4LIFE TRANSFER FACTOR® TRI-FACTOR FORMULA

PRODUCT DESCRIPTION

TECHNICAL DESCRIPTION

Transfer factors were first discovered in 1949 by H. Sherwood Lawrence when he demonstrated that CMI could be transferred from one individual to another by way of low molecular weight extracts of white blood cells. Transfer factors could transfer DTH of a specific form from a skin test positive individual to a skin test negative individual who subsequent to the transfer would skin test positive for that antigen.[6] In a subsequent study in 1955 he demonstrated that DTH could be passed serially, first from a skin test positive individual to a test negative individual, who became test positive, then 6 months later from the second individual to another test negative individual who became test positive.[7] At the time antibodies were the focus of immune research and little was known of the importance of DTH and of the involvement of T-cells in immune response. Transfer factors promote wellness via cell mediated immunity. These compounds are components of colostrum, an infant’s first meal. They bridge the generational gap by passing cell mediated immunity from mother to infant.


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See Mayo Clinic article on mumps

Some time ago a child my spouse was caring for came down with a runny nose which the following day became flu like symptoms with a fever. My wife had a pronounced swelling of the parotid gland. Frequencies were looking like a flue frequency set (see previous message below). She thought her lymph glands were swollen, but plate zapping lymph nodes with the frequencies detected did not do much.

A physician friend examined her and thought the swelling was lower on her jaw than the parotid gland. Since she was not noticably ill and mumps can be serious in an adult who was never vaccinated or had mumps, he discounted it. However, when I began treating her, the swelling was definitely above the jaw bone in the location of the parotid gland.

Since I happen to have a homeopathic Mumps nosode, I checked and she tested positive. Within a day or two the Mumps nosode along with some Oscillicosinum and frequency treatment kept her well and eliminated the swelling.

She, of course, infected me with the disease and over the course of a few days, I was able to identify the frequency set. I was never really ill because I detected the frequencies as soon as minor symptoms appeared.

More recently my spouse came back from the orthodontist with a swollen left jaw. After a few days she said it feels like mumps. Sure enough it was. Mumps is very infectious and I had to run frequencies for the whole family.

An upgraded frequency set for mumps is posted on the subscribers list.

National Institute of Allergy and Infectious Diseases

The malaria parasite is easily killed by electromagnetic frequencies and there are a number of small pilot projects using zappers in Africa. I’ve talked with some of the larger nonprofits about expanding these studies as I have seen 100% remission consistently with a few hours of application of exact frequencies. However, the response has been that if a non-profit research institute looked at anything other than conventional drugs they would get all their grants terminated.

It is important to keep up with the latest research on malaria as frequencies can also modify protein production. Virulent forms of this and other diseases (particular viral infections) can kill by evoking an overwhelming immune response. Thus frequencies must modulate immune response through reducing certain protein production as well as kill the pathogen. Those who are intelligent enough to use this technology can at least protect themselves.

Work on malaria frequencies at the recent Frequency Foundation workshop in San Diego has identified several new strains of the malaria parasite. These are available to subscribers as Malaria 2.0 frequencies.

Evolution of virulence in malaria
Bridget Penman email and Sunetra Gupta email
Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK
Journal of Biology 2008, 7:22doi:10.1186/jbiol83

The electronic version of this article is the complete one and can be found online at: http://jbiol.com/content/7/6/22
Published: 28 August 2008 © 2008 BioMed Central Ltd

Abstract
The pathogenesis of severe malarial disease is not yet fully understood. It is clear that host immunopathology plays a central role, and a recent paper in BMC Evolutionary Biology suggests that the ability of the parasite to stimulate interleukin-10 production is a major factor and speculates on its impact on the coevolution of host and parasite.

