The Google Adword links that have been showing up lately have been largely for sites that exploit vulnerable families with false claims and toxic treatments.
They're gone.
Sharing what I have learned supporting two atypical minds from childhood to adulthood.
Thursday, March 02, 2006
Tuesday, February 28, 2006
Omega 3 and autism: how to account for dietary aversion?
Recently The Economist, a news magazine, highlighted Omega 3 fatty acids in its science section. This got some attention, including this BBC article which confuses The Economist with an academic publication. The thesis is of great interest to parents of children with autism; although the article speaks of "lower IQs" the traits allegedly related to low fish intake sound primarily autistic:
Let's consider autism. Autism is a genetic disorder with complex inheritance and variable penetrance. The parents and siblings of autistic children show "autistic traits". Most autistic people have strong food aversions. It would not be surprising if persons with autism, or their relatives, avoided oily fish. If so, could that explain the entire relationship between Omega-3 intake and lower IQ and social isolation?
Even if Omega-3 intake was helpful to infants who didn't have autism, what's to say it would help those with autism? It might even hurt them.
Bottom line, this is an interesting study. It would be very good to know what the animal models tell us. I would not be surprised, however, if 10 years from now Omega-3 was not considered terribly important.
PS. I've noticed the Google Ads appearing on this page tend to favor 'alternative' therapies and remedies. That's not my gig, and if they keep doing that I'll take them off the page. The only reason they're there is to provide a service to readers -- I don't make anything from them.
BBC NEWS | Health | Oily fish makes 'babies brainier'Hmm. This may be one of the most flagrant examples of confusing correlation with causation I've seen in the past few years.
... Looking at the effects of Omega-3 intake on 9,000 mothers and their children, the team found mothers with the lowest intake of the essential fatty acid had children with a verbal IQ six points lower than the average.
While those with the highest consumption of mackerel and sardines and other sources of Omega-3 had children, at age three-and-a-half, with the best measures of fine-motor performance, researchers said.
Low intake of the crucial fatty acid also appeared to lead to more problems of social interactions - such as an inability to make friends.
Research leader Dr Joseph Hibbeln said "frightening data" showed 14% of 17-year-olds whose mother had eaten small quantities of Omega -3 during pregnancy demonstrated this sort of behaviour.
This compared with 8% of those born to the group with the highest intake, he said.
... Professor Jean Golding of Bristol University set up the original research - the Avon Longitudinal Study of Parents and Children -15 years ago to look at the predisposition to disease.
She told the BBC: "The baby's brain needs Omega-3 fatty acids. It doesn't create its own fatty acids so it needs to be something that the mother will eat." ...
The richest sources of Omega-3 are larger fish which eat other fish, but research shows that the larger the fish the more pollutants, such as mercury, they contain.
For this reason Mr Holford recommends women consume two portions of wild or organic salmon, trout or sardines weekly.
Seeds such as flax, pumpkin and hemp are good sources of Omega-3 for vegetarians, but large quantities need to be consumed to gain the same effect.
This might translate to two tablespoons of seeds daily, Mr Holford said, but women can also use a high quality Omega-3 supplements.
Let's consider autism. Autism is a genetic disorder with complex inheritance and variable penetrance. The parents and siblings of autistic children show "autistic traits". Most autistic people have strong food aversions. It would not be surprising if persons with autism, or their relatives, avoided oily fish. If so, could that explain the entire relationship between Omega-3 intake and lower IQ and social isolation?
Even if Omega-3 intake was helpful to infants who didn't have autism, what's to say it would help those with autism? It might even hurt them.
Bottom line, this is an interesting study. It would be very good to know what the animal models tell us. I would not be surprised, however, if 10 years from now Omega-3 was not considered terribly important.
PS. I've noticed the Google Ads appearing on this page tend to favor 'alternative' therapies and remedies. That's not my gig, and if they keep doing that I'll take them off the page. The only reason they're there is to provide a service to readers -- I don't make anything from them.
Thursday, February 23, 2006
Minnesota Special Hockey
Minnesota Special Hockey has a web site. Actually, it's a blogspot blog and a redirect from www.mnspecialhockey.org, but it is up.
Saturday, February 18, 2006
Winter sports and recreation for special needs: Hockey, Skiing and more (Twin City area)
[Update 2/21/06 with information from hockey flyer].
I'm amazed I'd not heard of this. Three Minneapolis suburbs offer courses and recreational activity for persons with disabilities. The fee for non-residents is said to be only slightly higher than the resident fee.
Together with the American Special Hockey Association the ARLE is now launching a MN Special Hockey program (first in the state) for ages 3 and older with a $60 fee for residents and non-residents. The program starts after regular hockey is over, it will run from March 5th 2006 to April 9th on Sunday evenings from 5:30-6:30 pm (952-826-0433).
