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Transfer Factor
Transfer factor was first reported in 1949 by Dr. H. Sherwood Lawrence. Dr. Lawrence named his discovery transfer factor because it was the factor that transferred tuberculosis immunity from a person who had an active immunity to tuberculosis to a naive individual. Latter it was discovered that this process is naturally accomplished between mammalian mothers and their newborns through the mother's colostrum.

Transfer factors were discovered to be universally effective regardless of the differences between the species of the donor and the recipient. The more essential a material or structure is the more common one sees this material or structure throughout living systems.

Dr. Lawrence has explained that transfer factors are essential components of even the most primitive immune systems. Unlike antibodies that are large proteins, transfer factors are small peptides containing about eight amino acids. The small size of the transfer factors makes them non-allergenic. Antibodies are consumed by directly attaching themselves to the offending cell or protein. Transfer factors perform a different role. Transfer factors are immune messenger molecules that educate and alert naive immune cells to an impending danger. In this regard transfer factors perform a catalytic role in the immune system, triggering the affect without themselves being consumed.

Transfer factor preparations consist of three identifiable fractions. These are an inducer fraction, a antigen specific fraction and a suppressor fraction. The immune system must be able to respond quickly, respond specifically and not exhaust itself by over responding and attacking normal tissue. The three transfer factor fractions were named because of the discovered affects they had on immune system. The inducer fraction triggers a general state of readiness in the immune system. The antigen specific fraction is an array of critical tags used by the immune system to identify a host of enemy microbes. The suppressor fraction is as important as the other fractions in that the components of this fraction keep the immune system from focusing all its strength on a defeated infection while ignoring new microbial threats. The suppressor fraction is also responsible for controlling allergic reactions and blocking autoimmune disorders.

Originally transfer factor preparations were administered by injection. Later studies showed that transfer factor was equally effective when taken orally. This means that the potency of transfer factor is not degraded by stomach acid or digestive enzymes.

The existence of multiple components in the antigen specific fraction leads to what is called a poly-valent transfer factor preparation. For example the transfer factor provided by the mother's colostrum to the newborn is a compilation of her own infectious experiences. Sometimes a transfer factor product is called a specific transfer factor. What this often means is not that the product is actually specific but rather that the batch was tested for and shown to contain activity against a specific microbe. Methods for generation of truly specific, or at least highly focused, transfer factor drugs involve live pathogen inoculation or pharmaceutical biotechnology.

Transfer factor drugs can be prepared in one of three ways. First, the blood of an individual who has either deliberately been inoculated or inadvertently contracts the desired infection can be processed to recover the specific transfer factor. Second, an expectant female can be deliberately infected prior to delivery. The expectant mother then generates an increased amount of transfer factor specific to the current pathogen. This specific transfer factor would be enhanced in the mother's colostrum which would then be harvested and the transfer factor isolated. Live pathogen inoculation can not be done in all cases since it is known that pathogens mutate as they pass through animal intermediaries. This was the case in the Hong Kong flu wherein chickens acted as the animal vector which lead to lethal human infections. In the case of diseases such as AIDS, HIV specific transfer factor drugs can be generated using a third technique. In this technique immune cells are grown in pharmaceutical cell-cultures under extreme containment conditions in the presence of the infectious agent. The problems with specific transfer factors prepared in this way are that they may lack the inducer and suppressor fractions.

Claim of activity against a specific infectious disease is a drug-like claim and not allowed under the 1994 Dietary Supplement Health and Education Act (DSHEA). Under DSHEA dietary supplements can be claimed to strengthen or support a normal body function. Thus strengthening the immune system through the use of transfer factors obtained as a "milk product" is well within the legal bound set up by law. Claims of efficacy against specific diseases has been the basis of FDA crackdowns on dietary supplement suppliers and users. Transfer factor products can be both dietary supplements and drugs depending on how they are prepared and marketed.

Antibody Supplements
Antibody therapy has been examined experimentally since the 1930's. At that time antibody-containing animal sera was delivered intravenously to successfully treat a number of illness. Any non-human antibody is rapidly rejected by the recipient's immune system leading to a severe side reaction called serum-sickness. This technique was largely abandoned due to the severity of the side-reactions.

Even with the recent development of human monoclonal antibodies the problem was not solved. Monoclonal antibodies are great research tools but they are also very expensive. Monoclonal antibodies have a critical weakness in that they are focused on a single antigen. An antigen is a recognizable feature on a foreign body that the immune system uses as a point of recognition. If the infectious agent mutates slightly the antigen would no longer be present and the microbe would become invisible to the antibody.

Clinically antibodies are administered by injection. Oral ingestion of antibodies is naturally observed in mammals wherein the mother provides colostrum to her offspring. Studies have shown that antibodies from colostrum are absorbed intact into the bloodstream of newborns. Absorption of intact antibodies usually ends within 24 hours of first feeding due to maturation of the infant's intestinal tract. Two features should be noted here. First the mother and infant are of the same species thus no anti-antibodies are formed. Second the recipient is an infant without a fully developed digestive system.

