Life Glow Plus
New Formula Changes
Posted on May 1, 1999
This formula will be available by about June 1, 1999
Prior to the receipt of this formula the "Life Glow with EDTA -- 20 Capsules" was shipped, at $70 for each set of two bottles, retail. Those bottles are all now sold out.
The current formula, Life Glow Plus, is sold in single bottles, at $50 per bottle, with the claim that ONE bottle of this new formula is equivalent in benefit to ONE bottle of the original 10-tablet Life Glow being sold at $70 for one bottle. Thus, from this viewpoint, the price of Life Glow Plus is LOWER than the previous "Life Glow" because of the increased power of the new ingredients. However, note that I recommend that you start using Life Glow Plus at the rate of 20 capsules per day until you have achieved a significant reduction in toxic metals -- such as lead, mercury, iron and others. Then, if cost considerations are a factor, go onto a maintenance dosage of 10 capsules per day indefinitely.
|
Life Glow Plus |
The items on this page are the ONLY ones that have changed. Two items had reductions in quantity, and all the other items are either brand new, or had increases in the quantity. Ingredient costs are far higher than the previous formula. |
|
|
|
N Acetyl Cysteine |
300 mg added, not previously included this is more than three times as expensive and powerful as regular cysteine. Click
Here to review hundreds of scientific studies on N Acetyl Cysteine. |
|
L Cysteine |
The amount is reduced from 1,000 mg to 300 mg, since NAC is so much more powerful. Cysteine, combined with N Acetyl Cysteine, gives the equivalent of far more than the 1,000 mg of cysteine in the original formula. Click
Here to review hundreds of scientific studies on cysteine. |
|
Methyl Sulfonyl Methane |
100 mg added. MSM makes cell walls more permeable, thus toxins get removed more easily and nutrients are absorbed more easily – makes all other vitamins more efficient. Thus lower quantities are needed for the same result. Organic sulfur is known for its anti-inflammatory and circulation enhancing
properties. It is a close chemical relative to the commonly known
dimethylsulfoxide (DMSO). Whereas DMSO has been noted for its association with
bad breath and dry itchy skin, MSM seems to provide all the benefits and
advantages without the troublesome side effects of its predecessor. MSM can be
used in the body in part to help build methionine and cysteine, rate-limiting
amino acids in our diet which have well established chelating benefits as well
as the ability to assist the body in many other organo-sulfur molecule pathways |
|
Garlic |
200 mg of organic, high Allicin content
garlic powder. This is a powerful
chelator and compliments many of the other ingredients. This is not only a large increase in the
item, but a much more expensive and powerful form of garlic powder. |
|
Hawthorne Berries – Homeopathic
Crataegus –
6X 100 mg |
Hawthorne Berry has always been recognized as good for the heart – there is now 100 mg of the extremely powerful homeopathic version of this substance. In its homeopathic form 100 mg is a massive dose. Hawthorne
Berry is known as
one of the most valuable cardiovascular tonics available. It has been used to bring high or low blood pressure back
to normal and reduce the severity and frequency of angina attacks. It has also
been used in the treatment of irregular heartbeats, artery spasms (Raynaud's),
and some nerve disorders such as insomnia |
Life Glow Plus™
Oral
Chelation Formula
Available about June 1, 1999
One
Bottle Of 300 Capsules -- $50.00
Take 20 Capsules Per Day to Start – you can cut back to 10 capsules per day if
you wish.
F1 (Return to text) Explanation of the use of "desferoxamine therapy" for which Malic Acid is a preferable treatment -- naturally. Read the entire section below, or click here for the exact reference to "desferoxamine therapy."
Diagnostic challenges can still arise: if
both alpha and beta thalassemia coexist, the changes in Hgb A2 and F
will not be apparent, and as noted above, there are instances of normal or
elevated levels of Hgb A2 and F in beta thalassemia trait. Family
studies and, if warranted, DNA analysis can be used to make a definitive
diagnosis.
Children who are diagnosed with Thalassemia Intermedia have a homozygous
or heterozygous
beta globin mutation that causes a decrease in beta chain production, but not to
the degree that chronic transfusion therapy is required. The phenotype can also
occur in children who have a mutation that increases production of c-globin, in children who have co-inherited alpha thalassemia
and beta thalassemia, and in other rarer mutations. Children who have
thalassemia intermedia are able to maintain a hemoglobin of 7 gm/dl or slightly
higher with a greatly expanded erythron and may manifest bony deformities,
pathologic fractures and growth retardation. Children who have thalassemia
intermedia can also have delayed pubescence, exercise intolerance, leg ulcers,
inflammatory arthritis and extramedullary
hematopoiesis causing spinal cord compression, a medical emergency requiring
radiation therapy and transfusion. They can also have iron overload due to
increased absorption of iron from the gastrointestinal tract and intermittent
transfusion. They are at risk for the cardiac and endocrine complications of
hemosiderosis, but usually at an older age than chronically transfused children.
Chelation therapy is indicated for increasing ferritin and elevated liver
iron.
Children who can not maintain a hemoglobin between 6 and 7 gm/dl
should have an alternative diagnosis considered. If thalassemia is the cause of
the anemia, transfusion and/or splenectomy should be considered. Frequently,
adolescents and adults are unable to tolerate the degree of anemia that is seen
in thalassemia intermedia. Hypersplenism,
splenic pain, congestive heart failure secondary to anemia, severe exercise
intolerance, thrombocytopenia
and leucopenia
should be considered indications for beginning transfusion therapy or for
splenectomy in the child who has severe hemolytic anemia.
Beta thalassemia major was first described by a Detroit
pediatrician, Thomas Cooley, in 1925.
The clinical picture he described is
prevalent today in countries without the necessary resources to provide patients
with chronic transfusions and desferoxamine therapy. Children who have untreated
thalassemia major have ineffective erythropoiesis, decreased red cell
deformability, and enhanced clearance of defective red cells by macrophages
(immune system cells). The result is a very hyper metabolic bone marrow with thrombocytosis, leukocytosis
and microcytic anemia in the young child prior to the enlargement of their
spleen. At presentation they have almost 100% percent Hgb F (these cells have a
longer life span due to a balanced globin ratio, as c
rather than b, globin is present Hgb F). These children
have little or no Hgb A2 and a low reticulocyte
count. The diagnosis can be confirmed by demonstrating thalassemia trait in both
parents, by globin biosynthetic ratios, or by beta gene screening. Beta gene
screening identifies the most common and some uncommon mutations, but not all
mutations. An electrophoresis showing only Hgb F, a complete blood count and a
smear will generally be diagnostic. In most states, these children will be
discovered by state screening or occasionally by the obstetrician who makes a
diagnosis of thalassemia trait in the mother and obtains a family history of
thalassemia or anemia in both parents prior to the birth of the baby.