The beautiful game of football (soccer) is a bit of national obsession here in the UK. In the bracing North-East of England, we have a particularly loyal following of fans who, every Saturday (or thereabouts) dress up in either red and white or black and white depending on their affinity to the Black Cats or the Magpies, and brave the elements to watch 90 minutes of sporting battle. Derby days when the two teams meet are something else!
I myself, whilst an interested follower of one of these teams (not saying which!), have never been as overly enthusiastic as some of my fellow North-Easterners, instead preferring to follow a different kind of sport, research. Funny you might think that he equates research with football, but it follows very similar principles: competition, goals, star players, money, esteem. Some would say that football is a matter of life or death; research is perhaps in some cases even more about life or death.
Within the autism research football division, several teams compete. At the moment, I would probably say that the team based at the UC Davis MIND Institute are the Manchester United of the Premier League. Indeed various papers from the MIND Institute have been covered on this blog. Their focus on the environmental as well as the genetic is perhaps what makes the MIND Institute stand out from the rest.
Why the long-winded introduction?
Well a paper has appeared recently which whilst outside of autism research could potentially tie into some areas covered by the MIND Institute team. The paper by Zota and colleagues* reports on a study looking at polybrominated diphenyl ethers (PBDEs) and related metabolites used as flame retardant materials alongside markers of thyroid function in pregnant mums based in California.
Many things contain PBDEs despite such compounds being banned in several parts of the world. Plastics, wire insulation, old furniture foam - much like asbestos, being banned does not necessarily mean that people are not exposed to such compounds (and for years after). Zota and colleagues sought to measure serum concentrations of PBDEs in mums-to-be who were in the second trimester of pregnancy. They found some of the highest concentrations of PBDE-related metabolites ever reported in pregnant women. Added to that they reported associations between PBDE findings and moderators of thyroid function such as thyroid-stimulating hormone (TSH).
Whilst it is not possible to say what specific effects such serum PBDE levels might have on the developing foetus bearing in mind their toxicity profile, it is fair to say that any potential disruption to maternal thyroid function caused by alterations in TSH levels is not likely to be good for the child. Foetal premature birth, low birth weight and even miscarriage and stillbirth have been noted in cases of gestational maternal hyper- and hypothyroidism.
So how does this relate back to the MIND Institute and autism research?
Levels of PBDEs and related metabolites in cases of autism have been examined by our intrepid UC Davis team. This paper from Hertz-Piciotto and colleagues measured serum PBDE levels in children with autism vs. developmental delay vs. asymptomatic controls. They did not report any significant differences among the groups, the groups made up of participants from California, but noted high levels of PBDEs in all. OK, you might say so there was no difference, but wait.. what if there might be some difference in the way that such compounds affect a person, a person with autism perhaps? During preliminary study this is what was hinted at in this paper by Ashwood and colleagues, who suggested an altered sensitivity to a specific PBDE, BDE-47 resulting in an increased inflammatory response in cells from people with autism spectrum conditions compared with controls. This finding follows other research suggestive of a potential association between BDE-47 and attention problems.
As with any environmental agent, it is nearly impossible to ascribe an effect in isolation because people do not live in a vacuum. As a population, we potentially face hundreds if not thousands of other exposures which might be contributory to any effect. Unless you measure them all, there is always doubt. Having said that, I don't want to take away from the findings of the study by Zota and colleagues. Findings which require replication and follow-up of infants born to mothers with such high levels, and if deemed necessary, urgent action to minimise any associated health or developmental risks.
I leave you with a song by a footballer which many North-Easterners will know well. It's probably not going to win a Grammy but harks back to happier times for the gentleman in question.
* Zota AR. Polybrominated diphenyl ethers (PBDEs), hydroxylated PBDEs (OH-PBDEs), and measures of thyroid function in second trimester pregnant women in California. Environmental Science & Technology. August 2011.
Saturday, 13 August 2011
Thursday, 11 August 2011
Amyloid precursor protein and autism
A cobbler should stick to his last. Meaning that people should generally stick to what they know and do best. I think most people would feel comfortable with this phrase. We would after all never (knowingly or willingly) go for surgery at a bakery or have our teeth fixed by a plumber. Likewise I probably wouldn't want my doctor to butcher my pork chops, even if she was handy with a scalpel.
I hope that I am not getting too out of my depth with this quite biochemistry-heavy post on some new findings on the amyloid precursor protein in relation to autism spectrum conditions. I have consulted with a few people who know a little more about this than I, just to check a few facts, but please do not assume I am an expert in this area. We will see if I do the science and research justice.
