Calcium phosphoricum Anhang 2
[Sankaran]
Calcarea phosphorica
is a tubercular remedy and belongs to the mineral kingdom. The main feeling of Calcarea phosphorica is: “I am
not loved at the place of security (home), so I should seek love elsewhere
(outside of home), and come home for security”. This is seen in the rubric:
Home, desires to go and when
there to go out.
Calcarea persons need to have people around,
they want to be protected as they feel insecure. The feeling of Phosphorus is:
“I must prepare to be alone, to be able to live on a distant island”. Thus Calcarea phosphorica has the need
for security, but ability to live alone if the need arises.
The ability to make new connections also comes from the Phosphorus
element of Calcarea phosphorica.
Calcarea phosphorica people
are friendly and make friends easily. They love to travel. Calcarea
phosphorica persons tend to make a new home wherever
they go. The friend’s home becomes their home. They care even for strangers in
such a way that they soon become part of that family.
This may seem like Phosphorus but the difference is that Phosphorus
persons do not make a home wherever they go – this additional element is found
in Calcarea phosphorica
because of the Calcarea element, with its need for
stability and security.
Calcarea phosphorica
is a chief mineral component of bone which not only provides security and stability
to the body but also facilitates its mobility. The Calcarea
phosphorica people are
active physically as well as mentally, and are very sensitive. They are
often found to be sportsmen. This is probably due to the fact that sports
involve friendliness, activity and mobility.
The Calcarea phosphorica
persons are often of an athletic build – tall, muscular, of rigid fibres. They
tend to be lean, have white spots on nails, and sweaty palms.
There is craving for meat, fish, spices, potato and potato chips.
Rubrics:
Anxiety in children when
lifted from the cradle.
House, desires to go, and when
there to go out.
Travel, desire to.
Violent, when hearing another
reproached.
Jealousy.
Kent:
Taste, bitter for water.
Desires smoked meat.
Desires fat, ham.
Phatak:
Craves condiments.
Growth, affected, disorders
of.
Mammae,
nodes in, walnut-like, in males.
[Jan Scholten]
The same is true for the discrepancy in diagnosis between regular
medicine and homeopathy. For example the regular diagnosis ”bronchitis” is a
symptom of the homeopathic diagnosis “Calc-p.”.
Calc-p. is the state of someone having a fear of not being interesting
for others. They fear that others see them as stupid, not clever and have
nothing interesting to say,
so they will have no friends. In school they study hard to overcome that
idea of being stupid, so they develop abdominal pains and headaches (around
examinations).
They have lung problems, bronchitis and pneumonia. They have
homesickness, desire for spicy, salt and fish and a fear of thunderstorm.
In this example we see that the regular diagnosis is just a symptom in a
homeopathic diagnosis.
The second difference is that no symptoms are excluded from diagnoses.
Disease is empirically observed as a whole, also the symptoms of the mind which
are included and regarded as essential. In the Calc-p. diagnosis we saw those
features in the form of the fear of having no friends. In contrast, regular
medicine sees mind symptoms more as artifacts of the
body machine. From a homeopathic perspective a whole range of symptoms are
artificially excluded from disease by regular medicine.
Another aspect of the difference is that the homeopathic classification
is based on the natural expression of diseases: in the form of intoxications.
These come from natural substances in the world in the form of minerals,
elements, plants and animals and are the basis of disease classifications.
Sulphur, a natural element, is an example of a homeopathic disease.
[Dr. Janice Block]
Exploration of the relationship between the remedy Calcarea
phosphorica and calcium and vitamin D metabolism.
Our homeopathic materia medica
states that calcarea phosphorica
is an effective remedy for rickets and bone disease, and that it is suited to
dark skinned people.
On a constitutional level, Calcarea phosphorica is often associated with unhappiness and
discontent.
[Vithoulkas]
“Discontent is the main theme around which the image of Calc. develops.
Calc. patients do not know what they want. They know something has gone wrong
with their system, but they do not know precisely what it is or what to do
about it….”
Why might calcarea phosphorica
be suited to dark skinned people? And what might be the common thread which
unites Calc., bone disease, joyless demeanor, and
dark skin? The answer is suggested in the hormonal regulation of bone
deposition, bone resorption, and vitamin D production
through the skin.
The relationship between Calc. and bone
Bone is the body’s main reservoir for calcium and phosphate: 99% of the
body’s calcium and 85% of the body’s phosphorus are bound up in bone, mostly in
the form of hydroxyapatite. Hydroxyapatite
, the most prevalent mineral component of bone, has a chemical composition of
Ca10(PO4)6(OH)2. In the presence of heat, hydroxyapatite
readily undergoes condensation
to Calc. (or “tricalcium phosphate,” as it is
known chemically) and water.
Calc. is one of the main combustion products of bone. With a chemical
composition of Ca3(PO4)2, Calc. is so similar to the bone mineral hydroxyapatite that it can behave almost in the
manner of a sarcode for bone.
