This is for informational purposes only.
It is not intended as medical advice, business
advice, or to be used for treatment of disease.
Transfer Factors are not a drug, they are a
dietary supplement that supports and educates the immune system. Although
there are definite benefits from supporting immune system activity with
transfer factor, there is insufficient research to consider the immune system
a drug.
The FDA considers Transfer Factors a
transferceutical in a classification of its own.
The intent of this article and information is
to give you a better understanding of the roles that transfer factors play in
the immune system and how the immune system operates to protect the body
against threats to health only.
Independent study results show an increase of
248% NK Cell activity over baseline! The NK Cells are our first line of
defense against viruses, tumor cells, etc.
Natural Killer (NK) Cells are a type of lethal
lymphocyte
Scientists estimate that NK
cells make up five to 16 percent of the total number of white blood cells that
the body uses to fight infections. Those with defective or absent NK cell
activity can contract a wide spectrum of diseases, particularly cancers. In
fact, results from a number of clinical trials indicate that NK cells can be
used to control tumor metastases. The therapeutic uses of NK cell activity
will likely increase as their relationships to healthy and diseased cells
becomes better known.
Natural Killer (NK)
cells - NK cells were discovered in the 1970's and are a subset of
large granular lymphocytes that are cytotoxic cells. They are called
"natural" killers because they, unlike cytotoxic T cells, do not
need to recognize a specific antigen before swinging into action. They are
capable of spontaneously killing tumor or virus-infected cells. In several
immuno-deficiency diseases, including AIDS, natural killer cell function is
abnormal. Natural killer cells may also contribute to immuno-regulation by
secreting high levels of influential lymphokines.
Natural Killer (NK) cells have no
immunological memory and are independent of the adaptive immune system, NK
cells make up approximately 15% of the human white blood cells. Their specific
function is to kill infected and cancerous cells.
Recent research reveals that NK cells are
involved in multiple effector, regulatory and developmental activities of the
immune system. Research has confirmed that low NK cell activity causes one to
be more susceptible to autoimmune diseases such as CFS, viral infections and
the development of cancer cells.
Any statement that natural killer (NK) cells
play an "important role" in human health is as casual as saying that
the brain is important for bodily function. If our brain is not present and
active we cannot continue "living". If our immune system is not
armed and working well we will also not continue "living" for very
long. NK cell activity is to the immune system, what brain activity is to the
body.
Activated NK cells produce a variety
of cytokines, including interferons,
interlukins, TNF (Tumor Necrosis Factor, hematopietic cell growth factors and
other growth factors. There is substantial evidence that indicates the
involvement of NK cells in the interactions of the immune system with the
neuroendocrine axis. They also appear to be responsible for activities at the
interface between the immune system and the reproductive and neurological
systems.
NK cell activity and NK cell count are not
the same. NK cells may be present in sufficient numbers, but unless they are
activated they are ineffective in doing their job. Decreased NK cell activity
is linked to the development and progression of many diseases. According to
the Center of Disease Control, low NK cell activity is present in all illness.
NK cell function appears to be a biologic marker for disease and is an
important indicator for declining or improving health.
The following assertion can be made; if one
is suffering from an illness, be it chronic, recurring or acute, the NK cell
activity would be below normal. The restoration of NK cell activity to a high
normal would be desirable, if not necessary, for recovery.
Low NK cell activity begins with stress of
some type. When the body is unable to adequately adapt to the environment
there is a resulting compromise of body function. Stress comes through loss of
sleep, overwork, emotional encounters, lack of exercise, poor nutrition,
exposure to toxins, exposure to germs etc.
Excessive stress causes many detrimental
changes in the body physiology and particularly the immune system. There is
research evidence that there is a relationship between Natural Killer (NK)
cell activity and reaction to emotional stress. There is low NK cell activity
in individuals who have difficulty in handing stress and those suffering from
behavioral disorders.
Acute low NK cell activity resulting from
temporary stress can be eliminated with the elimination of the stress factor.
For example, if we are over-tired and under-nourished we can simply rest and
eat properly for a few days and recover. However when we become continually
immune compromised we start developing recurring problems which may lead into
serious or chronic conditions.
NK cell activity level is lowered in times
of stress and can become chronically low with chronic stress. Research shows
that normal NK cell activity is essential to the recovery and maintenance of
good health. One way to offset the effects of stress is to
support
normal
NK cell function.
When the immune system is overwhelmed the
communication pathways are compromised and remain compromised until
re-established. If the communication networks are not restored there is little
opportunity for the immune system to regain full defensive capability.
Communication in the immune system, is
accomplished through the cytokine mechanism. These messenger molecules must be
activated to energize the communication capability that is necessary for
immune system reliability.
Conversely, immune modulation that harnesses
the body's ability to regulate will have an all-encompassing immune response
that is not limited to one specific area of immune response. Regulation,
upward or downward, in accordance with the needs of the body will be achieved.
