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Visionamme on tuottaa oikeaa tietoa terveyden uhkatekijöistä.
Suurimpana ongelmana länsimaissa on jatkuva, yksipuolisesti liian hapan ruokavalio, jota elimistö ei kykene riittävästi puskuroimaan, vaan koko aineenvaihdunta -järjestelmä joutuu tekemään työtä happamuutta vastaan.
Lopulta elimistö alkaa tulehtua ja saavuttaa potilaan huomaamatta, jatkuvan tulehduksellisen tilan.
sunnuntai 26. helmikuuta 2017
GcMAF Goleic Therapy - 4 Verita Life Clinical Programmes
Macrophages are large immune cells found in our bodies that are able to recognise, engulf and digest cancer cells.
Also responsible for stimulating other immune cells,
macrophages can be activated by ‘MAF’ (macrophage activating factor), a naturally occurring protein. The precursor of MAF inside the body is called the Gc protein.
How Tumours prevent Macrophages
Tumour cells produce nagalase, a special enzyme inhibiting the
Gc protein’s function leading to high nagalase levels resulting in lower
MAF levels. The body’s macrophages subsequently cannot be activated,
leading to the suppression of the immune system.
Complementary oncology utilises breakthrough GcMAF therapy to
counteract this effect and enhance the immune system.
GcMAF Goleic Therapy
GcMAF therapy regulates the human protein required to reactivate immune
cells and boost patients’ immune systems. Many published peer reviewed
studies have proven that GcMAF Goleic therapy is not only an immune
activator, but can be used as a natural cancer treatment. In addition
to rebuilding a diminished immune system, GcMAF Goleic inhibits
angiogenesis (stops blood supply to tumours), activates macrophages
and apoptosis (suicide of cancer cells); reverts cancer cells’ phenotype
(characteristics) to normal healthy cells; reduces the metastatic
potential of human cancer cells and increases energy production at
the mitochondrial level. The treatments available at Verita Life > GcMAF Goleic is one of 15 separate core cancer treatments that can be
combined into your personal protocol. The exact combination and frequency of treatments is planned according to your specific needs. Chosen for proven effectiveness, every treatment has been shown, through
numerous medical studies and extensive experience, to attack and defeat
Following your enquiry and review of your case by our medical team, you
will receive a Doctor consultation. A full personalised protocol will follow and this will recommend the treatments needed.
Treatments are delivered in 4 Verita Life Clinical Programmes
Whatever phase of treatment, or Stage you are at, Verita Life can help treat your
Cancer and your cancer-related symptoms.
GcMAF Goleic and the other treatments are combined and delivered in 4 separate
Clinical Programmes, one of which is best for you, or your loved one.
1. If you are currently having Chemo or Radio therapy – maximise results
and minimise side effects. Verita Life Oncoboost™ protects your organs and
boosts your immune system.
2. If you are looking for Alternative treatments to defeat cancer
– Verita Life 360 ™
– Complete treatment protocols combining cancer-specific treatments if you don’t
want to, or can’t, undergo conventional treatments.
3. If you have not started treatment yet – Prepare your Immune system and
organs to withstand chemo and radio therapy with uniquely combined treatment protocols. Verita BodyBoost™.
4. If you are in remission. Recover from cancer side effects with All Clear Aftercare™
– rebuild a weakened immune system and damaged organs.
Regain your health and prevent cancer returning.
ALL TREATMENTS ARE WELL TOLERATED
1. We treat the cancer and support the immune system at the same time.
2. We ensure a diet and lifestyle change so that patients remove the conditions that promoted or supported tumour growth.
3. We give patients a chance to heal or maintain the status quo, even when conventional medicine has given up.
4. In almost all cases, we achieve a stronger immune system and improved quality of life.
R. A w iki for the life sciences w here authorship matters. Nature
Genetics (2008) Disease
relevance of Gc
maintained on vitamin D-deficient diets for a brief period, the
not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying
bone changes associated with vitamin D deficiency .
and resistance to vitamin D toxicity in mice null for vitamin D binding
an overload of vitamin D, DBP-/- mice were unexpectedly less
to hypercalcemia and its toxic effects .
forms of renal Fanconi syndrome are associated with endocytic
dysfunction with disruption of megalin-mediated uptake DBP/25- (OH)D3
complex, producing metabolic bone disease in affected individuals as a
prominent clinical finding .
utility of serum alpha-N-acetylgalactosaminidase and
resulted from deglycosylation of serum Gc protein in oral
cancer patients .
related information on Gc
homozygous for a DBP-null allele display less locomotor activity and free-run
with a shorter period than otherwise isogenic wild-type animals
impact information on Gc
show that 25-(OH) vitamin D3 in complex with its plasma carrier, the vitamin
D-binding protein, is filtered through the glomerulus and reabsorbed in
the proximal tubules by the endocytic receptor megalin .