Given the similarity of Calc. to hydroxyapatite
and bone ash, it is not a surprise that Calc phos is
one of the homeopathic remedies suggested for treatment of rickets and other
developmental bone diseases. Clearly, not all patients who respond to Calc.
have rickets, or poorly mineralized bones on x-ray. But I have found that the
majority of them -including those who do not present with skeletal complaints-
present with incidental bow legs, knock knees, or some other skeletal
condition, however mild.
Hormonal regulation: parathyroid hormone, calcitonin
and activated vitamin D
Bone turnover, the process by which the old bone is removed and
replaced, occurs at a rate of about 100% per year in children and about 10% per
year in adults. These numbers are only averages, and there may be considerable
variability from one person to another.
Hormonal regulators of bone resorption and
deposition include calcitriol, otherwise known as
activated vitamin D; parathyroid hormone, which is secreted by the parathyroid gland;
and calcitonin, which is secreted by the parafollicular cells of the thyroid gland. In women, the
uptake of calcium into bone is also influenced by estrogen.
Parathyroid hormone moves calcium and phosphate out of bone and into the
circulation, and also influences the kidneys to reabsorb calcium and to excrete
phosphate. The net effect of parathyroid hormone secretion is to remove calcium
from bone, to increase calcium in blood, and to decrease phosphate in both
blood and bone. Parathyroid hormone also stimulates the
kidneys to convert 25 (OH) vitamin D into the activated form of vitamin
D, calcitriol.
Calcitonin opposes the action of parathyroid
hormone by moving calcium out of the blood circulation and into the bone. Its
net effect is to increase calcium deposition in bone and decrease calcium in
blood, in opposition to the effect of parathyroid hormone.
When it comes to strengthening and mineralization of bone, activated
vitamin D (otherwise known as calcitriol) is more
important than calcitonin. Activated vitamin D, or calcitriol, is
derived from a vitamin, but it is a hormone in every respect. It
improves absorption of calcium, phosphate, and magnesium from the digestive
tract, reduces calcium excretion into urine,
and stimulates breakdown of bone, with movement of calcium out of bone
and into circulation. Even though calcitriol
stimulates movement of calcium out of bone and into blood, its net
effect is the opposite: it increases the overall calcium content of
bone. Its strengthening effect on bone is related to its ability to increase
calcium absorption from food.
In order to make calcitriol, the body must
produce vitamin D. While some vitamin D is obtained through vitamin D-rich food
such as fish, most of the vitamin D is manufactured in the skin.
As the skin comes in contact with sunlight, solar ultraviolet light
(UV-B) triggers the conversion of a cholesterol metabolite into vitamin D. The
newly manufactured vitamin D courses from
the skin capillaries to the liver, where it is converted to calcifediol, a calcitriol prohormone. Then, under conditions of low ionized calcium
and high parathyroid hormone, the kidneys convert cacifediol
into calcitriol, the activated form of vitamin D.
It is interesting to note that routine blood measurements for vitamin D
actually measure calcifidiol, or 25(OH) vitamin D,
rather than vitamin D itself. Vitamin D itself cannot be measured
on a blood test, as it is unstable and quickly converted into 25(OH)
vitamin D. But a low 25(OH) vitamin D level indicates inadequate skin
conversion of cholesterol into vitamin D –
“vitamin D deficiency.”
Dark skin and vitamin D deficiency rickets
Melanin, a brown to black skin pigment which is plentiful in the skin of
darker skinned people, is capable of blocking vitamin D synthesis in the skin.
Dark melanin pigment filters out solar
UV-B radiation. This has the beneficial effect of protecting against
sunburn, but it also limits the skin’s ability to manufacture vitamin D.
Throughout the millennia, dark skin rich in melanin has been
advantageous in hot, sunny environments - environments in which sun exposure is
plentiful, vitamin D is plentiful, and sunburn
is a significant risk. Pale skin has been advantageous in colder
environments with longer winters, during which time sun exposure is limited,
vitamin D production is limited, and sunburn is
less of a risk. The rise of cities in modern times has also had an
impact on vitamin D levels in the body. Since people in cities spend much more
of their time indoors, vitamin D deficiency has become a significant risk even
in lighter skinned people.
In children, vitamin D deficiency may result in rickets, a disease of
bone malformation which the body does not have enough activated vitamin D,
calcium, or phosphate to meet the needs
of the developing bone. While some forms of rickets involve vitamin D
resistance rather than deficiency, historically, the most common cause of
rickets is due to nutritional deficiency of vitamin D.
In the absence of active vitamin D, calcium is poorly absorbed from
foodstuffs, and there is insufficient mineral (calcium and phosphate) available
to harden the developing bone. As blood calcium plummets, parathyroid hormone
rises. Parathyroid hormone stimulates the movement of calcium and phosphate out
of bone and into blood, weakening the bone, and inhibits the movement of
calcium and phosphate from blood back into bone.
The result is rachetic bone - developing bone
which is soft, stunted, poorly mineralized, and thickened in places. The soft
bones bow easily under the strain of a weight they cannot support.
And as unmineralized bone matrix accumulates,
the rachetic child’s wrists become wider, his cranial
bones become thicker, and his ribs begin to bend.