The hockey program is not yet on the main web site. Email me (jfaughnan@spamcop.net) prior to 2/24 for a PDF of the flyer. A JPG scan (will print oddly, click on it for larger view) is below. The initial location is the Richfield Ice Arena 636 East 66th Street.
I'm amazed I'd not heard of this. Three Minneapolis suburbs offer courses and recreational activity for persons with disabilities. The fee for non-residents is said to be only slightly higher than the resident fee.
Adaptive Recreation and Learning ExchangeThe 17 page winter catalog (PDF on site) includes ski lessons (GACK! We'd have done that!).
The Cities and school districts of Edina, Eden Prairie, Bloomington and Richfield work together to provide recreation and education for people with disabilities. This cooperative is known as the Adaptive Recreation & Learning Exchange (AR&LE).
Together with the American Special Hockey Association the ARLE is now launching a MN Special Hockey program (first in the state) for ages 3 and older with a $60 fee for residents and non-residents. The program starts after regular hockey is over, it will run from March 5th 2006 to April 9th on Sunday evenings from 5:30-6:30 pm (952-826-0433).
The hockey program is not yet on the main web site. Email me (jfaughnan@spamcop.net) prior to 2/24 for a PDF of the flyer. A JPG scan (will print oddly, click on it for larger view) is below. The initial location is the Richfield Ice Arena 636 East 66th Street.

Friday, February 17, 2006
Correct decisions with limited conscious cognitive abilities
I am often surprised by the correct decisions of at least one person with a very limited verbal reasoning capability. Perhaps there's an explanation:
Gordon's Notes: Better decisions without the prefrontal cortex
... I wonder if this goes some way to explaining why some children and adults with poor prefrontal cortex functions (low measured IQ, severe ADHD) may make surprisingly correct decisions given complex problems. If their unconscious reason is less impaired than their PF cortex ...
Tuesday, January 10, 2006
Mirron neurons and autism
Mirror neurons may play an important role in autism. Is this a primary cause of autism, or is the loss of mirror neuron function an adaptation to a diffuse defect in the development of neuronal interconnectivity? Are mirror neuron abilities being sacrificed to compensate for other problems?
Monday, January 02, 2006
Tolerance and Ritalin in ADHD: We know nothing
You'd think that after 30 years we might know something about how much of a problem tolerance is in the treatment of ADHD with methylphenidate (Ritalin), a stimulant medication. You'd think we'd have done to research to find out what happens when children take this medication for years.
You'd think. You'd be wrong.
One retrospective study done in 1989 on 108 boys with good responses, a highly selected group, seemed to show ongoing benefit without tolerance. It would have been interesting to see how well these children would have done with no medication at all. That's it.
On the other hand, the Google search on Ritalin and Tolerance had 190,000 hits today. Heck, some bored medical student could do a qualitative review of the Googleplex and compare it to the indexed literature. It could be exhibit A in the indictment of biomedicine. This is a topic of interest that is not being addressed by our research.
It boggles the mind. This is a scandal and a crime. All physicians and researchers ought to hang their heads in shame. Why aren't we screaming about this lack of work? (I mean, other than my screaming?)
I know the studies are terribly expensive and very hard to do. I suspect there's no tenure at the end of the tunnel. There's probably no NIH funding and no pharma money. I think I understand why we haven't done to the work. It's still a scandal. The way we do biomedicine is broken.
You'd think. You'd be wrong.
One retrospective study done in 1989 on 108 boys with good responses, a highly selected group, seemed to show ongoing benefit without tolerance. It would have been interesting to see how well these children would have done with no medication at all. That's it.
On the other hand, the Google search on Ritalin and Tolerance had 190,000 hits today. Heck, some bored medical student could do a qualitative review of the Googleplex and compare it to the indexed literature. It could be exhibit A in the indictment of biomedicine. This is a topic of interest that is not being addressed by our research.
It boggles the mind. This is a scandal and a crime. All physicians and researchers ought to hang their heads in shame. Why aren't we screaming about this lack of work? (I mean, other than my screaming?)
I know the studies are terribly expensive and very hard to do. I suspect there's no tenure at the end of the tunnel. There's probably no NIH funding and no pharma money. I think I understand why we haven't done to the work. It's still a scandal. The way we do biomedicine is broken.
Friday, December 09, 2005
Oxytocin: hope for autism and other social disorders?
The psychiatry I studied twenty years ago is, sadly, almost current today. We haven't really had many substantially new therapies (so much for the speed of medical advancement!). Lately, though, there are signs of a break in the drought. The endocannabinoids may one day provide us new therapies, and more recently oxytocin is looking very interesting:
I'd guess we have as much as a 20% probability of a new useful therapy -- which is pretty good in this world. Of course the probability of abuse is 100%. Colognes may again become popular among men ...
