It is common for people to have heard that ascorbic acid can be used for “chelation” purposes. This is a complicated topic at best as the data in support or opposition to the claim are not in synchrony from a methodological point of view. A review of the data available (focusing on lead and mercury) shows:
– Anecdotal reports from 1939 and 1940 [1,2] suggested that ascorbic acid may be beneficial in treating occupational lead exposure. Subsequent small trials among humans yielded inconclusive results [3-8]
– In a 1999 human trial [8] researchers showed decrease in blood lead in the group taking 1 gram QD oral ascorbate (versus no change in 200 mg ascorbate or placebo.)
– A study using human volunteers in 1994 [12] using intravenous ascorbic acid (infusion of 750 mg of ascorbic acid/kg body weight, up to 60 g ascorbic acid) showed no significantly different excretion of lead or mercury after the intravenous infusion of ascorbate over a 24 hour period post IV.
– A 1999 JAMA published human trial [9] showed “Our data suggest that high serum levels of ascorbic acid are independently associated with a decreased prevalence of elevated blood lead levels. If these associations are related causally, ascorbic acid intake may have public health implications for control of lead toxicity.”
– Animal and cell line studies in 2007 and 2016 [10,11] showed neuronal protection from lead damage by ascorbate and lower blood lead levels with improved neuro protection in a two generation study.
– In an interesting rabbit study looking at ascorbic acid versus DMSA and assessing lead ion concentration in blood, liver, kidney and brain before and after treatments application, as well as apoptotic related proteins P53 and Bcl2 were estimated beside histological studies of tissues it was shown that ascorbate was more active a chelator than DMSA for lead during active lead exposure.
Discussion:
These disparate data show that we have a number of potential benefits from ascorbic acid (AA) in heavy metal toxicology, and some confusing conclusions to contend with. AA does appear to be protective to neurological tissue. It appears to lower blood lead levels but not urinary excretion. In the case of mercury is similarly is protective to cell and ReDox activities but unlikely to increase excretion.
The obvious question is “if we lower blood lead and do not increase urinary excretion where does the lead go?” – The only possibilities are either body wide redistribution or deposition in bone and solid organs.
My personal conclusion is that while neuroprotective and able to lower blood lead levels AA is a piece of the depuration and detoxification and not the only therapy appropriate to employ. Oral AA should be used as a cell protectant in any exposed person (some would argue all people). In every course on detoxification and depuration I teach we stress an encompassing view of metal removal and cell protection. AA is certainly an economical part of the base protocol as a protective substance especially during exposures – which can be considered as “during chelation” as well.
If aiming at lowering total body burden a whole person strategy is better than using a single agent. The use of a direct chelator or ideally chelators along with ReDox support with agents such as AA, tocopherols, glutathione and others are the best plan, along with whole body depuration. Using AA as a sole chelation agent is as ill-advised as using EDTA alone as a chelating agent.
References:
1. Holmes HN, Campbell K, Amberg EJ. The effect of vitamin C on lead poisoning. J Lab Clin Med.1939;24:1119-1127.
2. Marchmont-Robinson SW. Effect of vitamin C on workers exposed to lead dust. J Lab Clin Med.1940;26:1478-1481.
3. Sohler A, Kruesi M, Pfeiffer CC. Blood lead levels in psychiatric outpatients reduced by zinc and vitamin C. J Orthomolecular Psych.1977;6:272-276.
4. Flanagan PR, Chamberlain MJ, Valberg LS. The relationship between iron and lead absorption in humans. Am J Clin Nutr.1982;36:823-829.
5. Lauwerys R, Roels H, Buchet JP, Bernard AA, Verhoeven L, Konings J. The influence of orally-administered vitamin C or zinc on the absorption of and the biological response to lead. J Occup Med.1983;25:668-678.
6. Calabrese EJ, Stoddard A, Leonard DA, Dinardi SR. The effects of vitamin C supplementation on blood and hair levels of cadmium, lead, and mercury. Ann N Y Acad Sci.1987;498:347-353.
7. Dawson EB, Harris WA. Effect of ascorbic acid supplementation on blood lead levels [abstract]. J Am Coll Nutr.1997;16:480.
8. Dawson EB, Evans DR, Harris WA, Teter MC, McGanity WJ. The effect of ascorbic acid supplementation on the blood lead levels of smokers. J Am Coll Nutr. 1999 Apr;18(2):166-70. PMID: 10204833
9. Joel A. Simon, Esther S. Hudes. Relationship of Ascorbic Acid to Blood Lead Levels. JAMA. 1999;281(24):2289-2293. doi:10.1001/jama.281.24.2289.
10. Han JM, Chang BJ, Li TZ, Choe NH, Quan FS, Jang BJ, Cho IH, Hong HN, Lee JH. Protective effects of ascorbic acid against lead-induced apoptotic neurodegeneration in the developing rat hippocampus in vivo. Brain Res. 2007 Dec 14;1185:68-74. Epub 2007 Sep 26. PMID: 17959157
11. Sepehri H, Ganji F. The protective role of ascorbic acid on hippocampal CA1 pyramidal neurons in a rat model of maternal lead exposure. J Chem Neuroanat. 2016 Jan 16;74:5-10. doi: 10.1016/j.jchemneu.2016.01.005. [Epub ahead of print] PMID: 26783884
12. Dirks MJ, Davis DR, Cheraskin E, Jackson JA. Mercury excretion and intravenous ascorbic acid. Arch Environ Health. 1994 Jan-Feb;49(1):49-52. PMID: 8117147
13. Bassem M. Raafat, Ahmed El-Barbary, Ehab Touson, Samir Aziz. Di-Mercapto Succinic Acid (DMSA) and vitamin C chelating potency in lead intoxication, regarding oxidative stress and apoptotic related proteins in rabbits. Journal of Genetic Engineering and Biotechnology (2011) 9, 121–131. http://dx.doi.org/10.1016/j.jgeb.2011.09.004