Transfer Factor Plus: An
In Vitro Study -
Hosted
by the Institute of Longevity Medicine 11/5/99
PRELIMINARY REPORT
(additional test results to follow) Transfer Factor
Immune
System Support Testing
Background and
rationale '.) Cancer is the
second leading cause of death in the US. The rate of nearly every type of
cancer is on the rise. Despite billions of dollars in research, the mortality
rate has remained nearly unchanged and morbidity has increased slightly since
the 1960's using conventional treatments such as radiation, surgery and
chemotherapy. Thus, there is considerable interest in using immune modulation
support as a non drug for adjuvant cancer therapy. Natural Killer cells are
particularly important in destroying cancer cells.
Purpose of study : 1)
To determine the in vitro anti-cancer effects of
the immune system activity supported by Transfer
Factor and Transfer Factor Plus using PBMC isolated from human volunteers and
assaying the increased ability of the NK cell population to kill K562
erythroleukemic cells.
Methods: 1) PBMC
killing of K562 (erythroleukemic) cells
Results: 1)
Transfer Factor increased NK-cell killing by 103% and
Transfer Factor Plus by 248%
Conclusions :
Transfer Factor and Transfer Factor Plus supported an immune-based lysis of
K562 cells at a level unprecedented in the director's experience or in the
known medical literature. Since NK cell function is so crucial in killing
cancer cells, these non drug products are ideal candidates to support immune
system activity during cancer adjuvant therapy. In addition, NK cells form a
first line of defense against infections from viruses and certain
microorganisms. Killing assays against K562 cells have also been correlated
with increased activity against chronic and acute infections as well.
Director, Bioassay Laboratory
Institute of Longevity Medicine
Immune System Study with 20
Cancer Patients
Darryl See, M.D. conducted the following studies.
Twenty patients, 12 men and 8
women, were selected for this in vivo study. The average age was 49.3. The
twenty individuals were each level 3 or level 4 cancer patients. Each patient
was basically sent home by his or her oncologist to die. The average life
expectancy was 3.7 months. The protocol was to place each patient on 9
capsules per day of Transfer Factor Plus™. The patients were given a number
of other general nutrients (Antioxidants, Digestive Enzymes, Probiotics, and
multi-vitamins). After eight months, 16 of these 20 individuals were still
living and were either in remission, improving or stabilized.
The baseline for natural killer cell
function was 6.4. Within 4 weeks the average NK Cell function was increased to
25.7 and in 6 months it increased to 27.6. This represented a 400% increase in
NK Cell function. This is an ongoing study. This study has been submitted to a
peer reviewed publication.
The following study was conducted at the
Institute of Longevity. The purpose of the study was to examine the
synergistic effects of the components of Transfer Factor Plus
™.
Each component was tested separately and then tested as a whole unit. Together
the proprietary blend increased NK Cell functions more than the sum total of
all of the ingredients tested separately. This study indicates that the
intelligence contained in Transfer Factor™
molecules has
an enhancing effect on other nutrients.
In vitro study:...
Ingredient 10 GM /ml NK Function
PBMC (Control) 25.6%
Zinc 26.8% NS
Proprietary Blend 59.9% <0.02 (Mushrooms etc)
Zinc +Prop. Blend 95.4 <0.01
Transfer Factor
™ alone
128.5% <0.01
Complete Prod. (Transfer Factor Plus™)
273.6% <0.01
The sum of the individual product is less than the Complete Product (Transfer
Factor Plus™).
There is synergy in having a combination of Transfer Factor Plus™.
Transfer Factor and Clinical Applications
by Steven J. Bock, MD
Reprinted with Permission from the International Journal of Integrative
Medicine
The immune system is amazingly complex.
Fortunately, nature gives neonates a little help. We are realizing the
importance of breast-feeding and immune competency. In this increasingly
dangerous world, we are being assaulted by pathogen after pathogen. Our immune
systems are faltering. Transfer factor (TF), the premier immune factor in
colostrum, can be a vital part of our armamentarium. Transfer factor trains
and continually educates the immune system. H.S. Lawrence discovered transfer
factor in 1949, when he demonstrated that an immune fraction of a person’s
white blood cells was able to transfer immunity in a nonsensitized individual.
Transfer factors are small molecules of 3,500-6,000 kDa molecular weight,
consisting of oligoribonucleotides attached to a peptide molecule. In the
past, they were derived from dialyzed white blood cells (WBC), but now they
can be purified from bovine colostrum or egg yolks. Transfer factors are
produced by T-lymphocytes and can transfer the ability to recognize a pathogen
to cells that have not been in contact with the pathogen (memory function).
