I am creating this thread in hopes to get a discussion going related to the preservative and bleaching agent, sodium metabisulfite and the potential health implications arising from of ingesting it. There does not seem to be much literature online other than sulfite alergies in general. Sodium metabisulfite induces oxadative stress in rat cerebellum and gastric mucosa and has been found to cause various problems with the skin and respiratory systems. Feel free to discuss closely related sulfite preservatives such as sodium bisulfite and potassium bisulfite as well. Based on the body of evidence on PUBMED, my reaction to it, and other anecdotal accounts related to sulfite preservatives, it does not seem beneficial to one's health to consume anything at all with sodium metabisulfite in it. For the sake of longevity and healthy living, it would be wise to avoid these preservatives.
The past few days prior to writing this, I've had a terrible reaction to sodium metabisulfite after consuming a large quantity of a coconut snacks containing sodium metabisulfite. The past 48 hours I have experienced "Ice-Pick-Headaches", skin reaction, brain fog, and slightly enlarged lymph nodes. I seldom get headaches let alone icepick headaches. I've had similar headaches from ingesting spinach and certain peppers at Subway years ago.
Sulfites are used as anti-microbial and anti-oxidant agents in the food and pharmaceutical industries. Curcumin, a flavonoid, is an Asian spice that shows neuroprotective activities. The current study aimed to stereologically assess the rats' cerebellar cortex and rotarod performance following sulfite exposure and determine the possible neuroprotective potential of curcumin. The rats were divided into five groups: distilled water, olive oil, curcumin (100 mg/kg/day), sodium metabisulfite (25 mg/kg/day), and sodium metabisulfite+curcumin. At 56 days after treatment, rotarod performance was tested, and then the cerebellum was removed for stereological analysis. The study results revealed 31%, 36%, 19% and 24% decrease in the total volume of the cerebellum, cortex, the total number of the Purkinje cells and length of the nerve fibers in the cortex per Purkinje, respectively in the sodium metabisulfite-treated rats compared to the distilled water group (p<0.01). The pre-trained animals on the rotarod apparatus were tested first on the fixed speed rotarod protocol followed by the accelerating rotarod protocol two days later. The results showed a significant decrease in the latency to fall in both test in sulfite-treated rats. The sulfite effects on the structural parameters and rotarod performance were significantly protected by the concomitant curcumin treatment (p<0.001). Sulfite can induce structural and functional changes in the rats' cerebellum and concomitant curcumin prescription plays a neuroprotective role.
www.ncbi.nlm.nih.gov/pubmed/24465141
→ source (external link)www.ncbi.nlm.nih.gov/pubmed/24465141
This study aimed to investigate the effect of ghrelin administration on sulfite induced oxidative and apoptotic changes in rat gastric mucosa. Forty male albino Wistar rats were randomized into control ©, sodium metabisulfite (Na2S2O5) treated (S), ghrelin treated (G) and, Na2S2O5+ghrelin treated (SG) groups. Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage and, ghrelin (20 μg/kg/day) was given intraperitoneally for 5 weeks. Plasma-S-sulfonate level was increased in S and SG groups. Na2S2O5 administration significantly elevated total oxidant status (TOS) levels while depleting total antioxidant status (TAS) levels in gastric mucosa. Ghrelin significantly decreased gastric TOS levels in the SG group compared with the S group. Additionally, TAS levels were found to be higher in SG group in reference to S group. Na2S2O5 administration also markedly increased the number of apoptotic cells, cleaved caspase-3 and PAR expression (PARP activity indicator) and, decreased Ki67 expression (cell proliferation index) in gastric mucosal cells. Ghrelin treatment decreased the number apoptotic cells, cytochrome C release, PAR and, caspase-3 expressions while increasing Ki67 expression in gastric mucosa exposed to Na2S2O5. In conclusion, we suggest that ghrelin treatment might ameliorate ingested-Na2S2O5 induced gastric mucosal injury stemming from apoptosis and oxidative stress in rats.
www.ncbi.nlm.nih.gov/pubmed/23439480
CONCLUSIONS:
Allergic contact dermatitis caused by sulfites is frequent and often relevant. One should be aware of possible relevant sources of exposure, particularly in occupational settings such as hairdressing and the food industry, and in pharmaceutical and cosmetic products. Patch testing with sodium metabisulfite, which seems to be the best indicator for sulfite contact allergy, is also useful in cases of immediate reactions to sulfite-containing products.
www.ncbi.nlm.nih.gov/pubmed/23039002
→ source (external link)Allergic contact dermatitis caused by sulfites is frequent and often relevant. One should be aware of possible relevant sources of exposure, particularly in occupational settings such as hairdressing and the food industry, and in pharmaceutical and cosmetic products. Patch testing with sodium metabisulfite, which seems to be the best indicator for sulfite contact allergy, is also useful in cases of immediate reactions to sulfite-containing products.
www.ncbi.nlm.nih.gov/pubmed/23039002
Skin-sensitizing chemicals that cause allergic contact dermatitis do so by reacting with self-proteins such that the modified structure becomes antigenic. The reaction chemistry involved is well characterized, but there are exceptions, such as the occasional allergen sodium metabisulfite.
