Autism Studies and Related Medical Conditions, January 2009 - TACA

An organism with an internal skeleton must accumulate calcium while
maintaining body fluids at a well-regulated, constant calcium concentration.
Neither calcium absorption nor excretion plays a significant regulatory role.
Instead, isoionic calcium uptake and release by bone surfaces causes plasma
calcium to be well regulated. Very rapid shape changes of osteoblasts and
osteoclasts, in response to hormonal signals, modulate the available bone
surfaces so that plasma calcium can increase when more low-affinity bone
calcium binding sites are made available and can decrease when more highaffinity
binding sites are exposed. The intracellular free calcium concentration of
body cells is also regulated, but because cells are bathed by fluids with vastly
higher calcium concentration, their major regulatory mechanism is severe entry
restriction. All cells have a calcium-sensing receptor that modulates cell function
via its response to extracellular calcium. In duodenal cells, the apical calcium
entry structure functions as both transporter and a vitamin D--responsive
channel. The channel upregulates calcium entry, with intracellular transport
mediated by the mobile, vitamin D-dependent buffer, calbindin D9K, which binds
and transports more than 90% of the transcellular calcium flux. Fixed
intracellular calcium binding sites can, like the body's skeleton, take up and
release calcium that has entered the cell, but the principal regulatory tool of the
cell is restricted entry.
PMID: 12805727 [PubMed - indexed for MEDLINE]
Bu B, Ashwood P, Harvey D, King IB, Water JV, Jin LW. Fatty acid compositions of red
blood cell phospholipids in children with autism. Prostaglandins Leukot Essent Fatty
Acids. 2006 Apr;74(4):215-21.
Department of Pathology, M.I.N.D. Institute, University of California at Davis,
2805 50th Street, Sacramento, CA 95817, USA.
We compared the compositions of fatty acids including n-3, n-6 polyunsaturated
fatty acids, trans- and cis-monounsaturated fatty acids, and saturated fatty acids
in the red blood cell membranes of 40 children with autism (20 with early onset
autism and 20 with developmental regression) and age-matched, 20 typically
developing controls and 20 subjects with non-autistic developmental disabilities.
The main findings include increased levels of eicosenoic acid (20:1n9) and erucic
acid (22:1n9) in autistic subjects with developmental regression when compared
with typically developing controls. In addition, an increase in 20:2n6 and a
decrease in 16:1n7t were observed in children with clinical regression compared
to those with early onset autism. Our results do not provide strong evidence for
the hypothesis that abnormal fatty acid metabolism plays a role in the
pathogenesis of autism spectrum disorder, although they suggest some
metabolic or dietary abnormalities in the regressive form of autism.
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