They also heighten the immune system’s ability to react (increased
reactivity or inducer function) to pathogens. Transfer factor probably
produces a trigger for T-cell recognition of antigens. On the other hand, it
may act as a gene product that assists in antigen presentation to other
T-cells.(1) This inducer fraction of transfer factor links the immune cells
with an antigen-binding site, thereby increasing their reactivity to an
antigenic stimulus. The suppressor fraction, known as nano factors, blocks the
response of the T-cells,(2) and signals a down regulation of the immune
response. This is useful in allergic or autoimmune conditions.
Role of TH1, TH2
Before one can understand the usefulness of
transfer factor, it is helpful to have an understanding of the TH1 helper/TH2
helper paradigm. T helper lymphocytes develop along two lines of cell
populations. TH1 cells, which modulate cell-mediated immunity, produce the
cytokines: IL-2, IFN-gamma, and TNF-alpha. TH2 cells, which modulate humoral
immunity, or antibody production, produce IL-4, IL-5, IL-6, IL-10, and IL-13.
Once you’re familiar with the particular TH1/TH2 predominant phenotypes in a
patient, you can more easily identify certain constellations of
health,
and tailor your support.
Cell-mediated or TH1 helper responses are important in the body’s ability to
defend itself against viruses, fungi, parasites, cancer, and intracellular
organisms. Cell-mediated immunity can be tested by:
1. Skin tests–delayed hypersensitivity skin
testing;
2. Response to non-specific mitogens, such as
phytohemagglutinin (PHA), concavalina, or pokeweed mitogens;
3. Response to specific mitogens, such as
diptheria, tetanus, or candida;
4. Response to alloantigens—mixed lymphocyte
reaction;
5. T-cell subsets;
6. IL-2R;
7. NK cell level;
8. NK cell activity;
9. IL1 assay; and
10. IL2 and interferon gamma, and other
cytokines. If one has a TH2-dominated condition, with decreased cellular
immunity and heightened humoral immunity, the conditions that tend to prevail
are:
1. Allergies
2. Chronic sinusitis
3. Atopic eczema
4. Asthma
5. Systemic autoimmune conditions such as lupus
erythematosus and mercury-induced autoimmunity
6. Vaccination-induced state
7. Certain cases of autism
8. Hyperinsulinism
9. Pertussis vaccination
10. Malaria
11. Helminth infection
12. Hepatitis C
13. Chronic giardiasis
14. Hypercortisolism
15. Chronic candidiasis
16. Cancer
17. Viral infections
18. Ulcerative colitis
A TH1-dominated picture would include
the following medical states:
1. Diabetes type 1
2. Multiple sclerosis
3. Rheumatoid arthritis
4. Uveitis
5. Crohn’s
6. Hashimoto’s
7. Sj
ögren’s
syndrome
8. Psoriasis
9. Sarcoidosis
10. Chronic Lyme
11. H. pylori infections
12. E. histolytica
Pregnancy is a TH2-dominant state. This is
an advantage during pregnancy, since a TH1- dominant state, or cell-mediated
immune response, would induce rejection of the fetus and placenta.(3) Because
it stimulates a TH1 response in most cases, transfer factor should not be used
in pregnancy. Certain autoimmune
responses,
such as multiple sclerosis and rheumatoid arthritis, which are TH1-dominant
states, are ameliorated during pregnancy.(4)
Transfer Factor
immune
system support in
Gynecological Conditions
• HPV infections
• Chronic vaginitis
• Chronic candidiasis
• Gynecologic cancer
• Genital herpes
TH1-dominant states are
generally not helped by transfer factor, and could be exacerbated. Many of
them, such as rheumatoid arthritis, multiple sclerosis, and Crohn’s, are
thought to be possibly caused by an infection or reaction to a pathogen. If
the TH1 response is an inadequate attempt of the immune system to fight off a
microbe, then transfer factor would augment that process and be effective in
certain cases. Clinically, this is seen in certain events, e.g., Crohn’s,
mutiple sclerosis, and chronic Lyme response, where transfer factor helps a
TH1-dominant condition. Transfer factor augments cell-mediated immunity or
pushes a TH2 to a TH1 state. This is useful in TH2-dominated conditions.
Normally, on exposure to gut-related microbes and childhood infections, a
child’s TH2-dominated immune system is subject to TH1 stimulation and
TH1/TH2 balance ensues.(5) If TH2 dominance remains, this can lead to atopic,
or allergic states. We see this in the increased incidence of allergic
symptoms, postnasal drip, asthma, etc., in clinical practice. The other side
of this TH2 state is a decreased TH1 or cell-mediated immunity. With this, we
see an increased incidence of viral infection, fungal infection, and cancer.
Vaccinations tend to push the immune system toward a TH2-dominant state. To
help overcome this tendency, we can use transfer factor pre- and
post-immunization.
*We would inject that the
advent of transfer factor nano-factor may change this scenario as nano-factor
wisely decreases immune system activity. We still do not recommend transfer
factor or tri-factor during pregnancy as sufficient testing is not completed
(WH. 2009).
