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Calcium AEP
by Ward Dean, MD and Jim English
In 1941, a unique form of calcium, Calcium 2-amino
ethyl phosphoric acid (Ca-AEP or Ca-2AEP) was discovered by the
eminent biochemist Erwin Chargaff. Chargaff found that Ca-AEP was
a vital component in the structure of cell membranes. The significance
of Chargaff’s work was largely ignored for the next two decades,
but studies over the last 30 years have shown that Ca-AEP plays
a vital role in maintaining cell membrane integrity and improving
cellular functions. It has also been shown to be effective in supporting
a host of conditions, including multiple sclerosis, diabetes, asthma
and immune disorders.
Ca-AEP is one of a number of colamine phosphates—vitamin-like
metabolites and cell membrane integrity factors, that are required
for cellular membrane functions. Among these functions, Ca-AEP is
known to acts as:
Cells allow entry of vital nutrients through pores spread across
the cellular membrane. Two types of pores predominate: free lipid
pores and peptide-lined transport pores. Lipidic pores can permit
the unwanted penetration into cells by harmful agents. Ca-AEP
decreases water solubility and seals the lipid cellular membrane
pores, decreasing the permeability of the outer cell membrane
by foreign substances. This action protects cells from invasion
by toxins, bacteria, viruses, antibodies and other harmful agents.
Ca-AEP facilitates the cellular exchange of inorganic electrolytes
in cells and aids the absorption of nutrient substances such as
fatty acids, amino acids, carbohydrates, vitamins, hormones and
steroids through the ‘active transport pores’ of cell
membranes.
Ca-AEP maintains and repairs cellular neurotransmission, vital
for the electrobiological connection of cells. Ca-AEP helps the
cells to retain the electrical charges of calcium, potassium and
magnesium ions residing on the membrane surface where they serve
to increase the conductivity of nerve tissue. It does this by
causing calcium and other minerals to bind to cellular membranes
where they serve as electrical condensers, essential for cellular
regulation.
This condenser function of the cell membrane plays
an active role in disease prevention. If there is an insufficient
amount of colamine phosphate salts, the cell’s electrical
charge and condenser function will be abnormal. A significant loss
of the electrical charge of the cell membrane may be catastrophic—especially
for the circulatory system, immune system and neuromuscular system.
Some illnesses are initiated when the body is unable to synthesize
and incorporate into cell membranes adequate amounts of colamine
phosphates such as Ca-AEP. Conversely, restoring levels of Ca-AEP
to proper levels has been shown to improve membrane integrity and
produce actions that are both therapeutic and preventive in nature.
Among the diseases initiated or influenced by disturbances in cellular
membranes are:
- Multiple Sclerosis and sclerotic disorders,
including Amyotrophic lateral sclerosis and progressive systemic
sclerosis
- Inflammatory disorders, including rheumatoid
arthritis
- Diabetes, both Insulin Dependent Diabetes Mellitus
(IDDM) and Non-Insulin Dependent Diabetes Mellitus (NIDDM)
- Diabetic complications, including diabetic
nephropathy and retinopathy
- Osteoporosis
- Lung diseases, including asthma, emphysema
and other conditions characterized by poor gaseous exchange in
the alveoli
- Immune disorders such as sarcoidosis.
The first trial applications of Ca-AEP were for the treatment of
multiple sclerosis (MS). In 1967 the German Health Authority approved
the use of Ca-AEP for MS. MS, an inflammatory demyelinating condition,
is one of the most common diseases of the central nervous system
(brain and spinal cord). Myelin, the fatty material that surrounds
nerves, acts as an insulator, much like the covering of an electric
wire.
It is the speed and efficiency with which electrical
impulses are conducted that permits smooth, rapid and coordinated
movements to be performed with little conscious effort. In MS, the
loss of the myelin sheath (demyelination) leads to a disruption
in the ability of the nerves to conduct electrical impulses. It
is believed that the loss of the ability of nerves to transmit impulses
rapidly to and from the brain is what produces the various symptoms
of MS.
The sites where myelin is lost (plaques or lesions)
appear as hardened scars. In multiple sclerosis these scars appear
at different times and in different areas of the brain and spinal
cord — thus, the term Multiple Sclerosis literally means "many
scars."
An analysis of more than 2,000 patients who were
treated with colamine salts in Germany over the course of 24 years
revealed greater efficacy from Ca-AEP treatments than other known
treatments. In 1986, Dr. George Morrissette conducted a retrospective
poll of patients in the USA who originally had begun Ca-AEP treatment
in Germany for MS. 82% of the almost 300 patients that entered the
study showed a positive benefit from Ca-AEP therapy. And when treatment
began in the early stages of MS, positive results rose to 92%.
