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Some aspects of autism do run in families, according to a new study about how parents of autistic children process facial expressions. As noted in today’s Science Daily, neuroscientist Ralph Adolphs of the California Institute of Technology and psychiatrist Joe Piven at the University of North Carolina at Chapel Hill studied 42 parents of autistic children and found that some of the parents evaluated facial expressions in ways similar to autistic individuals. 15 of the parents were classified as “aloof”—not preferring interactions with others or having “few close friendships involving sharing and mutual support”— according to psychological testing.
The parents participated in an experiment that measured how they make use of the face to judge emotions. The subjects were shown images depicting facial expressions of emotion that were digitally filtered so that only certain regions of the face were discernible–the left eye, for example, or the mouth. The subjects were then asked to decide as quickly as possible if the emotion depicted was “happy” or “fear.” The part of the face shown, and the size of the revealed area, randomly varied from trial to trial.
An analysis of the subjects’ correct responses revealed that “aloof” parents relied much more heavily on the mouth to recognize emotion than they did on the eyes, as compared to nonaloof parents and, to a greater extent, to a group of parents of children without autism. Prior studies by Adolphs and his colleagues have shown that humans normally evaluate emotions by looking at the eyes–but studies by Adolphs and Piven have shown that individuals with autism do not.
“We found that some parents who have a child with autism process face information in a subtly, but clearly different way from other parents,” says Adolphs. “This is evidence for the hypothesis that the parents with the autistic child have brains that function somewhat differently as well”–an idea that he and other researchers are currently investigating through brain imaging studies. One area of interest is the amygdala, a region located on either side of the brain in the medial temporal lobe that is known to process information about facial emotions and may have abnormal volume in both autistic individuals and their nonautistic siblings.
Researchers suggest that the study (which is published in Current Biology) may lead to research about genes that are responsible for face-processing.
I am pretty sure I look at people’s eyes—now I will be very conscious of this.
1320 days ago
[...] have also found that the parents of autistic children tend to evaluate facial expressions in ways similar to autistic individ…, and am now watching to see what Charlie’s eyes are drawn to. Tags: asd, asperger, autism, [...]
I can’t handle eyes, unless they are of someone I am very close to (this limits me to my girlfriend, two best friends, and parents). I find the experience too intimate-feeling, and very intense. Photos of eyes don’t do it to me (I have a mild heterochromia and enjoy learning about it, which involves a lot of photos of eyes), but being in person and having to maintain eye contact is difficult. I tend to look at one eye alone, or ears, or mouths. Hands, too, sometimes.
And now the whole study has been turned into Parents of Autistic Children Are Often Aloof Themselves—-and that word keeps reappearing.
@Tony Bateson, while the comment thread wandered into issues besides the study, there are plenty of other posts here on which to discuss vaccines. Very best.
MY further comments seemed to have got lost in the fog of words. I say again there are no unvaccinated autistic kids. Please tell me if you know of any we can invite their parents input into this debate. But don’t tell me about Madsen nonsense. Madsen herself is related to an established figure in vaccination and the Danish Institute involved in this research makes and sells vaccines for export, at that time 80% of its profits coming from DTP type vaccines, please.
Just speak to me if you are a parent with an unvaccinated autistic child or get someone else to speak to me if you wish to remain anonymous.
Tony Bateson
RAJ, once again, your point seems to be in a different country from my point. All I can say to what you’ve posted is (1) Duh, and (2) nothing I said would be counter to that.
“Environmental relevance is determined by what exposures levels and exposure routes are. There’s no point in widespread testing of the effects of living immersed in seawater 24-7 if no one actually does that. But using actually occuring exposures and exposure routes would be relevant”.
Not necessarily. Genetic susceptabilty plays an important role in gene-environment interactions that result in increased susceptabilty or resistance to disease after an exposure.
Microdeletions in the gene CCL31 have been found to increase susceptability to HIV after an exposure.
http://www.phgfoundation.org/news/861/
There is no sharp line where all individuals exposed to an equivelant amount of an environmental pthogen will all be effected or where no one will be effected..
I honestly have trouble looking at both eyes on a face I’m not very familiar with at the same time. I’ll focus on one eye or the other, or the mouth or somewhere else. But trying to watch an entire face at once throws me quite a lot. I think the most common incident where I use eyes for non verbal communication is that silent pact between the distracted driver and the invisible bicyclist that the cyclist won’t be killed while crossing the street. Such agreements are so unstable that only the sacred pact of eye contact can ensure fulfillment.
Otherwise I tend to avoid eye contact altogether, especially with people I haven’t met before.
ok. if you get amanda peet and jenny mccarthy in the same room to talk about the V-word, will they look at each others’ mouths or eyes.
pD, I believe you, and I’m sorry if that comes across as rude. It’s just not the best interface for “teaching,” you know?
Emily -
generally don’t get into deeper-level science discussions with people who don’t have the background because it leads to miscomprehension and digressions that I find tedious. I especially don’t like to do it online. Sorry.
Hehehe. No apologies necessary.
(my curiosity is geniune, btw)
OK!
- pD
Also, sorry if that “sounded” rude; there’s a reason I give birth to children on the spectrum.
pD, yes, I have specifics in mind, as do plenty of other people who do real research in this field.
Your criticism of vaccine studies is a standing critcism of all toxicology studies. It’s nothing new, and anyone who has actually done toxicological research knows that replicating the “environment” is not possible. I didn’t say we should replicate the environment, I said we should use environmentally relevant exposures and exposure routes, and those are two different beasts.