Cancer,
Cell-mediated Immunity and Transfer Factor Immune System
Support
|
S
ince
cancer can be associated with a TH1-deficient state, use of transfer factor
should be considered as part of your support for immune augmentation in
cancer. Factors that decrease cell-mediated immunity and TH2 dominance are
age, cytotoxic cancer treatments, post-surgery stress, metastatic response,
etc.(6) Cell-mediated immunity (CMI) can be a predictor of morbidity and
mortality over the age of 60. In patients with liver metastases or colon
rectal carcinoma, CMI is predictive of survival.(7) Decrease in cell-mediated
immunity, along with an increase in circulating immune complexes, indicates
unfavorable prognosis in cancer patients.(8) Studies show that patients who
have multiple skin cancers had impaired CMI.(9) In a study of gynecological
cancer patients compared to control groups, those on chemotherapy had a
decrease in immune perimeters (i.e., refractory decreased cell-mediated
immunity), whereas the group getting immunotherapy (in this case, thymopeptin)
maintained their immune perimeters at normal levels.(10,11)
Immunologically deficient cancer patients
are susceptible to infection by viral pathogens, such as herpes zoster and
cytomegalovirus (CMV). Infection occurs as a result of cytotoxic therapy and
deficiency of cell-mediated immunity.(12) TH1-dominant states, characterized
by increased amounts of IL-2 and IFN-gamma, are immuno-stimulatory and limit
tumor growth. In contrast, TH2-predominant patterns, characterized by IL-4 and
IL-10 cytokines, are immuno-inhibiting and stimulate tumor growth. HIV
progression to HHV8 infection with Kaposi sarcoma, ulcerative colitis,
progression to colon cancer, and obesity with increased incidence of
carcinoma, are all associated with the increased TH2 state (and decreased
cell-mediated immunity). Studies suggest that this shift to TH2 dominance
precedes the cancerous transformation. As the cancer grows, it becomes
increasingly hypoxic. This leads to further suppression of cell-mediated
immunity, allowing decreased immune surveillance. Studies show that a TH2
immune response is associated with a proangiogenesis state, which facilitates
cancer growth.(13)
Transfer factor immune system
support has been shown to improve cellular immunity in patients with immune
defects.(14) Since it augments TH1 or cell-mediated immunity, transfer factor
immune system support is helpful in these situations. For example, by
conveying cell-mediated immunity against bladder and prostate tissue-specific
antigen, transfer factor immune system support was efficacious in stage D3
hormone-unresponsive metastatic prostate cancer. Follow up showed increased
survival rates in 50 patients, with complete remission in two, possible
remission in six, and no progression of metastatic responses in (14,15)
Transfer factor immune system support was shown to improve survival as an
adjunct to resection in non-small cell lung carcinoma.(16)
Before transfer factor was derived from
colostrum, it was obtained from dialyzed leukocyte extract (DLE). The
literature has many citations of DLE of an antigen-specific nature being used
for various viral conditions, autoimmune conditions, and certain cancers. It
has been found that DLE facilitated immunity to tumor-associated antigen.
Fudenburg showed that transfer factor could, from selected donors, increase
the
immune system cell-mediated
responses to tumor-associated antigens in human osteogenic sarcoma patients.
One of the compromises on our
cell-mediated immunity is environmental stress (e.g., chemical or heavy metal
pollution). It has been shown that long-term exposure to polychlorinated
hydrocarbons suppresses phagocytosis, decreases NK cell activity, and reduces
lymphocyte response to mitogens in mice.(17) Alterations in immune
dysregulation, with a predominantly TH2 response, occurs with lead and mercury
exposure. This leads to impaired cell-mediated immunity, increased incidence
of infectious activity or cancer, and can end with an autoimmune response.(18)
Transfer Factor immune
support in Allergy and ENT Patients
•
Chronic sinusitis
• Chronic allergies
• Postnasal drip
• Atopic
• Asthma
• ENT cancer
Transfer Factor
immune
support in GI
Practice
• Ulcerative colitis
• Viral hepatitis
• Chronic candidiasis
• Gastroenteritis
• GI cancer
Viral Infections
Currently in medicine, we are seeing
increased problems with viral infections, such as otitis media, measles,
chronic fatigue, Epstein-Barr virus (EBV), CMV, acquired immunodeficiency
syndrome (AIDS), hepatitis, and West Nile virus. We utilize regimens that
range from interferon to azidothymidine (AZT), ribavirin, and relenza.
However, even with all the high-tech immune weapons available, we are still
losing the battle.
With Immune
support in viral infections, transfer factor immune support provides an
advantage at a fundamental level. The immune system has been shown to induce
interferon in patients with viral infections.(19)
Viruses tend to increase TH2 and decreased
TH1. This is also seen with fungi, parasites, and cancer. Bacteria are
associated with decreased TH2-dominant states.