The vitamin D(3)-binding protein (Gc protein)-derived
activating factor (GcMAF) activates tumoricidal macrophages against
a variety of cancers indiscriminately .
steady-state mRNA levels of the vitamin D-dependent calbindin-D9K gene
were induced by 1,25(OH)2D more rapidly in the DBP-/- mice .
line of mice deficient in vitamin D binding protein (DBP) was
generated by targeted
mutagenesis to establish a model for analysis of DBP's biological functions
in vitamin D metabolism and action .
the role of DBP is to maintain stable serum stores of vitamin D
and modulate the rates of its bioavailability, activation, and
compound and disease context of Gc
esters with short alkyl chains, such as di-ethyl (DEP), di-n-propyl (DPP),
and di-butyl phthalate (DBP), have adjuvant effects on an FITCinduced contact
hypersensitivity mouse model .
context of Gc
fourth gene, Gc, encoding vitamin D-binding protein or group-specific component,
maps to the same chromosome as the other family members,but
linkage has not been established .
report describes the genetic and physical mapping of Gc in mouse and establishes
that, although Gc is genetically linked to the other genes, its physical
distance from them extends beyond the resolution range of yeast artificial
chromosome cloning and pulsed-field gel electrophoresis .
gene frequencies for these proteins binding vitamin D were in the range
of those reported for Gc, and individuals of known Gc phenotype were found
to have the corresponding vitamin-D-binding phenotype .
D-binding protein (DBP) has been reported to contribute to innate immunity
antibodies produced a similar reduction in DBP/25-(OH)D3
context of Gc
studies revealed a marked defect in the ability of these DBP(-/-)
recruit cells to the peritoneum after localized thioglycolate
verify prior in vitro and cell-based observations supporting this
role, we assessed
the ability of a recently developed DBP-null mouse line to recruit neutrophils
and macrophages to a site of chemical inflammation .
interrupted DBP allele had been generated by homologous recombination in
129X1/SvJ embryonic stem cells and these cells were subsequently used to
generate a line of DBP(-/-) (null) mice .
of intercellular signal transmission among nonadherent (B and T) cells
revealed that lyso-PC-treated B cells modify Gc protein to yield a proactivating
factor, which can be converted by T cells to the macrophage activating factor
of the serum factor required for in vitro activation of
Role of vitamin D3-binding protein (group specific component, Gc)
in lysophospholipid activation of mouse peritoneal macrophages
of Gc with chemical compounds
lines of evidence are reported: (1) Polyacrylamide gel
autoradiography of serum labeled with (14-C)vitamin D3 revealed patterns
of radioactive bands identical to those expected of the two Gc alleles
component (Gc) proteins bind vitamin D and 25-
review describes these new pathways for uptake of 25-hydroxyvitamin- D3
and the gonadal sex-steroids (17beta-estradiol and testosterone)
bound to vitamin D-binding protein and sex hormone-binding globulin
rapid process of macrophage activation was found to require a serum factor,
the vitamin D3 binding protein (the human protein is known as group-specific
component; Gc) .
D3-binding protein (Gc protein), a serum glycoprotein, is the
for the macrophage activating factor .
interactions of Gc
studies have shown that vitamin D-binding protein (DBP)/25-(OH)D3 complex
is one of the megalin/cubilin ligands .
influence of age, sex and strain on the serum concentration of
(corticosteroid-binding globulin) and vitamin D-binding protein (DBP)
in mice was investigated .
interactions of Gc
between vitamin D-binding protein and alpha-fetoprotein in the
a previous study, the s locus was included in the same linkage group
albumin (Alb) and vitamin-D binding protein (GC) which are mapped on
chicken (Gallus gallus) chromosome 4 (GGA4) .
of Gc protein with a mixture of beta-galactosidase and sialidase efficiently
generated the macrophage-activating factor .
antibody was subtyped IgG2b kappa and had a kd of 3.0 x 10(-8) M for antigen
and vitamin D-binding protein levels in mouse serum .
diagnostic and therapeutic context of Gc
Immunoelectrophoresis and autoradiography of labeled serum reacted against
antiserum to human Gc revealed labeling by (14-C)vitamin D3 of
Gc protein cannot be converted to macrophage activating factor,
leading to immunosuppression .
assays with vitamin D3 and Gc in enzyme-linked immunosorbent assay
indicate that the epitope of hDBP-1 on the Gc molecule may be related to
the vitamin-D3-binding site .
The difference of isoelectric focusing mobility in Gc protein and GcMAF
would be useful to develop a GcMAF detection method . Gc
protein from human serum was purified by affinity chromatography with 25-hydroxyvitamin
Osteopathy and resistance to vitamin D toxicity in mice null for