerebrum, 1.53 and 4.89 in the nucleus lentiformis, 1.95 and 5.02 in the cerebellum, 1.05 and 3.27 in the brain stem, 3.40 and 8.15 in the liver and 0.42 and 0.44 in the kidney cortex. In contrast, comparing all individuals under investigation with only 0-2 teeth with amalgam no correlation between Ag and inorg. Hg could be found in liver, kidney cortex or cerebral cortex. These results show that amalgam fillings release Ag as well. Considering the different toxicokinetics of Ag and Hg it can be concluded that Ag is a reliable marker for the fact that the elevated concentrations of in org. Hg found in tissues of individuals with amalgam fillings derive mainly from these fillings and not from other theoretically possible sources.

J Trace Elem Med Biol 1995 Jul;9(2):82-7

Influence of low frequency magnetic fields on the intra-oral release of mercury vapor from amalgam restorations.

Since the results of a preliminary study have shown that the magnetic fields of some visual display units (VDUs) increased the release of mercury from amalgam specimens, the aim of the present study was to examine whether exposure to magnetic fields might affect the mercury vapor release from amalgam restorations in humans. The test group consisted of five subjects with an average of 31.4 amalgam surfaces (range 13-48). In each of the subjects tested, the intra-oral release of mercury vapor was measured during three 9-h periods at intervals of 30 to 90 min, using a standardized schedule and standardized food. During the first 9-h period which served as control, no intentional magnetic fields were applied. During the second and the third 9-h period, magnetic fields with flux densities of 20 microT at 30 kHz or 500 microT at 50 Hz, respectively, were applied. Although these flux densities were one thousand times higher than those caused by VDUs, no effects could be found on the release of mercury vapor from the amalgam restorations. The results of the present study do not support the assumption that exposure to magnetic fields increases the mercury vapor release from amalgam restorations in humans.

Eur J Oral Sci 1998 Apr;106(2 Pt 1):671-4

Release of mercury vapor from dental amalgam.

Because of its long-term clinical use there is more information and research data available about dental amalgam than about any other dental restorative material. However, on and off the safety of dental amalgam has been called in question and during the 80's the mercury controversy came to the fore, not only within the profession but also among the general public. Sources of mercury vapor contamination within dentistry were identified and attempts made to evaluate the contributions to the daily mercury uptake which can be attributed to dental amalgam. Mercury can be released from dental amalgam by evaporation and electrochemical corrosion as well as from amalgam particles which have been swallowed. A major route for mercury uptake from amalgam restorations is through inhalation of mercury vapor. The present study focused on experimental and analytical difficulties associated with the measurement of mercury vapor released in the oral cavity. A careful methodological study of the kind of source of mercury vapor that is prevalent and on the methods for measuring the intra-oral release of mercury vapor was carried out. With this as a basis quantitative determinations of the release rate of mercury vapor from amalgam restorations were made on healthy human subjects not occupationally exposed to mercury. The daily uptake of mercury from inhaled mercury vapor was calculated and salivary and urinary mercury levels were determined. In addition the release rate of mercury vapor from different types of amalgam was studied in vitro and in vivo. The findings may be summarized as follows: The only relevant measurable quantity when determining the mercury vapor released from amalgam restorations is the amount released per time unit, i.e. the amount of mercury vapor collected during intra-oral sampling is proportional to the sampling time. The diffusion of mercury atoms inside an amalgam restoration results in the formation of a concentration gradient in the surface of the amalgam. This mercury diffusion is the rate-determining step for mercury vapor release in the long run. In the short run the mercury concentration gradient prevalent on the amalgam surface on the measuring occasion is the apparent rate-determining step. The daily uptake of mercury from inhaled mercury vapor released from dental amalgam seems to make a very small contribution to the total body burden of mercury, in comparison with what can be tolerated in the work environment. The in vitro results revealed obvious differences regarding the release rate of mercury vapor from dissimilar amalgam types.

