by Seth
Bittker
My name is Seth Bittker, and I am the father of
a boy with ASD. My son’s development was slow up until about 2 1/2 years
of age. Around this time, his milk consumption increased, and it began
crowding out other sources of sustenance. Within a few months he
regressed, and we received an autism diagnosis soon after this. Stopping his milk consumption was the first
step in helping him get better.
Like some other parents of those with ASD
children, I noticed that his behavior varies significantly with what he eats.
When he consumes large amounts of calcium fortified foods or beverages, his
behavior gets worse: he becomes more autistic in a behavioral sense. Since milk has a lot of calcium, and calcium
fortified foods do as well, it seemed like there might be some connection to calcium
and his symptoms. Later based on a doctor’s recommendation we gave him
supplemental vitamin D. We did not notice much initially, but a few weeks
later he developed hives, and he regressed. Since supplementation with
vitamin D increases absorption of calcium, it appeared that the bad reaction to
calcium and vitamin D might be connected. Based on these experiences and
others, I eventually inferred that we should keep him on a relatively low-calcium
diet and avoid vitamin D supplementation or fortification (milk as well as many
other foods in the US are fortified with vitamin D).
I also concluded that my son was different from
most others affected with autism as some have suggested that vitamin D
deficiency is involved in inducing autism,[1]
and he evidently did not have a deficiency based on the vitamin D trial even
though vitamin D levels in his blood were relatively low.
But is he really different than others with
autism? If one examines the evidence from a number of genetic syndromes
that are comorbid with autism, in many cases the cause is over-active calcium
channels (effectively too much intra-cellular calcium).[2]
You can see this by looking at syndromes such as Timothy syndrome, Williams
syndrome, and Sotos syndrome, which have high comorbidity with autism and seem
to be caused by too much intra-cellular calcium. In Williams syndrome the
connection is through a gene which upregulates vitamin D.[3] In some of these syndromes is it well known
that supplementation with calcium and vitamin D are contraindicated.[4]
In addition there are certain biochemical
markers that are typical in autism, and my son seems to have this same
biochemical gestalt. For example two types of immune system cells
released by the thymus are called “Th1” cells and “Th2” cells, and Th2 cell levels
relative to Th1 cells are much higher in the blood of those with autism than in
controls.[5] As Th2 is associated with extra-cellular
immunity, this suggests that those with autism will be prone to allergies,[6]
which fits with anecdotal observation. In addition with autism we see
elevated markers for oxidative stress and endothelial damage.[7]
Also those with autism typically have functional deficiencies of magnesium[8]
and potassium. By functional we mean the levels may not be low in the blood
relative to controls, but there is a biochemical need for greater consumption. To see the latter you can give somebody with
autism a small dose of supplemental potassium, and the result is generally a
reduction in autistic symptoms. For more on this, see Peter’s work: http://epiphanyasd.blogspot.com/2013/08/potassium-may-play-important-role-in.html.
It turns out that vitamin D skews the immune
system to produce elevated levels of Th2 cells.[9]
One can infer that it also produces functional deficiencies of potassium and
magnesium as these minerals offset the effect of calcium on calcium channels
and vitamin D increases the absorption of calcium. In addition in high
doses vitamin D causes oxidative stress and endothelial damage as we see in
autism.[10]Oral supplementation with vitamin D can cause other consequences as well. Supplementation with significant doses of vitamin D early in life, results in more cases of allergies, asthma, and dermatitis later.[11] Asthma, allergies, and dermatitis all feature high levels of Th2 cells like autism.[12] Is it too much of a stretch to suggest that supplementation with vitamin D early in life, might result in more cases of autism later as well?
On looking at the data we can see that my son as well as most other babies in much of the civilized world received, and in many cases continue to receive, large oral doses of vitamin D starting from birth. As a baby we gave him vitamin D drops, and he also occasionally received some formula. Starting at one year of age he consumed increasing amounts of milk (fortified with vitamin D in many countries) as well as children’s multivitamins, which also contained vitamin D. Here is a graph showing vitamin D content of various beverages:
We are giving babies today much more oral vitamin D than they would consume from human milk alone and also much more than they would have consumed in past decades through formula and food sources when vitamin D fortification was more restrained. In fact based on nutrition data and caloric intake, a baby just out of the womb consuming Similac baby formula today will receive approximately 855 IU per day of vitamin D.[13] I am 190 pounds. If we assume that dose should be proportional to weight, which is a good baseline assumption for most vitamins, I should consume 16,245 IU per day of vitamin D. This is a huge dose, and based on past experience I know it would have a devastating effect on my health. Why should it not be the same for some subset of babies?
When and where vitamin D consumption by the
young is high, is where autism rates are high.
For example, in the United States autism rates are high relative to much
of the rest of the world and they rose gradually starting around 1980 as much
of the population transitioned to lower fat milks, which increased consumption
of vitamin D.[14]
Later rates rose again in the early 1990s as the amount of vitamin D in milk
was increased significantly with no change in the label.[15] Rates continued rising with the
popularization of the Sippy Cup starting in the 1995.[16]
They rose further during the 2000s as the Institute of Medicine increased the
supplementation recommendations for babies in 2003 and again in 2008.[17]
When looking internationally, the evidence also
points to a role for oral consumption of vitamin D in inducing autism.
Cuba for example has extraordinarily low rates of autism.[18]
The Cuban Health Service does not supply vitamin D drops to babies. Nor do they fortify milk or other foods with
vitamin D in Cuba.[19]
The Amish also have very low rates of autism as well. They do not provide
vitamin D drops to babies, and the milk they consume comes straight from cows:
no vitamin D is added.[20]
In the United Kingdom rates of autism are lower than in the United States.[21] Fortification and supplementation are common
in the United Kingdom, but at somewhat lower levels than in the United States.[22]
Vitamin D is also used as a rodenticide, and
experiments in rats show that it is more deadly to male rats than female rats.[23]
Is it any coincidence that autism strikes many more males than females? Babies who get most of their sustenance from
formula also receive more vitamin D than those who receive vitamin D from human
milk. Not surprisingly autism rates are
higher among those who are formula fed.[24]
Vitamin D’s involvement also explains why some with
autism benefit from a “casein” free diet as such diets avoid milk, which has
high calcium content and is fortified with vitamin D in many countries.
It also explains why low-oxalate diets are beneficial as well as ketogenic diets.
Oxalates cause excess calcium salts to precipitate in the body and ketones
effectively remove excess calcium due to acidity.[25]
Both lower the calcium load. Oral
supplementation with vitamin D also explains why some with autism have a
favorable reaction to chelation. Chelation agents remove excess calcium
at the same time as they remove other metals.[26] So they also lower the calcium load.
So the evidence suggests that over-consumption
of vitamin D by babies and toddlers may induce autism in a genetically
susceptible subset of the population. This
explains the biochemistry of autism as well as the nature of the autism
epidemic. There are a number of other data points that fit with this hypothesis. If you are interested in this topic, here is
an ebook with a lot more detail: http://www.amazon.com/dp/B00GVB46ES.I want to thank Peter for allowing me to be a guest blogger here, and I also want to thank you for reading this. How do you view this hypothesis? Do you have observations that are relevant to it? Are you aware of existing data that would help confirm it or refute it?
[2]
For more on calcium channels and autism, please see http://www.autismcalciumchannelopathy.com/Genetic_Factors.html.
[10] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052582/
and Gross, David Ross, Animal Models in Cardiovascular
Research, p. 316.
[15] FDA,
M-I-92-13.