Here are some blood results from a patient with rickets:
Calcium: 8.6 mg/dL
(normal 8.8 – 10.8 mg/dL)
Phosphorus: 3.3 mg/dL
(normal 3.8 – 6.5 mg/dL)
Alkaline phosphatase:
1506 U/L (normal 100-320 U/L)
25(OH) vitamin D: 4.6 ng/ml
(normal 30 ng/ml)
This child presented with growth stunting and motor delay. She was a
stubborn, fearful child, often irritable, and also adept at communication. At
the age of two, her language development was appropriate or even advanced for
her age, yet she was still unable to walk. On physical examination, she was a
thin but not emaciated child with dark skin. She was bowlegged, her wrists were
abnormally thick, and she had the beginnings of a “rachitic rosary” on the
chest: bead-like prominences of ribs, at the locations where bone meets
cartilage on the rib cage. The picture, including details not discussed here,
was consistent with Calc.
On the blood test panel, 25(OH) vitamin D was low, as would be expected
for a child with clinical rickets. Calcium and phosphorus were low on account
of poor absorption of calcium and phosphorus from the digestive tract. However,
it should be noted that at various other times, her calcium was normal, thanks
to increased activity of parathyroid hormone in moving calcium out of bone and
into blood.
Alkaline phosphatase was extremely high on
account of the injuries to soft rachitic bone and increased rate of bone resorption, which increased the need for bone remodelling
and for building of new bone. Alkaline phosphatase is
an enzyme involved in building bone matrix, and it is elevated under conditions
of increased bone remodeling. In rickets, alkaline phosphatase contributes to the characteristic bony
thickening of wrists and ribs seen in these children.
Vitamin D deficient rickets has become rare in the developed world, but
it still occurs occasionally in city dwellers - in children who spend most of
their time indoors, or children who live in cities where air pollution limits
sun exposure. In my more than 20 years of pediatric
practice in the United States and Israel, I have seen thousands of patients
with vitamin D deficiency.
Some were “white” or “Asian,” some were tanned, some were “olive
skinned,” and some were “black.” But among all of the patients I have seen with
vitamin D deficiency, only two children presented with the full picture of
vitamin D deficiency rickets, with soft bones, bony deformation, and stunted
growth. Both had dark skin.
Vitamin D and depression
A decrease in sun exposure is associated with a decrease in vitamin D
production, and also, in some people, with an increase in depressive symptoms.
Patients with seasonal affective disorder (SAD) have winter depression (or
summer depression in the southern hemisphere) which is induced by a decrease in
sun exposure. Since the problem in SAD is insufficient exposure to solar UV-B
radiation, the treatment for SAD is a UV-B lamp. But given that the same UV-B
frequencies are associated with production of vitamin D, could deficiency of
vitamin D be contributing to depressive illness?
Premkumar, et. al. (Arch. Osteoporos,
2013) studied subjects living in Antarctica for a year. In the study, those
subjects who had lower serum levels of vitamin D and higher serum levels of
parathyroid hormone were significantly more likely to suffer from symptoms of
winter stress and depression than were subjects who had normal levels of
vitamin D and parathyroid hormone. This study suggests that SAD - at least in
its extreme form, during a polar winter lasting many months - is associated
with deficiency of vitamin D.
Vitamin D deficiency has also been associated with non-seasonal
depression. In a meta-analysis of 15 randomized controlled trials (Spedding, Nutrients, 2014), vitamin D supplementation was
found to be effective for treatment of depression in patients with low levels
of vitamin D. This is not to say that vitamin D is a treatment for depressive
patients who are not deficient in vitamin D. Vitamin D therapy is appropriate
treatment only in those depressed individuals whose depression is associated
with deficiency of the vitamin.
In my own clinical experience, patients with vitamin D deficiency often
complain of weakness, fatigue, and lack of joy. As 25(OH) vitamin D levels
rise, these patients feel better.
The message seems clear: some forms of depression are related to vitamin
D, vitamin D production is related to sun exposure, and sun exposure is related
to melanin in the skin. If so, then in people who have more melanin pigment in
the skin, i.e. dark skinned people, the depressive effect should be greater
than in light skinned people.
Calc. – the remedy
Having come full circle, we are now able to peek into the logic of
homeopathic Calc. Calc. is related to bone mineral, and bone mineral, in turn,
is related to both vitamin D and parathyroid hormone. Since both bone
mineralization (by hydroxyapatite and other
calcium-phosphate complexes) and mood depend on vitamin D and parathyroid
hormone, and since Calc. is integrally tied up in this process, it is logical
that Calc. exhibits actions in both of these spheres. Calc. is a potential
treatment for bone disease, but it is also a potential treatment for joyless
depression.
Also, we have seen that vitamin D production depends on sun exposure,
and that the ability to absorb the sun’s rays depends in part on the
concentration of melanin in skin. Perhaps this is the reason why our materia medica states that Calc.
is “suited to dark skinned people.” But in our modern urban world, in which
much of our time is spent indoors, we might expect Calc. to be effective in
lighter skinned people, as well. This is exactly what I have seen in my own
patients.