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 wrote in Essences of Materia Medica, “discontent is the main theme around which the image of Calcarea phos. develops. Calcarea phos. 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 Calcarea phos., 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. phos. 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 Calcarea phos. (or “tricalcium phosphate,” as it is known chemically) and water.
Calcarea phos. is one of the main combustion products of bone. With a chemical composition of Ca3(PO4)2, Calc. phos. 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 Calcarea phos. to hydroxyapatite and bone ash, it is not a surprise that Calcarea phos is one of the homeopathic remedies suggested for treatment of rickets and other developmental bone diseases. Clearly, not all patients who respond to Calcarea phos. 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 to 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 bead.
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. phos.
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.
Calcarea phos. – the remedy
Having come full circle, we are now able to peek into the logic of homeopathic Calcarea phos. Calcarea phos. 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 Calcarea phos. is integrally tied up in this process, it is logical that Calcarea phos. exhibits actions in both of these spheres. Calcarea phos. 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 Calcarea phos. is “suited to dark skinned people.” But in our modern urban world, in which much of our time is spent indoors, we might expect Calcarea phos. to be effective in lighter skinned people, as well. This is exactly what I have seen in my own patients.