NIMH: Trust-Building Hormone Short-Circuits Fear In HumansSince Oxytocin is an "old" drug with existing FDA approval, there's a modest chance recent research may produce new treatments within 10 years. This particular result is not surprising given all the recent discoveries about Oxytocin and the amygdala, but it's still interesting and useful. The possibilities for treatment in autism, "attachment disorder" (assuming that's different from autism), and anxiety and paranoid disorders are tantalizing -- all conditions for which we have no effective medications.
...Scans of the hormone oxytocin's effect on human brain function reveal that it quells the brain's fear hub, the amygdala, and its brainstem relay stations in response to fearful stimuli....
... "The observed changes in the amygdala are exciting as they suggest that a long-acting analogue of oxytocin could have therapeutic value in disorders characterized by social avoidance," added Insel.
... Having just discovered decreased amygdala activity in response to social stimuli in people with a rare genetic brain disorder that rendered them overly trusting of others, Meyer-Lindenberg hypothesized that oxytocin boosts trust by suppressing the amygdala and its fear-processing networks.
To test this idea, he asked 15 healthy men to sniff oxytocin or a placebo prior to undergoing a functional magnetic resonance imaging (fMRI) scan, which reveals what parts of the brain that are activated by particular activities. While in the scanner, the men performed tasks known to activate the amygdala — matching angry or fearful faces and threatening scenes.
... People with autism characteristically avert their gaze from faces. A fMRI study4 reported earlier this year by NIMH grantee Richard Davidson, Ph.D., University of Wisconsin, and colleagues, found over-activation of the amygdala in people with autism when they were looking at faces. Meyer-Lindenberg said future studies may test oxytocin as a treatment for such social anxiety symptoms in children with autism...
I'd guess we have as much as a 20% probability of a new useful therapy -- which is pretty good in this world. Of course the probability of abuse is 100%. Colognes may again become popular among men ...
Monday, December 05, 2005
Autism-class social disorder correlates with blood flow to the inferior frontal gyrus
The researchers studied "high functioning" autistic children, so they were isolating "pure" social disabilities from the cognitive disorders common in many forms of autism. In this group a functional MRI study provided one of the first objective tests for evaluating autism:
Science & Technology at Scientific American.com: Lack of "Mirror Neurons" May Help Explain AutismThese children could be said to suffer from 'isolated hypofunction of the inferior frontal gyrus' syndrome' (IHIFG Syndrome). If these results hold up we will be able to tease out some of the different conditions subsumed by the generic label of "autism".
... Neuroscientist Mirella Dapretto of the University of California Los Angeles and her colleagues surveyed the brains of 10 autistic children and an equal number of nonautistic children as they watched and imitated 80 different faces displaying either anger, fear, happiness, sadness or no emotion. By measuring the amount of blood flowing to certain regions of the children's brains with a magnetic resonance imaging (MRI) machine, the researchers could determine what parts of the brain were being used as the subjects completed the tasks. The autistic children differed from their peers in only one respect: each showed reduced activity in the pars opercularis of the inferior frontal gyrus--a brain region located near the temple.
This section of the brain has been shown by other studies to be part of the so-called mirror neuron system, which allows humans to understand the intentions of other human beings by observing their actions or imitating their behavior. When damaged, it can interfere with speech.
Although the high-functioning autistic children were able to imitate the facial expressions, they had trouble understanding the corresponding emotional state. The study suggests that the incompletely activated mirror neuron system is to blame. In fact, the less blood that flowed to this region of the brain in each autistic child, the less social ability that child showed--providing more support for the apparent link.
Thursday, December 01, 2005
Autism, communication disorders and FOXP2 mutations
The FOXP2 gene is currently thought to have been a critical factor in the evolution of human communication. It may be one of the things that allowed the pre-human primate to dominate the world.
Researchers are exploring whether mutations in FOXP2 may be associated with communication disorders, of which autism may be considered one example:
Researchers are exploring whether mutations in FOXP2 may be associated with communication disorders, of which autism may be considered one example:
Entrez PubMed - Am J Hum Genet. 2005 Jun;76(6):1074-80. Epub 2005 Apr 22. Identification of FOXP2 truncation as a novel cause of developmental speech and language deficits.
FOXP2, the first gene to have been implicated in a developmental communication disorder, offers a unique entry point into neuromolecular mechanisms influencing human speech and language acquisition...
...Our discovery of the first nonsense mutation in FOXP2 now opens the door for detailed investigations of neurodevelopment in people carrying different etiological variants of the gene. This endeavor will be crucial for gaining insight into the role of FOXP2 in human cognition.
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