I generally don’t get into deeper-level science discussions with people who don’t have the background because it leads to miscomprehension and digressions that I find tedious. I especially don’t like to do it online. Sorry.
Mouth, eyes–>vaccines.
Fair assessment and sorry. No more from me on this thread. [but I didn't start it!]
Though I work with computers all day, it’s eyes for me when folks are around.
- pD
Mouth, eyes–>vaccines.
Okey-dokey.
I tried to be a better observer, of this behavior and I tend to, when within close speaking distance, to flit between mouth and eyes. From this end, continuous eye contact feels too *volitional*, but on standing further back the focus is more on the eyes of the listener.
Data point of one.
Hi Emily -
when they identify polymorphisms, etc., that occur at a higher rate in an autistic population than in a non-autistic population, that provides just one opportunity for mechanistic studies. There are pretty well-trodden paths to follow to pursue these. And there are pretty well-trodden tox paths to follow to pursue candidate environmental agents in the context of these mechanisms.
Hm. But do you have any specific notions on what should be pursued; i.e,. which agents, the particular biological results of a specific polymorphism that we may want to look for alternative mechanisms of achieving? Or is your idea more along the line of looking for agents that might cause the polymorphisms associated with autism? (My head hurts trying to figure out how that might work).
While there is, of course, problems with annectodes; at this point, I’m not sure if we understand enough about the disparate physiological findings in autism to know where to start looking if we exclude what has been observed. There seem to be so many things gone haywire inside these children, and great difficulty teasing out which one(s) are the ’cause’ of autism versus which ones are the results of of having autism.
I sort of thought you had some details in mind; i.e. we know mutation X is associated with autism and eventually results in calcium influx problems in neurons that should correspond with altered brain structure, now lets look for agents that also result in calcium influx problems in neurons. [and that list of agents contain. . .]
Environmental relevance is determined by what exposures levels and exposure routes are. There’s no point in widespread testing of the effects of living immersed in seawater 24-7 if no one actually does that. But using actually occuring exposures and exposure routes would be relevant. . .
Agreed, but I again, I thought you might have some specific agents, or even classes of agents in mind.
Your statement, it turns out, is a perfect argument of the often not understood problems with existing vaccine studies; which involve only presence or absence of a specific preservative, or the presence or absence of a single stimulated immune challenge from a series of challenges. They do not, in fact, test the environment everyone is exposed to.
Thanks!
- pD
FYI – I just posted link and not here so must be in moderation. It was to my new blog and I am trying to spread the word on it. Looking for feedback and a place for comments since BellaOnline does not have that. Expanding my base in the autism community, or something like that.
I read this last nite. Behind in reading here, but busy with my new blog and wanted to share
http://autismfamiily.blogspot.com/2008/07/announcing-virtual-cat.html
Did you ever find that post I did from NJ blogger? I got it from twitter and might have saved it, but think I posted it here, will do a google search for it.
I like how the blogs get comments since I dont get them at BellaOnline so wanted to be more in the mix and have discussions, etc.
pD, when they identify polymorphisms, etc., that occur at a higher rate in an autistic population than in a non-autistic population, that provides just one opportunity for mechanistic studies. There are pretty well-trodden paths to follow to pursue these. And there are pretty well-trodden tox paths to follow to pursue candidate environmental agents in the context of these mechanisms. But as long as we keep throwing anecdotes at the wall to see what sticks, we won’t be plodding down those paths, or at least not as quickly.
Environmental relevance is determined by what exposures levels and exposure routes are. There’s no point in widespread testing of the effects of living immersed in seawater 24-7 if no one actually does that. Doing research on that question would be irrelevant. But using actually occuring exposures and exposure routes would be relevant…if done in the mechanistic context, or hell, even in a good model of autism without the mechanism in hand.
Hi Emily –
“Or, we could do the right thing and focus on real research in real models with environmentally relevant exposures to whatever seems likely with examinations at the genetic and mechanistic level and really get some answers, but…oh, wait, let’s just poison children with DMSA instead.”
I am geniunely curious as towards which environmentally relevant exposures you think merit research resources. Likewise, I am interested if you have specifics on a mechanistic level you think would be worthwhile for analysis.
FYI – The Madsen studies in Denmark suffer from notoriously poor methodology; and were studying only MRI and thimerosal, as opposed to vaccinated vs. unvaccinated status. The fact that they are frequently classified as ‘among the best studies performed’ is what has me so skeptical.
This is not meant in any way to say that I don’t believe in unvaccinated children with autism; of course they exist. What we have no way of knowing is if they exist at different rates than their vaccinated peers.
- pD
Chuck, of course they are exposed to things. But the question at hand was whether or not there are any children who have not been vaccinated but who have autism, and the answer is, “Yes.” Yes. Yes.
I’m assuming that we’ll have to go to Mars and find a child with autism there who’s never been exposed to anything except the natural Mars environment before anyone will believe that it’s not necessarily something that evil people–doctors, scientists, CDC employees, the UN, the drug companies–have done, deliberately or otherwise, to cause autism. Or, we could do the right thing and focus on real research in real models with environmentally relevant exposures to whatever seems likely with examinations at the genetic and mechanistic level and really get some answers, but…oh, wait, let’s just poison children with DMSA instead.