OBJECTIVES:
To identify the potential in cutaneo reaction chemistry of sodium metabisulfite.
METHODS:
The established protein reaction chemistry associated with aqueous sulfite chemistry was explored in the context of the protein modification stage in allergic contact dermatitis.
RESULTS:
A probable mechanism for the in cutaneo modification of proteins by sodium metabisulfite involves the sulfite di-anion, acting as a nucleophile towards electrophilic centres in proteins, which is a rare mechanism, as most known skin-sensitizing chemicals behave as electrophiles.
CONCLUSIONS:
Sodium metabisulfite is an unusual but not infrequent contact allergen whose chemistry suggests a previously unrecognized protein modification mechanism involving nucleophilic attack by sulfite di-anions on target electrophilic centres in skin proteins. The chemical properties required for sensitization by nucleophilic attack on skin proteins are quite restrictive, so the domain of nucleophilic sensitizers is expected to be small. Thiourea derivatives are among the sensitizers likely to act by this mechanism.
www.ncbi.nlm.nih.gov/pubmed/22320665
Sodium metabisulphite induced airways disease in the fishing and fish-processing industry.
BACKGROUND:
Sodium metabisulphite (SMBS) is recognized as a potential cause of airway irritation and possibly occupational asthma, but awareness of its use in the fishing and fish-processing industry is low.
AIMS AND METHODS:
To describe three cases of occupational airways disease due to SMBS exposure and to review the literature.
RESULTS:
Three patients, one trawlerman and two prawn processors, developed work-related airways disease due to exposure to SMBS, one with irritant-induced asthma with a positive-specific bronchial challenge associated with very high sulphur dioxide exposures, one with occupational asthma and one with vocal cord dysfunction and underlying asthma. Of the nine cases recorded in the literature, most were non-atopic and responses to specific bronchial challenge when undertaken showed an immediate response. Exposures to sulphur dioxide in these settings are very high, in excess of 30 ppm.
CONCLUSION:
SMBS should be regarded as a cause of occupational airways disease and its use in the fish and prawn-processing industry investigated further to better identify risks from exposure and handling of the agent in the workplace.
http://www.ncbi.nlm....pubmed/18832347
Sulfite, which is continuously formed in the body during metabolism of sulfur-containing amino acids, is commonly used in preservatives. It has been shown that there are toxic effects of sulfite on many cellular components. The aim of this study was to investigate the possible toxic effects of sulfite on pyramidal neurons by counting cell numbers in CA1 and CA2-CA3 subdivisions of the rat hippocampus. For this purpose, male albino rats were divided into a control group and a sulfite group (25 mg/kg). Sulfite was administered to the animals via drinking water for 8 weeks. At the end of the experimental period, brains were removed and neurons were estimated in total and in a known fraction of CA1 and CA2-CA3 subdivisions of the left hippocampus by using the optical fractionator method--a stereological method. Results showed that sulfite treatment caused a significant decrease in the total number of pyramidal neurons in three subdivisions of the hippocampus (CA1 and CA2-CA3) in the sulfite group compared with the control group (p < 0.05, Mann Whitney U test). It was concluded that exogenous administration of sulfite causes loss of pyramidal neurons in CA1 and CA2-CA3 subdivisions of the rat hippocampus.
www.ncbi.nlm.nih.gov/pubmed/21511899
Furthermore, sodium metabisulfite and sodium bisulfite have been found to impede the absorbtion of Thiamine (Vitamin B1) http://www.ncbi.nlm..../pubmed/7325171
I plan on updating this thread with more evidence and a list of foodstuff that commonly that contain sodium metabisulfite. My apologies for the sloppy apperance of the thread (i.e. additional URLs), the reference tool was not working properly. Please click the URL that I pasted into the references below the abstract, both the reference URL and the reference link are not working properly.
Edited by FW900, 04 March 2014 - 12:32 AM.