Oral administration of antibodies to adults leads to rapid degradation of the antibodies due to both the acidity of the stomach and the action of intestinal enzymes. This leads to the recommendation that both stomach acid and intestinal enzymes be neutralized to obtain maximum benefit from orally administered antibodies. Antibodies from colostrum and egg yolk have been found to be more resistant to stomach acid than serum antibodies. Antibodies, from these and other sources, are not well absorbed except in newborns as noted above.

Rapid transit and incomplete digestion are the hallmarks of diarrhea. It is in just such a condition that oral ingestion of antibodies is most effective. No absorption of the intact antibodies is required since the troublesome agent is in the intestines.

The use of the immunoglobulin fraction of colostrum has been patented as a source of sulfur amino acids. The availability of these amino acids is essential for the biosynthesis of glutathione. Glutathione is a critical natural antioxidant and detoxification agent in humans.

The proper use of antibodies from colostrum, hyperimmune milk, and hyperimmune egg yolk require multigram quantities for effectiveness. For example one company supplies a product in single-dose, 45 gram pouches. This is in contrast with other companies who sell bottles of 90 capsules each capsule containing 500 mg of dried colostrum or 45 grams total material. These products are represented as a one month supply instead of a daily dose.

A general antibody product from colostrum or egg yolk would clearly be a dietary supplement. The production and isolation of antibodies for specific diseases would create a products whose claims would make them drugs by current legal terminology and thus restrict their use to licenced medical practice.

Lactoferrin
"Lactoferrin is an 80-kDa, iron-binding glycoprotein present in milk and, to a lesser extent, in exocrine fluids such as bile and tears." "Owing to its iron-binding properties, lactoferrin has been proposed ...to act as a bacteriostatic agent by withholding iron from iron-requiring bacteria."¹⁸ Lactoferrin is found in high concentrations in human colostrum but the level of lactoferrin in bovine colostrum is very low.¹⁸

REFERENCES
1 The cellular transfer of cutaneous hypersensitivity to tuberculin in man. Lawrence HS. Proc Soc Exp Biol Med 1949, 71, 516.

2 Process for obtaining transfer factor from colostrum transfer factor so obtained and use thereof. Wilson GB, Paddock GV. US Patent Number 4816563; Mar. 28, 1989.

3 A new basis for the immunoregulatory activities of transfer factor__an arcane dialect in the language of cells. Lawrence HS, Borkowsky W. Cell Immunol 1983, 82, 102_16.

4 Structural Nature and Functions of Transfer_Factors. Kirkpatrick CH. Annals of The New York Academy of Sciences 1993, 685, 362_368.

5 Effect of in vitro produced transfer factor on the immune response of cancer patients. Pizza G, Visa D, Boucheix CI, Corrado F. Eur J Cancer 1977, 13, 917-23.

6 Roda E, Viza D, Pizza G, Mastroroberto L, Phillips J, De Vinci c, Barbara L. Transfer factor for the treatment of HbsAg-positive chronic active hepatitis. Proc Soc Exp Med 1985, 178, 468-75.

7 Transfer factor 1993: New frontiers. Fudenberg HH, Pizza G. Progress in Drug Res. 1994, 42, 309-400.

8 Transfer factor _ current status and future prospects. Lawrence HS, Borkowsky W. Biotherapy 1996, 9(1-3), 1_5.

9 Activities and characteristics of transfer factors. Kirkpatrick CH. Biotherapy 1996, 9, 13_6.

10 a) Investigators present latest findings on Hong Kong 'bird flu' to the FDA. Marwick C. JAMA 1998, 279, 643_4.

b) Questions remain as Hong Kong's avian flu crisis continues. McManus J. Brit Med J 1998, 316, 91.

11 Return to the past: the case for antibody-based therapies in infectious diseases. Casadevall A, Scharff MD. Clinical Infectious Diseases 1995, 21, 150-61.

12 Antibody Therapy. Wawrzynczak EJ. Oxford, UK: BIOS Scientific Publishers Limited, 1995, p 9-10.

13 The renaissance of antibody therapy. Burnie JP, Matthews RC. J. Antimicrobial Chemotherapy 1998, 41, 319-322.

14 [The absorption of colostral immunoglobulins in newborn piglets. II. Effect of water or glucose solutions on the permeability of the newborn intestine] Klobasa F, Habe F, Werhahn E. Berl Munch Tierarztl Wochenschr 1991, 104, 37_41.

15 Reduction in virus_neutralizing activity of a bovine colostrum immunoglobulin concentrate by gastric acid and digestive enzymes. Petschow BW, Talbott RD. J Pediatr Gastroenterol Nutr. 1994, 19, 228_35.

16 Antibody Therapy. Wawrzynczak EJ. Oxford, UK: BIOS Scientific Publishers Limited, 1995, p 32.

17 Treatment of diarrhoea in human immunodeficiency virus_infected patients with immunoglobulins from bovine colostrum. Rump JA, Arndt R, Arnold A, Bendick C, Dichtelmuller H, Franke M, Helm EB, Jager H, Kampmann B, Kolb P, et al. Clin Investig 1992, 70, 588_94.

18 Lactoferrin: Molecular Structure and Biological Function. Lonnerdal B, Iyer S. Annual Reviews in Nutrition 1995, 15, 93-110.