Swed Dent J Suppl 1992;85:1-52

The future of dental amalgam: a review of the literature. Part 7: Possible alternative materials to amalgam for the restoration of posterior teeth.

This is the last in a series of articles on the future of dental amalgam. It considers possible alternative materials to amalgam for the restoration of posterior teeth. The materials discussed are gold inlays, gold foil, gallium alloys, and tooth coloured non-metal alternatives including glass-ionomer cements, composite resins, glass-ionomer-resin hybrids, compomers and ceramics. The clinical indications for these restorations are first described along with their potential clinical problems and their mean survival rates in comparison with dental amalgam. Secondly, the safety of composite resins is considered and potential toxic and hypersensitive effects of these materials are discussed. Finally, it is concluded that the present evidence does not appear to demonstrate that dental amalgam is hazardous to the health of the general population. It does, however, recommend that in continuing to use amalgam dentists must use strict mercury hygiene procedures to avoid risk to their staff and contamination of the environment. It seems that mercury contamination of the environment is likely to be the main reason for any future government action against the continued clinical use of dental amalgam.

Br Dent J 1997 Jul 12;183(1):11-4


Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin.

OBJECTIVE: To determine whether a nutritional supplement of selenium will decrease the incidence of cancer. DESIGN: A multicenter, double-blind, randomized, placebo-controlled cancer prevention trial. SETTING: Seven dermatology clinics in the eastern United States. PATIENTS: A total of 1312 patients (mean age, 63 years; range, 18-80 years) with a history of basal cell or squamous cell carcinomas of the skin were randomized from 1983 through 1991. Patients were treated for a mean (SD) of 4.5 (2.8) years and had a total follow-up of 6.4 (2.0) years. INTERVENTIONS: Oral administration of 200 microg of selenium per day or placebo. MAIN OUTCOME MEASURES: The primary end points for the trial were the incidences of basal and squamous cell carcinomas of the skin. The secondary end points, established in 1990, were all-cause mortality and total cancer mortality, total cancer incidence, and the incidences of lung, prostate, and colorectal cancers. RESULTS: After a total follow-up of 8271 person-years, selenium treatment did not significantly affect the incidence of basal cell or squamous cell skin cancer. There were 377 new cases of basal cell skin cancer among patients in the selenium group and 350 cases among the control group (relative risk [RR], 1.10; 95% confidence interval [CI], 0.95-1.28), and 218 new squamous cell skin cancers in the selenium group and 190 cases among the controls (RR, 1.14; 95% CI, 0.93-1.39). Analysis of secondary end points revealed that, compared with controls, patients treated with selenium had a nonsignificant reduction in all-cause mortality (108 deaths in the selenium group and 129 deaths in the control group [RR; 0.83; 95% CI, 0.63-1.08]) and significant reductions in total cancer mortality (29 deaths in the selenium treatment group and 57 deaths in controls [RR, 0.50; 95% CI, 0.31-0.80]), total cancer incidence (77 cancers in the selenium group and 119 in controls [RR, 0.63; 95% CI, 0.47-0.85]), and incidences of lung, colorectal, and prostate cancers. Primarily because of the apparent reductions in total cancer mortality and total cancer incidence in the selenium group, the blinded phase of the trial was stopped early. No cases of selenium toxicity occurred. CONCLUSIONS: Selenium treatment did not protect against development of basal or squamous cell carcinomas of the skin. However, results from secondary end-point analyses support the hypothesis that supplemental selenium may reduce the incidence of, and mortality from, carcinomas of several sites. These effects of selenium require confirmation in an independent trial of appropriate design before new public health recommendations regarding selenium supplementation can be made.

JAMA 1996 Dec 25;276(24):1957-63

Dietary selenium and arsenic affect DNA methylation In vitro in caco-2 cells and In vivo in rat liver and colon.