By stimulating TH1, transfer
factor immune system support may be advantageous in hepatitis. In hepatitis C,
the activation of the TH2 dominance plays a role in the development of chronic
hepatitis changes. TH1 stimulation may result in clearance of viral particles
and improvement in the hepatitis.(20,21) Studies show that severe complicated
measles has been helped successfully with non-specific transfer factor immune
system support. Symptoms were ameliorated within 24 hours, without side
effects.(22)
One theory claims that one of
the mechanisms involved in the autistic spectrum is an immune imbalance toward
a dominant TH2 pattern, resulting from measles, mumps, and rubella (MMR)
vaccination. Currently, a study is ongoing to test the efficacy of transfer
factor immune system support to act as an immune modulator.
It is well-known that viruses play an
important role in the etiology of acute otitis media (AOM) in children. In a
study of AOM, 75% of the children were positive for viruses such as
respiratory syncytial virus (RSV), para influenza, and influenza, and 48% had
the causal viruses in the middle ear effusion.(23) These viruses probably act
as antecedents to the bacterial infections typical of AOM.(24) This could
account for the excellent results seen in otitis media using transfer factor
to support the immune system.
A certain percentage of
asthmatics have their symptoms precipitated by respiratory infection, most of
these secondary to viral infections. A study conducted with transfer factor
immune system support and asthmatic patients showed that approximately 50%
discontinued their steroid medication and the other half decreased their
steroid use. Overall, there was a decrease in hospital admissions.
Administration of transfer factor immune system support improved cellular
immunity. No adverse effects or allergic reactions were observed.(25)
In Annals of Allergy, Kahn reported the
increased incidence of infection, such as para influenza virus, syncytial
virus, adenovirus, etc., as precipitating factors in children who have asthma.
It was also found that children with asthma have a propensity toward frequent
infection.(26) Twelve of 15 children exhibited defects in T-cell immunity,
many of which were not drastic.(27) This should emphasize that functional,
suboptimal defects in cell-mediated immune function can be a factor in viral
illnesses, as measured with sensitive immunological testing. Once again, we
see that transfer factor
immune
system support can
help with increased susceptibility to viruses, a dominant TH2 (decreased
cell-mediated) profile.
It was found that women with extended human
papilloma virus (HPV) infections have defective protective mechanisms of
cell-mediated immunity.(28) A pronounced shift from TH1 to TH2 cytokine
pattern is associated with more extensive HPV infection. Increased
gynecological problems are found secondary to HPV. The potential of transfer
factor
immune system support in
HPV infections needs to be further explored.
Chronic Infection
The addition of transfer factor can help an
impaired immune system that is subject to chronic infections. How many
practitioners see this scenario: A child comes down with recurrent bronchitis
or tonsillitis, starting shortly after birth, necessitating frequent courses
of antibiotics. This can then lead to symptoms of chronic candidiasis. A
history of chronic eczema or allergic diathesis can also be found.
Immunological or skin testing shows a mild defect in cell-mediated immunity,
but no abnormalities. Grohn reported on several similar cases and obtained
successful treatment with administration of transfer factor.(29) Here we see
that transfer factor is helpful for elevated TH2 states, allergy, chronic
candidiasis, and eczema.
Transfer factor immune system
support has ameliorated cases of recurrent, non-bacterial cystitis (NBRC) when
treatment with antibiotics and non-steroidal drugs was unsuccessful, and
cell-mediated immunity to herpes simplex and candida was decreased.(30)
Various studies show positive results with transfer factor in chronic
mucocutaneous candidiasis.(31)
With Lyme, cytotoxic production
of a TH2 phenotype is correlated to resistance, while that of a TH1 phenotype
is correlated to susceptibility.(32) This suggests that certain people have an
immune glitch that makes their immune system prone to either the TH1 or TH2
pattern, and therefore more susceptible to different diseases. This may be
precisely where transfer factor immune system support, having
immune-modulating effects, can be helpful. For instance, in Lyme patients we
usually see a TH1-dominated pattern, but transfer factor immune
system support works
very well for certain subsets of Lyme patients.
Chronic Fatigue
Transfer factor immune system
support has been used in chronic fatigue, especially if a viral etiology can
be found. It has had varied success, although one may need to use increased
dosages. If polyvalent transfer factor immune system support is not
successful, the use of antigen specific transfer factor immune system support
may need to be explored.(33)
In elderly patients with
cellular immunodeficiency and chronic fatigue syndrome, age-related decrease
in recovery occurred after treatment with transfer factor.34 Success with
transfer factor in chronic fatigue syndrome secondary to human herpes virus 6
(HHV6), genital or labial herpes, and recurrent ocular herpes has been
well-documented.35-37 A study on the effect of transfer factor immune system
support on the course of multiple sclerosis showed that it retarded the
progression in mild to moderate situations.(38)
The Treatment
Treatment with transfer factor is dose
dependent. In viral infections, one usually starts with three capsules three
times a day. The dose is then tapered down to one capsule three times a day.
