Rickets, Seizures, and Vitamin D
"Rickets on the Rise," "Elderly at Risk of Vitamin D Deficiency." These are just a few headlines making world news about vitamin D Deficiency. Research is now linking the development of many chronic diseases to low levels of vitamin D.
If you take anticonvulsants, this link is significant because anticonvulsants can rob the body of its supply of vitamin D. Low levels of vitamin D can set off psychological, neuromuscular, skeletal, and nervous system disorders. However, research indicates these symptoms may be preventable.
x-ray of a 2 year
old child with rickets
In its active form, vitamin D is calcitriol, a hormone, not a true vitamin. Sunlight reacts with oil in the skin to form vitamin D3. In the liver it is metabolized into calcidiol (25 hydroxy vitamin D) and stored in blood and fat. Throughout the body calcidiol is converted into calcitriol as it is needed. In the early eighteen hundreds, a Polish physician recognized a connection between lack of sunlight, our main source of vitamin D, and the development of rickets, the bone deforming disease of early childhood.
Vitamin D deficiency has been called the enduring epidemic. Widespread throughout the world today, vitamin D deficiency was pervasive a hundred years ago when rickets was endemic. About 80% of children in American cities had rickets in 1900. Some studies of this era in northeastern cities found the rate among Blacks and Italians, people originating from warmer climates, to be 100%.
At that time, it was difficult to find a child in London not suffering from what was called "The English Disease." Rickets was also common among children in Glasgow, Paris, and Berlin. The lifestyles of the world's most industrialized areas included too little sunlight to nurture life and prevent illness.
Smoke and pollution from factories, and too much time spent indoors, contributed to the problem. Rickets and osteomalacia (adult rickets) were common in all age groups, all social classes. Sometimes entire families were afflicted.
Along with bone deformities, other problems are linked to nutritional rickets. Sir William Gowers, a major figure in the history of neurology, saw a strong connection between rickets and the development of seizure disorders more than a century ago. Children suffering from rickets often developed seizure disorders when teething and he thought the two were related.
Everyone has a seizure threshold, a tolerance level for seizures. Anything that increases your risk of having a seizure, such as fevers in children, or metabolic distress lowers the seizure threshold. Whatever raises your seizure threshold reduces your chances of having a seizure. Vitamin D deficiency may trigger mineral and electrolyte imbalances that can lower the seizure threshold.
Gowers conducted a study of 180 young children with seizures in the 1880s. The seizures first occurred in 72 of the cases when the child was teething. Expressing the opinions of his time, Gowers wrote that nearly all cases of convulsions beginning during this period of childhood could be attributed to the "irritability of the nervous system" due to rickets. He made his observations forty years before vitamin D was identified and recognized as crucial to the development of healthy teeth and bones. Cod liver oil, one of the richest food sources of vitamin D, was a common prescription for rickets and seizures in the 1800s and well into the twentieth century.
Public Health and education campaigns beginning in the 1930's promoted food fortification and healthy sunbathing to prevent vitamin D deficiency and rickets. By the 1960s, it appeared rickets had been eradicated. However, neither rickets nor vitamin D deficiency were eliminated and deficiency continues to be widespread.
People who take anti-seizure medications face a greater risk of developing vitamin D deficiency than the rest of the population because these drugs can interfere with the body's metabolism of vitamin D leading to drug induced deficiency. Rickets, osteomalacia, osteopenia (thinning bones) and osteoporosis are the most noted vitamin D related side effects of anticonvulsants.
However, we are just as dependent on vitamin D for a healthy nervous system as for sturdy bones. Fat soluble vitamin D is needed to absorb and metabolize calcium and phosphorus, the two most abundant nutrients in our bodies. As minerals, calcium and phosphorus form hydroxyapatite, the hard crystals which make our bones solid and strong. As electrolytes calcium and phosphorus create nerve and muscle impulses.
If we develop vitamin D deficiency, calcium and phosphorous levels may also fall. Calcium deficiency (hypocalcemia) can cause many health problems. Symptoms may include tingling sensations, nervousness, cardiac arrythmia, muscle spasms and twitching. Neuropsychiatric symptoms include irritability, mental confusion, and behavioral changes.