Selenium is an essential trace element for human health, and it has received considerable attention for its possible role as an anticarcinogenic agent. The purpose of the present study was to determine whether changes in the amount and the chemical form of selenium would affect DNA methylation and whether this effect would be modified by arsenic. Caco-2 cells, a human colon cancer cell line, were exposed to 0, 1 or 2 &mgr;mol supplemental selenite/L and 0, 1 or 2 &mgr;mol supplemental arsenite/L for 7 d. DNA isolated from Caco-2 cells not treated with selenite was significantly (P: < 0. 0001) hypomethylated compared with that from cells treated with 1 or 2 &mgr;mol selenite/L. DNA isolated from Caco-2 cells not treated with arsenite was significantly (P: < 0.0001) hypomethylated compared with DNA isolated from cells treated with 1 or 2 &mgr;mol arsenite/L. In addition, methylation of the p53 promoter region of Caco-2 cells decreased when cells were cultured in the absence of selenite and in the absence of arsenite. Sixty weanling male Fischer 344 rats were fed a torula yeast-based diet supplemented with 0, 0.1 or 2 mg selenium/kg diet as either selenite or selenomethionine in the presence or absence of 5 mg arsenic/kg diet as arsenite for 6 wk. Similar to the results with Caco-2 cells, rats fed selenium-deficient diets had significantly (P: < 0.0001) hypomethylated liver and colon DNA compared with rats fed 0.1 or 2.0 &mgr;g selenium/g diets as either selenite or selenomethionine. Thus, alterations in DNA methylation may be a potential mechanism, whereby deficient dietary selenium increases liver and colon tumorigenesis.

J Nutr 2000 Dec;130(12):2903-9

Selenium from high selenium broccoli protects rats from colon cancer.

Colon cancer is the third most common newly diagnosed cancer in the United States and the third most common cause of cancer-related deaths. Previous supplementation studies have demonstrated the efficacy of selenium (Se) for prevention of colon cancer in humans. The metabolism of Se depends on its chemical form, and studies have shown that the chemical form of Se in broccoli does not accumulate in the body as fast as other forms of Se and may be especially beneficial for prevention of cancer. In the first experiment of the present study, Fisher F-344 rats (n = 45) were allotted randomly to torula yeast-based diets supplemented with the following: 1) no Se; 2) 0.1 microg Se/g diet as selenate; 3) 1.0 microg Se/g diet as selenate; 4) 0.1 microg Se/g diet as selenized broccoli (Se concentration of approximately 500 microg/g); or 5) 1.0 microg Se/g diet as selenized broccoli. In Experiment 2, rats (n = 80) were allotted randomly to the same basal diet supplemented with the following: 1) no added Se; 2) 2.0 microg Se/g diet as selenite; 3) 2. 0 microg Se/g diet as selenite + low Se broccoli; and 4) 2.0 microg Se/g diet as selenized broccoli. Rats were fed the diets for 2 wk and injected with a chemical carcinogen (3,2 dimethyl 4-amino biphenyl or dimethyl-hydrazine in Experiment 1 or dimethyl hydrazine in Experiment 2; 2 rats/treatment were used as vehicle controls). Supranutritional amounts of Se supplied as high Se broccoli significantly decreased (P: < 0.05) the incidence of aberrant crypts (AC) and aberrant crypt foci (ACF; preneoplastic lesions indicative of colon cancer) compared with other dietary treatments. Diets were controlled for the presence or absence of broccoli and for the total amount of Se. The reduction in AC and ACF was a function of Se in high Se broccoli and not a result of broccoli alone or Se alone. Adequate dietary Se supplied as high Se broccoli did not accumulate in tissues or increase glutathione peroxidase activity as well as other forms and amounts of Se. Thus, Se from high Se broccoli may be metabolized in a manner that diverts much of the Se into a pool that provides protection against colon cancer.

J Nutr 2000 Sep;130(9):2384-9

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