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• The prevention of vaccine reactions
  C Alan B Clemetson, M.D.
  Published on: 10 December 2004

• Published on: 10 December 2004

  The prevention of vaccine reactions

  • C Alan B Clemetson, M.D., Professor Emeritus

  Dear Editor

  I read the article by Jefferson[1] with interest. Although they are rare, vaccine reactions do occur and are suspected of having severe consequences.[2-4] It is here suggested that it is mainly those infants who already have somewhat depleted vitamin C stores, who are affected most. We now know that even modest ascorbate depletion is associated with very high blood histamine levels,[5], as shown in figu...

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  Dear Editor

  I read the article by Jefferson[1] with interest. Although they are rare, vaccine reactions do occur and are suspected of having severe consequences.[2-4] It is here suggested that it is mainly those infants who already have somewhat depleted vitamin C stores, who are affected most. We now know that even modest ascorbate depletion is associated with very high blood histamine levels,[5], as shown in figure 1; so any additional histamine due to infection or vaccinations can cause a toxic histaminaemia leading to capillary fragility.

  

  Figure 1. Results of plasma ascorbic acid (reduced form) and whole blood histamine concentrations in the same blood samples from 437 volunteers in Brooklyn, NY (4). A highly significant increase in the blood histamine level was evident when the plasma ascorbic acid level fell below 0.7 mg/100 mL. This comprised 150 of the 437 (34 percent) men and women. Data from Clemetson 1980.

  A very simple remedy is suggested. There is no doubt that a vitamin C supplement can be used to prevent the adverse vaccine reactions brought on by increased blood histamine levels, both in animals and in man. We know that vitamin C acts to remove histamine from the blood by converting it to hydantoin-5-acetic acid.

  We also know that a dose of vitamin C appropriate for this purpose may be much greater than the usually recommended dietary allowance. Ascorbic acid has been shown to be life-saving when given with vaccines, even in rats, mice, and rabbits, which make their own ascorbic acid in the liver and do not normally need it in their diet. It seems that even these animals do not always make enough ascorbic acid for their own needs.

  As for human infants, the appropriate dose of vitamin C to be given with vaccines -- and the best method of administering it -- still need to be determined. Ascorbic acid is not toxic, so I have suggested 500 mg to be given to infants in fruit juice on the day of vaccination. Some authorities may decide to give sodium ascorbate intramuscularly, already prepared with the vaccine.

  Much has been written on the specific toxicity of individual vaccines, but histamine toxicity is a general effect. Now that infants receive as many as six vaccines together at eight weeks of age, we have to think of the cumulative histamine increase as a general toxicity. Excellent work on vitamin C and vaccine reactions was done many years ago and was summarized in 1999.[6] The results of all the experiments were consistent and showed that ascorbic acid reduces both the morbidity and the mortality due to all the bacterial antigens studied, and in all the different animals tested.

  The observation that borderline ascorbic acid deficiency increases the morbidity and mortality from diphtheria antigen in guinea pigs goes back to work by Harde[7] in 1934 and by King and Menten[8] in 1935, not long after the isolation of ascorbic acid by Svirbely and Szent-Gyorgyi[9] and by King and Waugh[10] in 1932. King and Menten observed that there is a wide zone of vitamin C depletion, without the appearance of scurvy, wherein physiological processes are subnormal and an animal is more sensitive to bacterial toxins.

  In addition to providing protection against diphtheria toxoid, vitamin C is also protective against the toxoids of four different varieties of gas gangrene bacteria in mice, as shown by Buller-Souto and Lima[11] in Table 1, and against tetanus toxoid in rats, as shown by Dey[12] in Table 2.

  Table 1
  Protective activity of L-ascorbic acid 10mg daily, given intramuscularly to mice for 3 days preceding both a single and a double LD50 dose of four different gas gangrene toxins. Note the unsurprisingly good protective activity of ascorbic acid even in mice, which make their own ascorbic acid
  

  LD50 dose> of Toxin of Clostridium	AA treated		Controls		Percentage Survival of Controls	Percentage Survival of AA-treated Mice
  	n	dead at 48 hrs	n	dead at 48 hrs
  welchii	55	14	26	13	50	75
  septicum	30	7	10	5	50	77
  oedematiens	22	3	11	5	55	86
  histolyticum	18	3	15	6	60	83
  2 LD50 dose
  welchii	57	38	30	30	0	33
  septicum	31	15	12	10	17	52
  oedematiens	24	9	11	8	27	63
  histolyticum	18	16	15	15	0	11

  AA=L-ascorbic acid; n=number of animals
  An LD50 dose of toxin is that previously found to kill 50 percent of the animals
  2 LD50 is twice that dose
  From Büller-Souto and Lima.[11]. Translated and summarised by Clemetson,[6] reproduced with permission from the Journal of Orthomolecular Medicine

  Table 2. Efficiency of vitamin C in counteracting the toxicity of tetanus antigen in adult rats