Minireview
Plasmodium falciparum malaria is responsible for over 1 million deaths each year, mostly in children under the age of 5 living in sub-Saharan Africa. And yet the number of malaria infections which go on to become life threatening is proportionally very small, as the majority of these infections either remain asymptomatic (due to the acquisition of clinical but non-sterile immunity after repeated exposure) or progress to disease without lethal complications [1]. Viewed in an evolutionary context, the existence of severe disease presents a population-level compromise for the parasite between the necessity of bearing factors that increase survival and transmission and the risk that these will stimulate a host immune response that will either curtail the infection or perversely cause the death of the host (thus also spelling the end for the parasite). With the aim of identifying factors that may be relevant in the evolution of this balance, Long et al. in a recent article in BMC Evolutionary Biology [2] have investigated the influence of the inflammatory response on the severity of disease in a rodent model of malaria, and we discuss here how their results may bear on the coevolution of parasite and host, in the context of what is known about the determinants of severe malarial disease in humans.
Factors in the severity of malaria

Severe malaria can be resolved broadly into two different syndromes: cerebral malaria and severe malarial anemia. Cerebral malaria is associated with impaired consciousness and sometimes convulsions and coma, and can leave those who recover with long-term neurological problems. Its pathophysiology is not fully understood but it is probably due to a combination of the obstruction of cerebral capillaries by parasitized cells and an overactive inflammatory response. Severe malarial anemia occurs when the suppression of erythrocyte production, combined with the destruction of red blood cells by the parasite itself, leads to a particularly profound anemia – which can cause shock and respiratory distress. Both syndromes can involve a range of metabolic complications such as acidosis or hypoglycemia [3].

Both host and parasite factors are likely to contribute to the processes leading to severe disease, and Long et al. have examined one possible interaction using mice infected with different clones of the rodent malaria parasite Plasmodium chabaudi chabaudi. Specifically, they have shown that blockade of the receptor for the anti-inflammatory cytokine interleukin-10 (IL-10) has a dramatic impact on time to death of the infected animal, particularly where the infecting parasite clones are normally avirulent. This result certainly implies that IL-10 plays a fundamental role in controlling the inflammatory response to malaria and that its absence can contribute to the demise of the murine host; Long et al. propose that the ability of the parasite to stimulate IL-10 production is a factor determining its relative virulence. However, whether regulation of the inflammatory response by IL-10 actually plays a part in the evolution of parasite virulence remains an open question and requires a careful consideration of the population-level consequences of interactions between host susceptibility and parasite virulence factors.

4Life Glutamine prime is a new product that will enhance your immune system. Check it out …

Sick Indonesians turn to ‘railway therapy’

Telomeres and Aging
GERALDINE AUBERT AND PETER M. LANSDORP
Terry Fox Laboratory, British Columbia Cancer Agency, and Division of Hematology, Department of
Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Aubert G, Lansdorp PM. Telomeres and Aging. Physiol Rev 88: 557–579, 2008;
Telomeres play a central role in cell fate and aging by adjusting the cellular response to stress and growth stimulation on the basis of previous cell divisions and DNA damage. At least a few hundred nucleotides of telomere repeats must “cap” each chromosome end to avoid activation of DNA repair pathways. Repair of critically short or “uncapped” telomeres by telomerase or recombination is limited in most somatic cells and apoptosis or cellular senescence is triggered when too many “uncapped” telomeres accumulate. The chance of the latter increases as the average telomere length decreases. The average telomere length is set and maintained in cells of the germline which typically express high levels of telomerase. In somatic cells, telomere length is very heterogeneous but typically declines with age, posing a barrier to tumor growth but also contributing to loss of cells with age. Loss of (stem) cells via telomere attrition provides strong selection for abnormal and malignant cells, a process facilitated by the genome instability and aneuploidy triggered by dysfunctional telomeres. The crucial role of telomeres in cell turnover and aging is highlighted by patients with 50% of normal telomerase levels resulting from a mutation in one of the telomerase genes. Short telomeres in such patients are implicated in a variety of disorders including dyskeratosis congenita, aplastic anemia, pulmonary fibrosis, and cancer. Here the role of telomeres and telomerase in human aging and aging associated diseases is reviewed.