In LA Times article, Temple Grandin sees the advantages that she and others with autism bring to society.
Thanks to ADResearchInitiative blog for the tip on this message.
On another note, our family is off to E Africa for 3 weeks to give lectures (me, viruses and mental health; wife Carolyn, special education) in Uganda, Kenya and Tanzania. We are also looking forward to touring national parks, including tracking mountain gorillas in Biwindi. So I’ll be out of touch till July, but may come back with some interesting stories.
This conference received virtually no press coverage at all.
“A feverish debate” – Excellent new article on PANDAS etc by Alison Motluck.
In the past few decades there has been a marked increase in autoimmune disease. This has been correlated with the increased population of the Western diet and processed foods. The latter contain far more salt than homemade foods. Now, two recent papers in Nature provide compelling evidence that a modest increase in salt in the diet of a mouse model of multiple sclerosis strongly increases the symptoms (earlier onset and more severe disease), and induce a pro-inflammatory state. The authors of one paper suggest that, “…clinical trials with severe curtailment of salt intake for individuals at risk for developing autoimmune disease are required.” Given the inflammatory component in mental illness, might this also apply to these disorders?
On the other hand, it has become apparent that changing to a very low salt diet does not lessen the heart attacks or strokes in people at risk, although the American Heart Association is not convinced about the newer data. Nonetheless, there is no necessary connection between heart disease and mental illness studies.
Readers of this book and blog are well aware that influenza infection during pregnancy increases the risk for schizophrenia and autism in the offspring. Now Alan Brown and colleagues at Columbia Univ expand that risk to bipolar disorder (BD). The new paper provides evidence that the risk for BD increases nearly 4-fold, with nearly a 6-fold increase for a BD subtype with psychotic features. These numbers are similar to the 3-7-fold increase for schizophrenia risk that Brown found found previously. While the most significant risk for a schizophrenia outcome was associated with infection during the first half of pregnancy (primarily late first and early second trimester; not third), the increased risk for BD in the offspring appears to be associated with infection at any time during pregnancy. There is a very slightly increased risk for infection during the 2nd or 3rd trimesters. Thus, it is possible that the timing of the infection may influence the outcome, although genetic background and the intensity of the infection could also play a role.
Several people have inquired about a new paper tying abnormalities in the placenta with an autism outcome in the offspring. This work involved a collaboration between Cheryl Walker and colleagues at UC Davis and Harvey Kliman at Yale in which they analyzed 217 placentas. Those placentas that came from families at high risk for having an autistic child were more likely to have abnormal cell growths called trophoblast inclusions. The at-risk placentas had as many as 15 inclusions while control placentas had no more than 2 such abnormalities. At-risk here means that the family already had a child with autism, which increases the risk 9-fold for the second child to have autism, although that risk is still relatively small (2-7% have autism). Unfortunately, it will be at least a year before we find out how many of the placentas with high numbers of inclusions actually gave rise to autistic children. Kliman had already published a much smaller study in 2006 that indicated that children with autism were 3 times more likely than controls to have inclusions in their placentas.
Elaine Hsiao and I recently reviewed the literature on the placenta and mental disorders, and discussed findings that the placenta is immune activated by maternal infection/immune activation in mouse models. This activation results in altered endocrine function in the placenta. In our own work, we did not see any gross morphological changes in the placenta, however. Surprisingly, Fatemi and colleagues did report morphological changes in the placenta following maternal flu infection in mice. Histology changes in the placenta were also reported following LPS challenge (to mimic bacterial infection) during pregnancy. The most intriguing part of the Yale findings in the human study is that maternal infection would have only occurred in a minority of those cases, so the placental changes must have been caused by other factors, and so placental pathology may be a common mechanism leading to an autistic outcome. It would be really important if maternal infection is tapping into a general mechanism for increasing ASD risk. It may be, of course, the the inclusions are a sign of general placental stress or immune activation, and could be caused by a variety of stressful conditions, and would therefore not be specific to an autism outcome. It will be interesting to determine which types of conditions lead to the formation of inclusions.