While too little calcium is associated with bone loss, too little phosphorous (hypophosphatemia) causes soft, weak, and poorly formed bones as well as muscle weakness, confusion, heart problems, and difficulty with speech. Phosphorus is crucial for converting food to energy and needed by all cells in the body. Deficiencies of either calcium or phosphorus lower the seizure threshold.
Sometimes, after years of being seizure free on anticonvulsants, the seizures return. The problem may be the medication. A recent medical report from Kuwait describes how hypocalcemia, a side effect of anti-seizure medication, led to a patient's loss of seizure control after five years of successful drug therapy. His seizures stopped and he regained control following treatment with vitamin D and calcium. The authors concluded loss of seizure control while taking anti-seizure medication is a warning sign to check calcium levels.
By triggering deficiencies of calcium or phosphorus, low levels of vitamin D can be a factor in the development of seizures. But what about preventing seizures? Vitamin D may have a role here as well. A 1984 research study found the seizure threshold of laboratory rats increased when vitamin D3 was injected into their hippocampi, an area of the brain that is very susceptible to seizures.
An exploration of sunlight as vitamin D therapy for seizure patients showed promising results. During the 1982 study, 450 institutionalized patients taking anticonvulsants received sunlight exposure in addition to their medications. The results indicated sunlight therapy may be the reason most of those patients did not develop osteomalacia or rickets from using anticonvulsants.
These and other studies suggest that osteoporosis, mental confusion, and other side effects of anticonvulsants may not be inevitable. The key is maintaining adequate levels of vitamin D, calcium, and other nutrients.
Seizures may be the first noticeable symptom of vitamin D deficiency. Over the last decade physicians from coast to coast have expressed surprise and alarm at discovering children whose seizures are due to vitamin D deficiency rickets. Not all the children appeared to be malnourished, yet they were not receiving enough vitamin D from diet and sunlight to prevent the development of rickets and seizures. Breast fed infants may not receive enough vitamin D from breast milk alone to meet their needs. They must also get vitamin D from sunlight, diet or supplements.
Gowers suspected a nutritional factor at work when children developed seizures while teething. That factor was vitamin D. Today this link may be overlooked in the mistaken belief that vitamin D deficiency is rare. Some of the world's most eminent vitamin D researchers believe up to half the population has below optimum levels of vitamin D. Vitamin D deficiency is common among all age groups in North America.
Vitamin D deficiency is a problem we can fix. The American Academy of Pediatrics revised its recommendations for Vitamin D in 2003. The Academy now recommends 200 IU of vitamin D for children who are not getting adequate vitamin D in their diets or from sunlight.
Speaking out on these concerns is Dr. John Cannell, Executive Director of the Vitamin D Council, whose mission is to raise awareness about vitamin D deficiency. According to Cannell, " A lot of people just won't go into the sun. They just won't; their doctors have told them not to. The Federal Government tells them it causes cancer, which it does. It also prevents cancer. Very little time in the sun is needed for the body to make its own stores of vitamin D."
A quick and easy solution to vitamin D deficiency may be a walk on the sunny side of the street. Writing in "The UV Advantage," Dr. Michael Holick says that just a little sunlight is quite enough to meet our needs. For light skinned people living in the United States, Holick writes, 15-20 minutes skin exposure to sunlight several days a week can produce the as much vitamin D as the body needs from March through October. People with dark pigment will need much longer exposure, up to an hour or more.
Supplements may be the safest means for people who take anticonvulsants to get adequate amounts of vitamin D. Many anti-seizure drugs also cause increased sensitivity to sunlight. If you take anticonvulsants you can check with your pharmacist to see if your medication puts you at risk of becoming sensitive to ultra violet rays from the sun or tanning lights.
Despite decades of reports indicating bone disease is a side effect of using anticonvulsants, most physicians are unaware of the risks or preventive effect of maintaining adequate levels of vitamin D and calcium. A study reported in 2001 found only 7% of adults' neurologists, and 9% of children's' neurologists prescribe calcium and vitamin D to their patients who have seizure disorders. The study concluded more awareness of the problem could improve the bone health of many patients with seizure disorders.
Vitamin D deficiency, and the problems deficiency can initiate, may not be an unavoidable side effect of anticonvulsants. By screening for deficiency and being sure you maintain normal levels of vitamin D and calcium, some of the dreaded side effects of anticonvulsants may never develop. With careful attention to nutrition, some cases of seizures, as Gowers suspected, may indeed be preventable.
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