That dose is maintained in cases of chronic viruses, chronic herpes infection,
chronic fatigue secondary to CMV or EBV, chronic colds, and impaired
resistance. If there is any flare-up in viral infections, the dose can be
increased to three capsules three times a day. Usually, patients report
decreased susceptibility to colds, decreased nasal symptoms (for instance,
postnasal drip and chronic sinus symptoms). In allergic conditions, an adult
starts with two capsules three times a day, increasing to three capsules three
times a day if symptoms get worse. Again, the dose is tapered to a maintenance
level with amelioration of allergic symptoms.
In cases of chronic fatigue syndrome, patients start on
three capsules three times a day. One may need to increase the dose patients
undergoing chemotherapy and/or radiation therapy, with a resulting decrease in
cellular immune function.
Immune System Modulators
For Immune Imbalances
• Fibromyalgia
• Lyme (certain subsets)
• EBV, CMV, HHV6, and other viral
infections
Various immune function tests, especially
those measuring CMI, can be done to gauge maintenance dosage. One can also
perform a cytokine panel, measuring IL-2, IL-4, IFN-U, IL-10, etc. An elevated
IL-2 and interferon gamma would indicate a TH1-predominant state, while an
elevated IL-4 and IL-10 would point to a TH2-dominated state. NK cell
activity, which is usually decreased in cases of cancer, is increased
secondary to transfer factor administration, and can be periodically measured.
In pediatric cases with increased
susceptibility to viruses, asthma, allergic chronic sinus symptoms, and
chronic candida symptoms, initial dosage is:
Under 1 Year: 1/2 capsule a
day (200mg of transfer factor per capsule).
1-5 Years: 1/2
capsule a day.
6-12 Years: 1
capsule 2 times a day.
Over 12 Years 1
capsule 3 times a day
These are starting doses; the doses can be
gradually increased depending on the severity of the case.
Occasionally, when a person
starts transfer factor immune system support, he or she may experience
flu-like symptoms, nausea, or gastrointestinal symptoms. Since transfer factor
is a small peptide and does not contain milk protein, allergic reactions are
rare. These symptoms are usually classified as Jared Herxheimer mechanisms,
and they probably signify a direct reaction of transfer factor on gut or
systemic pathogens. If people are informed of these possible mild reactions,
they are more likely to continue using the the transfer factor supplements.
Factor in Pediatric Practice
• Chronic pharyngitis
• Eczema
• Allergies
• Asthma
• Food allergies
• Autism (certain subsets)
• Prevention of vaccination-induced TH2
states
• Chronic infection
• Thrush and candidiasis
• Otitis media
• Cancer
• Autoimmune states: lupus and ulcerative
colitis
• Chronic fatigue
• Fibromyalgia
• Lyme (certain subsets)
• EBV, CMV, HHV6, and other viral
infections
Transfer Factor
Immune
System Support vs. Alternative Therapies
In complicated immune cases or in adjunct
cancer treatment, it is advantageous to add complementary classes of herbs and
nutrients to augment the immune
system-support
effects. These auxiliary factors boost natural killer cell activity, increase
phagocytosis, increase maturation of T- cells, enhance general immunity, and
trigger the complement cascade, helping cytotoxicity. Compounds that act
synergistically with transfer factor include thymic protein factors, Chinese
herbs (such as astragalus, cordyceps, shiitake, maitake, and reishi), inositol
hexaphosphate, melatonin 1-3 beta glucan glutathione and associated
antioxidants Vitamins A D and B6 promote the TH2 pattern, while vitamins E, C,
and folate support the production of a TH1 response.(39) Vitamin B12
suppresses the TH1 response.(40) In addition, acupuncture has been found to
increase the immune perimeters of CMI. Levels of CD 3+, CD 4+, CD 4+/CD8+, and
beta-endorphins were found to be increased in patients with malignant tumors
after a course of acupuncture treatment.(41)
Thymic factors cause maturation of na
Vve
T-cells and increase cell-mediated immunity. It is known that transfer factor
is more effective in post-thymic cells. Therefore, both thymic factors and
transfer factors are recommended for mild thymic primary
immunodeficiency.(42,43) A recent study by Dr. D. See showed that transfer
factor immune system support enhanced
natural killer cell cytotoxic activity. The effect of transfer factor immune
system support was
greater than that observed with other well-known NK cell activity enhancers,
such as echinacea, acemannan, 1-3 beta glucan, IP-6, and certain Chinese
mushrooms. Colostrum had 1/4 the potency. Other immune parameters, such as
T-cell function and test of cellular immunity, were not done in this
particular study.(44)
Conclusion
Immune system functioning is at
the heart of the increasing infectious and immunologic health seen in clinical
practices. Through its unique properties and activities, transfer factor
immune system support is an extremely useful, relatively risk-free alternative
to adjunctive therapy for treatment of cell- mediated or TH1-deficient
conditions. Think of immune system potential with cancer, fatigue, viruses,
allergies, fungus, chronic infections, and autoimmune responses.