According to the work of Dr. Hans Nieper, MS should not be viewed
as just a neurological disorder. MS is a generalized disease of
the cellular membrane system that affects the nerves, bones, kidneys,
lungs, red blood cells, blood vessels and many other organs and
sites.
Long-term observation of Ca-AEP’s effects
on more than 2,000 MS patients revealed a host of additional benefits.
MS patients receiving Ca-AEP showed less signs of aging in their
outward appearance, increased tissue elasticity and skeletal firmness
and a marked absence of osteoporosis. Second to the destruction
of the myelin sheath of the nerve fibers, MS patients are especially
at risk of kidney infection due to insufficient membrane polarization
at the cellular level.
While formerly one-third of all MS patients died
due to lost nerve functions, one-third from increased tendency to
bone fractures, and the last one-third from kidney failure, only
two patients out of 2,200 treated with Ca-AEP suffered from these
problems. Unusual bone fractures and problems with kidney functions
were not observed at all.
The supplementation of Ca-AEP repairs cell membrane
function and maintains it at optimal levels. It raises the depressed
energy in the membrane system of the nerves’ myelin sheath
of MS patients by several-fold, restoring proper synaptic function
in the affected organs.
MS patients receiving Ca-AEP treatments have experienced
facial and upper extremity mobility, body heat generation, greater
relief from exhaustion and decreased spasticity.
Every year over 1.3 million elderly Americans suffer from spontaneous
bone fractures due to osteoporosis and decalcification of the bones.
Both men and women experience a loss in bone density in middle age,
but postmenopausal women are particularly vulnerable due to declines
in estrogen production.
Osteoporosis is not a true biochemical disease,
but is being considered by some to be an electromagnetic illness.
The accumulation of crystallized bone salts requires the steady
pulsation of electric or electromagnetic potential at the surface
of the cell membrane of bone tissues. These pulses create a "piezoelectric"
pressure which, when applied to the salt crystals, builds up apatite
(calcium phosphate minerals) which in turn hardens and strengthens
the bone. Ca-AEP is indispensible in supporting the function of
the cell membranes that form bone.
After 30 years of Ca-AEP and Calcium Orotate therapies
with over 3,500 patients with multiple sclerosis, the risk of bone
fractures was drastically reduced. Furthermore, surgeons in six
surgical centers located in USA and Europe reported finding extremely
solid bone when implanting new joints in patients who were taking
Ca-AEP combined with calcium and magnesium orotate for at least
four years prior to their surgeries.
Ca-AEP, in conjunction with calcium orotate supplements,
has decreased bone decalcification and increased bone density and
strength. This most likely is a result of Ca-AEP’s ability
to improve the condenser function of the cell membranes of bone
tissues.
Ca-AEP protects the lungs against disease and repairs lung damage
by improving the gaseous exchange mechanism (uptake of oxygen and
elimination of carbon dioxide) of the alveoli. Colamine phosphate
salts have eliminated the tendency toward asthma, the development
of emphysema and elevated pulmonary pressure.
Ca-AEP’s actions in normalizing gas exchange
in the lungs may be the mechanism by which it benefits patients
with asthma and degenerative lung diseases. Researchers pointed
out that after a few weeks of therapy with Ca-AEP, asthmatic reactions
have subsided and almost disappeared. In addition, the bone-thinning
effects of these diseases is prevented by Ca-AEP. These disorders
of gas metabolism cause increased carbon dioxide stress in the blood,
resulting in the mobilization of calcium from the bones which causes
them to decalcify.
Diabetes
Ca-AEP has produced good results in treating Insulin-dependent Diabetes
Mellitus (IDDM), Non-insulin Dependent Diabetes Mellitus (NIDDM)
and the complications of diabetes. The treatment of IDDM with Ca-AEP
has resulted in lowered insulin requirements and in reduced sugar
excretion. Ca-AEP’s theraputic effect on diabetics is partly
due to its inhibiting pancreatic autoimmune disorders.
Ca-AEP has improved the regulation of blood glucose
in NIDDM. NIDDM is not a problem of reduced insulin production,
but rather insulin resistance and an inability to transport glucose
into cells. In such cases, eating excess carbohydrates causes an
abnormal rise in blood sugar. If, on the other hand, the individual
does not eat, hypoglycemia may result. When NIDDM patients are treated
with Ca-AEP, this abnormality practically disappears, because glucose
transport into cells is restored.
