We last spoke about the daily intake of vitamin D being suboptimal for most persons. Production of vitamin D by the skin is rapid and prolific. When light-skinned individuals sunbathe in the summer for about 20 minutes they are able to generate at least 10,000 IUs of vitamin D within 24 hours. A pregnant mother would have to drink 100 glasses of milk or consume 50 prenatal vitamins to equal this amount of vitamin D. Because of medical advice over the past 20 years to limit sun exposure and use sun-blocking agents, along with recommendations of the American Medical Association's Council on Scientific Affairs to "keep infants out of the sun as much as possible," generation of vitamin D by the skin has fallen dramatically. The consumption of vitamin D in food and supplemental form has not offset this deficit. This dramatically limits the exposure of the brain to optimal vitamin D during pregnancy and thereafter. Such limited exposure of the brain to vitamin D during key developmental stages is novel in the history of mankind and is chronologically associated with rising rates of autism.
Animal data from studies in vitamin D deficient maternal rats have documented abnormal nerve cell growth and proliferation. Reduced expression of a number of genes involved in determination of neuronal structure were observed as were alterations in memory and learning. Another group showed that vitamin D deficiency disrupts 36 proteins involved in mammalian brain development. This is consistent with anatomical studies in rats that revealed increased brain size and enlarged ventricles (the fluid spaces in the brain) similar to children with autism.
A human clinical study in 20 autistic children found that even low daily doses (150 IU) of vitamin D improved sleep and gastrointestinal problems. In other human studies investigating childhood cognition in 'normal' kids, improvements from 1% to 6% have been documented. In one fifth of the children, improvements of about 15% were detected. This may have been the most vitamin D deficient cohort. Recently, low maternal seafood consumption (a rich source of vitamin D) was linked to infants with low verbal IQs and poor outcomes in fine motor skills, communication, and social development. These are all seen to some degree in the autistic spectrum. Consistent with this observation is the association of increased fish intake during pregnancy with improved infant cognition.
When formula fed babies (formula contains significant amounts of vitamin D) are weaned to various juices, such as apple and grape juice, one might expect to see more cases of autism develop. A prospective study of 87 infants, some at high risk for development of autism, and others not, found no difference in cognition at age 6 months (prior to weaning to juice type diets). However, around the age of weaning initial signs developed in those who developed autism with rapid progression between 1 and 2 years of age. This timeline correlates with the age many children with autism deteriorate.
If vitamin D is somehow linked with autism, the prevalence should be lower in sunny climates or near the equator. Recent CDC (Center for Disease Control) data from 14 states showed the state with the highest prevalence was New Jersey (the second most northern state); Alabama, with the lowest prevalence, was the most southern state.
If there is an association between vitamin D deficiency and autism, drugs which lower vitamin D should be more likely to be related to the development of autism. There is little known about drugs that interfere with vitamin D metabolism, but sodium valproate is in this category. It is one of the few gestational drugs that are linked with autism.
Melanin is the skin pigment that makes skin dark and is also an efficient sunscreen. If this is the case, children born to dark skinned mothers might be expected to have more neurodevelopmental disorders. Four recent US studies found a higher incidence of autism in black children. Similar findings exist for dark-skinned immigrants in Europe. Low vitamin D levels are 150% more likely in pregnant black females than in white females. Furthermore, 45% of pregnant black females are severely deficient compared to only 2% of pregnant white women. The most startling observation is that prenatal vitamins containing 400 IUs of vitamin D offered little protection for mother or infant in either population.
The hormones estrogen and testosterone have dramatically different effects on vitamin D levels. Estrogen seems to be associated with higher vitamin D while testosterone is not. If estrogen increases neuronal vitamin D during pregnancy, while testosterone does not, this suggests male brains may not be as protected from vitamin D deficiencies.
These observations are consistent with the genetic basis of autism, the male and dark-skinned predominance, the timeline for development, and the timing of recommendations for sun avoidance.
If vitamin D deficiency contributes to the cause of autism, it has medical, social, and financial consequences. Simple preventative measures are at hand that are both widely available and inexpensive.