  Treatment	No. of Rats	Symptoms	Survival
  2 MLD tetanus toxin i.m.	5	All convulsed and died within 47-65 hrs	None
  2 MLD tetanus toxin i.m. with 1g AA (per body weight) i.p. and 1g AA/kg b.i.d. for 3 days i.p.	5	Only very mild local tetanus after 48 hrs	All
  AA 1g/kg b.i.d. for 3 days then 2 MLD tetanus toxin + AA 1g/kg b.i.d. for 3 days	5	No signs of toxicity	All
  2 MLD tetanus toxin, AA 1g/kg i.p. only when convulsions began after 16 to 26 hrs and continued b.i.d. for 3 days	5	Convulsions arrested	All
  2 MLD tetanus toxin. Animals anaesthetized after 40 to 47 hours when general tetanic convulsion occurred - then AA 300mg give IV	10		All

  AA=L-ascorbic acid; MLD=minimum lethal dose; 2 MLD=twice minimum lethal dose; i.m.=intramuscular injection; i.p.=intraperitoneal injection.
  Data from Dey.[12] Table reproduced with permission from the Journal of Orthomolecular Medicine.[6]

  Fukada and Koyama[13] demonstrated that pretreatment with ascorbic acid (500 mg/day), mixed in a soybean curd diet, protected their rabbits against the toxic effects of Salmonella typhi endotoxin. Ascorbic acid saturation markedly ameliorated the depletion of liver glycogen after endotoxin, both in intact and in adrenalectomised rabbits, and completely prevented the attendant hypoglycaemia.

  The seminal studies of Kalokerinos[14] showed that supplementary vitamin C was uniformly effective in preventing infant deaths following vaccination in Aborigine children in Australia.

  In view of all these most important and encouraging findings, one wonders why ascorbic acid has not yet been widely recommended for routine use with vaccinations. This reticence may have been due to a sense that such an anti-toxic action could possibly vitiate the purpose of a vaccine. However, now that we know that the anti-toxic effect of vitamin C is due to its role in the removal of histamine and does not affect the antigen, we can recommend it freely. Ascorbic acid acts as a co-enzyme in the elimination of histamine by converting it to hydantoin-5-acetic acid, and on to aspartic acid in vivo.[15] We can recommend vitamin C for general use with all vaccines, without any fear that the vaccine will lose its intended potency as a stimulant of immunity.

  The vaccine-ascorbate studies cited here are very old, and many, from abroad. It would be reassuring to hear of any new studies -- not that they would necessarily be any more reliable, but that plasma ascorbic acid and whole blood histamine studies could now be included.

  References

  1. Real or perceived adverse effects of vaccines and the media - a tale of our times. Jefferson T. J Epidemiol Community Health 2000; 54: 402-403

  2. Clemetson CAB. Elevated blood histamine caused by vaccinations and vitamin C deficiency may mimic the shaken baby syndrome. Medical Hypotheses 2004; 62:533-536.

  3. Clemetson CAB. Capillary fragility as a cause of subdural hemorrhage in infants. Medical Hypotheses and Research 2004; 1:121-129.

  4. Clemetson CAB. Is it "shaken baby," or Barlow's disease variant? Journal of American Physicians and Surgeons 2004; 9:78-80.

  5. Clemetson CAB. Histamine and ascorbic acid in human blood. Journal of Nutrition 1980; 110:662-668.

  6. Clemetson CAB. Vaccinations, inoculations and ascorbic acid. Journal of Orthomolecular Medicine 1999; 14:137-142.

  7. Harde E. Acide ascorbique (vitamin C) et intoxications. Comptes Rendus de l'Academie des Sciences Paris 1934; 119:618-620.

  8. King CG, Menten ML. The influence of vitamin C level upon resistance to diphtheria toxin. Journal of Nutrition 1935; 10:129-140.

  9. Svirbely JL,Szent-Gyorgyi A. The chemical nature of vitamin C. Biochemical Journal 1932; 27:279-285.

  10. King CG, Waugh WA. The chemical nature of vitamin C. Science 1932; 75:357-358.

  11. Buller-Souto A, Lima C. Activity of L-ascorbic acid on the toxins of gas gangrene. Memorias do instituto Butantan, Sao Paulo, Brasil, 1939; 12:265-295, in Portuguese; 297-311, in French (same data).

  12. Dey PK. Efficiency of vitamin C in counteracting tetanus toxin toxicity. Naturwissenschaften 1966; 53:310.

  13. Fukada T, Koyama T. Prevention by ascorbic acid of liver glycogen depletion in endotoxin intoxication. Nature (London) 1963; 200:1327.

  14. Kalokerinos A. Every Second Child. Thomas Nelson (Australia) Ltd. 1974. Now reprinted by Falconi O, Box 3345, Saratoga, CA 95070.

  15. Chatterjee IB, Majumder AK, Nandi BK, Subramanian N. Synthesis and some major functions of vitamin C in animals. Annals of New York Academy of Sciences 1975; 258:24-47

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  Conflict of Interest:
  None declared.

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