In diabetes the problem is not just the increase in blood sugar,
but the consequences of exposure to both elevated blood sugar and
elevated insulin over the course of a lifetime. Elevated glucose
levels produce toxic metabolites that are deposited in and damage
numerous structures of the body ranging from the red blood hemoglobin
to the cell membranes of blood vessels. This effect leads to degenerative
problems in 20-30 years.
Ca-AEP is beneficial in preventing and treating
the complications of diabetes. It seals the cell membrane that prevents
toxic glucose metabolites from entering and damaging the cells.
In the United States, diabetes is the second most
frequent cause of blindness. Diabetic retinopathy is caused by damage
to the small vessels in the retina as a consequence of sugar deposits
in the cell membranes. Diabetic retinopathy has been prevented and
reversed by treatment with Ca-AEP.
In European clinics, Ca-AEP is used in the treatment of gastritis,
duodenitis colitis, ulcer pain and other disturbances of the GI
tract. Ca-AEP therapies have also produced good results in relieving
tissue inflammation due to gastritis and GI tract autoimmune disorders.
Ca-AEP has produced exceptional therapeutic effects in patients
with chronic kidney diseases. The disorders include nephritis, nephrosis,
nephrosclerosis, cystic kidney and diabetic nephropathy (chronic
vessel and membrane damage in the kidney due to diabetes).
The kidneys are severely endangered by diabetes
on a long-term basis. The glomeruli, a small cluster of capillaries
in the kidney, are slowly destroyed by the burden of glucose. It
is a diabetic's fate to frequently suffer kidney failure. Ca-AEP
not only protects the kidneys against damage from diabetes and hypertension,
but also ameliorates the initial forms of diabetic kidney damage.
In addition, the increase in blood pressure caused
by diabetic nephropathy and abnormal elimination of protein are
often reduced, sometimes to completely normal values by Ca-AEP therapy.
Rheumatoid arthritic patients who were treated with Ca-AEP have
initially shown improved calcification of their joints and reduced
inflammation. Consequentially, Dr. Hans Nieper has recommended Ca-AEP
for the prophylaxis of rheumatic deformities of the joints. The
anti-inflammatory effects of Ca-AEP are a result of complex calcium
being introduced into the cell membrane, aiding its ability to prevent
pro-inflammatory materials from entering cells.
For many inflammatory tissue disorders, treatment
with Ca-AEP has produced results that were judged as effective as,
and in some cases more effective, than corticosteroid therapy. These
disorders included encephalitis, gastritis, nephritis, nephrosis,
arteritis, and spondylitis.
One should consider the fact that treatment with
Ca-AEP is non-toxic. On the other hand, corticosteroid therapy may
result in many harmful side effects that become more prevalent over
the course of treatment.
The role of Ca-AEP has been studied for more than 30 years. This
vitamin-like factor, like carnitine and coenzyme Q10, appears to
be very important for optimum health. The illnesses discussed above,
may be initiated by inadequate amounts of colamine phosphates and
respond favorably to Ca-AEP supplement therapy. Furthermore, I believe
that substances which have such a wide range of clinical benefits
in such a diverse number of pathological conditions may have profound
anti-aging/life-extending effects. This is particularly likely in
the case of Ca-AEP which specifically effects the integrity and
functional capacity of cellular membranes and their receptors.
1. Nieper HA. Mineral transporters. New Dynamics of Preventive Medicine;
1974: 43-54.
2. Nieper HA. A clinical study of the calcium transport substance
Ca l-d1-aspartate and Ca 2-aminoethyl phosphate as potent agents
against autoimmunity and other anticytological aggressions. Agressologie.
1967, 8:1-12.
3. Nieper HA. A comparative study of the clinical effect of Ca-1-d1-aspartate
(Calciretard), of Ca-2-aminoethanol phosphate (Ca-EAP) and of the
cortisones. Agressologie. 1968, 9: 471-474.
4. Nieper, HA. Suppression of cancer development by calcium colamine
phosphate and by calcium-l-d1-aspartate. The Townsend Letter for
Doctors and Patients. December 1995.
5. Nieper HA. Impairment of digestive potential in MS and osteoporosis
patients. Townsend Letter for Doctors and Patients. February/March
1991.
6. Ferrari V and Harkness RD: Increase of 2-amino-ethyl-phosphate
in regenerating liver tissue
J Phsiol, 113: 27, 1951.
7. Segal W: Biosynthesis of 2-aminoethaneohosphoradimic acid: A
phosphoramidic acid re-arrangement, Nature, 5017: 1284 1965.
Narrod SA and Jakoby WB: Metabolism of ethanolamine J biol chem
239: 2189, 1964.
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