Are there other states or national stats that show similar relationships between a rise in autism and an offsetting decrease in other diagnoses?

See the straight line?

The factors in the HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) are tied in with NO in that free hemoglobin (from lysed red blood cells) destroys NO ~600 times faster than does hemoglobin in RBCs. Elevated liver enzymes are a sign of low NO, and can be decreased by increasing basal NO levels (unpublished data). NO inhibits platelet aggregation and oxidative stress and low NO makes platelets and RBCs more sticky.

What is interesting is that placental metabolic stress seems to be pretty unique to humans. Other mammals don’t have it to the same extent as humans do. This is highly speculative, but that may be to purposefully induce low NO to cause neuronal hyperplasia and may be part of why humans have such uniquely large brains.

I see gestational diabetes as a sign of metabolic stress too, a feature to try and get more glucose to cells too far from a capillary. I have a recent blog on regulation of the vasculature by NO, and low NO is going to increase the capillary spacing. NO also regulates the number of mitochondria, and if cells don’t have enough mitochondria and switch some of their ATP production from oxidation to glycolysis, it takes 19 times more glucose to make ATP via glycolysis than by oxidation. Switching 5% of ATP from oxidation to glycolysis requires twice as much glucose. Glucose transport is active, with the “important” concentration being the concentration adjacent to the cell taking it in (not the value in bulk blood). If glucose demand goes up and capillary spacing gets farther apart due to low NO, the only way physiology can adapt is by increasing blood glucose levels. The cells closest to the capillary get enough and the cells too far don’t get enough (because the intervening cells consume it). The cells closest stop taking up extra glucose (glucose resistant) and stop taking up insulin (become insulin resistant) to leave glucose and insulin for the cells farther from a capillary. This is why tighter control of blood glucose leads to higher mortality. The glucose level that is important isn’t in bulk blood, it is in the extravascular space next to the cells taking it up.

There is cross-talk between vitamin D and NO signaling.

http://www.jbc.org/cgi/content/full/277/15/13294

mediated through zinc finger transcription factors. Zinc finger transcription factors are the largest class of transcription factors in humans, ~900. These authors previously found that NO isn’t important only in removing Zn from the zinc finger protein, but is also necessary for removing Zn from metallothionein, which is the normal physiological reservoir of Zn to put it on the Zn finger protein in the first place. It may take higher levels of vitamin D to achieve the same signaling when basal NO levels are compromised.

You may be interested in learning about the work of Dr. Ralph Reitan. The Reitan-Indiana Neurological Test Battery was developed to evaluate children from 5 to 8 years old. The Halstead-Reitan Neurolpsychological Test Battery for Adults is extremely useful. A complete neuropsychological evaluation is
required before using the DSM for diagnosis. SHALOM.

/S

E.g.
Fischer et al, Metabolism of vitamin D3 in the placental tissue of normal and preeclampsia complicated pregnancies and premature births. Clin Exp Obstet Gynecol. 2007;34(2):80-4.

Bodnar et al, Maternal vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab. 2007 Sep;92(9):3517-22. Epub 2007 May 29.

“Things that correlate positively with autism include uterine bleeding, Rh incompatibility, induced labor, prolonged labor, precipitous labor and hyperbilirubinaemia”

A few of these–uterine bleeding, induced labor, and precipitous labor–are also associated with Pre-eclampsia. Also, bleeding during the first trimester and second trimester of pregnancy has been associated with later ASD diagnosis, and this as well is seen pregnancies that become pre-eclamptic. Is there any link between pre-eclampsia and later ASD diagnosis? I have heard talk that there is, but I have not seen confirmation. And could pre-eclampsia also be associated with your NO hypothesis?