Steven J. Bock has been
practicing alternative and integrative medicine for over 20 years. He has
extensive experience in the integrative treatment of Lyme disease. Dr. Bock is
a certified acupuncturist. He is medical director of The Rhinebeck Health
Center, The Center for Progressive Medicine and www.PatientsAmerica.com. He is
the author of Natural Relief for Your Child
and Staying Young the Melatonin Way.
(New York: Plume Books, 1996).
Reprinted with Permission from the International Journal of
Integrative Medicine
References
1. Lawrence HS, Borkowsky W: Transfer factor: current
status and future prospects. Biotherapy 9:1-5, 1996.
2. Ibid.
3. Kim S, Lira SM, Dalal MA, Verity MA, Voskuhl RR: Estriol
ameliorates autoimmune demyelinating. Neurology
4:P1230-1237, 1999.
4. Formby: Immunologic response in pregnancy. Endocrine
Metabol Clinic North Am 24:187-205, 1995.
5. Bjorksten B: Environment and infant immunity. Proc Nutr
Soc 58(3):729-732, August 1999.
6. Nicolini A, Ferrari P, Spinelli R, Carpi A, Sagripanti
A, Amborgi F: Cell-mediated immunity in breast cancer patients. Biomed
Pharmacother 50(8):337-343, 1996.
7. Bansal AS, Bruce J, Devine PL, Scells B, Zimmermann PV:
Serum cytokines and tumor markers in patients with non-small
cell carcinoma of the lung. Dis Markers 13(3):195-199,
November 1997.
8. Aziz M, Akhtar S, Malik A: Evaluation of cell-mediated
immunity and circulating immune complexes as prognostic indicators
in cancer patients. Cancer Detect Prev 22(2):87-99, 1998.
9. Czarnechi D, Zaleberg J, Kulinshaya E, Kaz T: Impaired
cell-mediated immunity of apparently normal patients who had
multiple skin cancers. Cancer 76(2):228-231, July 15, 1995.
10. Mallmann P, Krebs D: The effect of immunotherapy with
thymopentin on the parameters of cellular immunity and the clinical course of
gynecologic tumor patients. (Abstract) Onkologie 12(Suppl 3):15-21, June 1989.
11. Mallmann P, Krebs D: Investigations on cell-mediated
immunity in patients with breast and ovarian carcinomas receiving a
combination of chemotherapy and immunotherapy with thymopentin. Methods Find
Exp Clin Pharmacol 12(5):333-340, June
1990.
12. Kitahara T, Takeaka T, Yoshino M: Infection and
immunosuppression in cancer patients. (Abstract) Gan To Kagaku Ryoho
16(4 Pt 2-1):1108-1114, April 1989.
13. O’Byrne KJ, Dalgleish AG, Browning MJ, Steward WP,
Harris AL: The relationship between angiogenesis and the immune
response in carcinogenesis and the progression of malignant
illness. European Journal of Cancer 36(2000):151-169, September 21, 1999.
14.Lawrence HS: Transfer factor in cellular immunity. The
Harvey Lecture Series 68. New York: Academic Press, 1987.
15. Pizza G, De Vinci C, Cuzzocrea D, Menniti D, Aiello E,
Maver P, Corrado G, Romagnoli P, Dragoni E, LoConte G, Riolo U, Palareti A,
Zucchelli P, Fornarola V, Viza D: A preliminary report on the use of transfer
factor for treating stage D3 hormone-
unresponsive metastatic prostate cancer. Biotherapy
9(3-1):123-132, 1996.
16. Pilotti V, Mastrotilli M, Pizza G, De Vinci C, Busutti
L, Palareti A, Gozzetti G, Cavallari A: Transfer factor as an adjuvant to
non-small cell lung cancer (NSCLC) therapy. Biotherapy 9:117-121, 1996.
17. Jirova D, Sperlingova I, Halaskova M, Bendova H,
Dabrowska L: Immunotoxic effects of carbon tetrachloride: the effect on
morphology and function of the immune system in mice. Cent Eur J Public Health
4(1):16-20, February 1996.
18. Heo Y, Lee WT, Lawrence DA: In vivo the environmental
pollutants lead and mercury induce oligoclonal T cell responses
skewed toward type-2 reactivities. Cell Immunol
179(2):185-195, August 1, 1997.
19. Khan A: Transfer factor in viral illnesses. The Lancet
1 (8059):328-329, February 11, 1978.
20. Milich DR, Chen MK, Hughes JL, Jones JE: The secreted
hepatitis precove antigen can modulate the immune response to the nucleocapsid:
a mechanism for persistence. J Immunol 160:2013-2021, 1998.
21. Tsai SL, Liaw TF, Chen MH, Huang LY, Kuo GC: Detection
of type-2 like T helper cells in hepatitis C detection: implications for
hepatitis C virus chronicity. Hepatology 25:449-458, 1997.
22. Ferrer-Argote VE, Romero-Cabello R, Hernandez-Medoza L,
Arista-Viveros A, Rojo-Medina J, Balseca-Olivera F, Fierro M, Gonzalez-Constandse
R: Successful treatment of severe complicated measles with non-specific
transfer factor. In Vivo
8:555-558, 1994.
23. McCormick DP, Lim-Melia E, Sneed K, Baldwin CD,
Chonmaitice T: Detection of respiratory viruses in middle ear fluids of
children with otitis media infections. Ped Infectious Disease Journal
19(3):256-258, March 2000.
24. Ramilio O: Role of respiratory viruses in acute otitis
media: implications for management of AOM. Ped Infectious Disease
18(12):1125-1129, December 1999.
25. Khan A, Sellars W, Grater W, Graham M, Pflanzer J,
Antonetti A, Bailey J, Hill NO: The usefulness of transfer factor in
asthma associated with frequent infections. Annals of
Allergy 40(4):229-232, April 1978.
26. Ibid.
27. Khan A: The syndrome of asthma, recurrent viral
infections and T-cell immuno-deficiency: investigations and management.
Annals of Allergy 43(2):69-72, August 1979.
28. Clerici M, Merola M, Ferrario E, Trabattoni D, Villa
ML, Stefanon B, Venzon DJ, Shearer GM, De Palo G, Clerici E: Cytokine
production patterns in cervical intraepithelial neoplasis: association with
human papillomavirus infection. J Natl Cancer Inst
89(3):245-250, February 5, 1997.
29. Grohn P: Transfer factor in chronic and recurrent
respiratory tract infections in children. Acta Paediatr Scand 66:211-217,
1977.
30. De Vinci C, Pizza G, Cuzzocrea D, Menniti D, Aiello E,
Maver P, Corrado G, Romagnoli P, Dragoni E, LoConte G, Riolo U, Masi M,
Severini G, Fornarola V, Viza D: Use of transfer factor for the treatment of
recurrent non-bacterial female cystitis
(NBRC): a preliminary report. Biotherapy 9(1-3):133-138,
1996.
31. Masi M, De Vinci C, Baricordi OR: Transfer factor in
chronic mucocutaneous candidiasis. Biotherapy 9(1-3):97-103, 1996.
32. Matyniak JE, Reiner SL: T helper phenotype and genetic
susceptibility in experimental Lyme disease. Journal Exp Med
181(3):1251-1254, March 1, 1995.
33. Sherwood Lawrence H, Borkowsky W: Transfer factor:
current status and future prospects. Biotherapy 9:1-5, 1996.
34. Hana I, Vrubel J, Pekarek J, Cech K: The influence of
age on transfer factor treatment of cellular immunodeficiency, chronic fatigue
syndrome and/or chronic viral infections. Biotherapy 9(1-3):91-95, 1996.
35. Ablashi DV, Levine PH, De Vinci C, Whitman JE Jr, Pizza
G, Viza D: Use of anti HHV-6 transfer factor for the treatment of two patients
with chronic fatigue syndrome (CFS): two case reports. Biotherapy
9(1-3):81-86, 1996.
36. Pizza G, Viza D, De Vinci C, Palareti A, Cuzzocrea D,
Fornarola V, Baricordi R: Orally administered HSV: specific transfer
factor (TF) prevents genital or labial herpes relapses.
Biotherapy 9(1-3):67-72, 1996.
37. Meduri R, Campos E, Scorolli L, De Vinci C, Pizza G,
Viza D: Efficacy of transfer factor in treating patients with recurrent
ocular herpes infections. Biotherapy 9(1-3):61-66, 1996.
38. Basten A, Pollard JD, Stewart GJ, Frith JA, McLeod JG,
Walsh JC, Garrick R, Van Der Brink CM: Transfer factor in
treatment of multiple sclerosis. The Lancet 931-934,
November 1980.
39. Long KZ, Santos JI: Vitamins and the regulation of the
immune response. Pediatr Infect Dis J 18:283-290, 1999.
40. Ibid.
41. Wu B: Effect of acupuncture on the regulation of
cell-mediated immunity in the patients with malignant tumors. (Abstract)
Chen Tzu Yen Chiu 20(3):67-71, 1995.
42. Lawrence HS: Immune Regulation in Transfer Factor. New
York: Academic Press, 1979, p. 613.
43. Khan A, Sellars WA, Gabela P, Thometz D: Transfer
factor, thymosin and E rosettes. NEJM 292:868, 1975.
44. See D, Gurnce K, Leclair M: An in vitro screening study
of 196 natural products for toxicity and efficacy. JAMA 2(1),
December 1999.