I start with some definition and description. Those with a medical or scientific background or possibly some family experience will probably already have heard of amyloid precursor protein (APP) in relation to Alzheimer's disease (AD). AD is the most common cause of dementia and the condition's profile is being elevated by people such as Sir Terry Pratchett (he of the Discworld novels). Without going too deeply into AD, the characteristic brain pathology of the condition is noted by the presence of neurofibrillary tangles and amyloid plaques. The plaques are made up of certain accumulated breakdown products of APP.
Nobody really knows how such pathology comes about in terms of genes and environment, but amongst the various investigations being undertaken into AD, one of the more widely suggested hypotheses involves APP and in particular, its peptide fragments, beta-amyloid, which are the main constituent of the plaques found in AD. Like any peptide, beta-amyloid is formed as a result of enzymatic processes involving a protease acting on APP, specifically the beta- and gamma-secretases. There are various other processes involved in this chain of events potentially related to AD but that's as far as I am going for now. I would perhaps also mention about the various pharmacotherapeutic measures currently available to tackle AD, based around two main classes of drug: the acetylcholinesterase inhibitors, which increase acetylcholine (often depleted in AD) and the glutamate-blocker, memantine. I have talked about acetylcholinesterase inhibitors previously in relation to autism (here). I note that memantine has also been trialled in cases of autism with some indications of positive symptom response.
A recent paper by Ray and colleagues* (open access copy available here) looked at some of the products of amyloid precursor protein (APP) in plasma from people with autism. The paper is a quite complicated one and not the easiest piece to follow, hence my use of bullet-points to break the methods and selected findings down:
These are interesting findings. Plasma levels of beta-amyloid peptides (particularly 42) are associated with cognitive decline and onset of AD. I would however caution before making too many statements about the study results and risk of AD based on things like the small participant numbers included in the current study, and also their young age.
This is not the first time that this particular research group have published in this area. Indeed in a previous study based on even smaller participant numbers, they reported increased total sAPP in severe autism relative to other groups and controls; contrasting with no overall difference in the current study. Perhaps more interesting however was the confirmation from the recent study of higher levels of non-plaque related sAPP combined with lower levels of plaque-related beta-amyloid-40 peptide in severe autism. Likewise another group has confirmed some of theses findings.
I would like to believe that there may be some good sense in conducting further, large-scale study of levels of sAPP-alpha in autism which some have suggested might be a potential biomarker for autism. There are also a few other potential tie-ins to sAPP-alpha which might also necessitate some further investigation including a peripheral nicotinic effect, the use of statins, and the effect of selected neuropeptides.
As per my initial caveat, I would perhaps advise interested readers to do a little confirmatory reading before taking my observations as any kind of truth. If on the other hand you need someone to name your Star Wars villains, well I'm yer man..
* Ray B. et al. Increased secreted amyloid precursor protein-α (sAPPα) in severe autism: proposal of a specific, anabolic pathway and putative biomarker. PLoS ONE. 2011: 6:6
I hope that I am not getting too out of my depth with this quite biochemistry-heavy post on some new findings on the amyloid precursor protein in relation to autism spectrum conditions. I have consulted with a few people who know a little more about this than I, just to check a few facts, but please do not assume I am an expert in this area. We will see if I do the science and research justice.
I start with some definition and description. Those with a medical or scientific background or possibly some family experience will probably already have heard of amyloid precursor protein (APP) in relation to Alzheimer's disease (AD). AD is the most common cause of dementia and the condition's profile is being elevated by people such as Sir Terry Pratchett (he of the Discworld novels). Without going too deeply into AD, the characteristic brain pathology of the condition is noted by the presence of neurofibrillary tangles and amyloid plaques. The plaques are made up of certain accumulated breakdown products of APP.
Nobody really knows how such pathology comes about in terms of genes and environment, but amongst the various investigations being undertaken into AD, one of the more widely suggested hypotheses involves APP and in particular, its peptide fragments, beta-amyloid, which are the main constituent of the plaques found in AD. Like any peptide, beta-amyloid is formed as a result of enzymatic processes involving a protease acting on APP, specifically the beta- and gamma-secretases. There are various other processes involved in this chain of events potentially related to AD but that's as far as I am going for now. I would perhaps also mention about the various pharmacotherapeutic measures currently available to tackle AD, based around two main classes of drug: the acetylcholinesterase inhibitors, which increase acetylcholine (often depleted in AD) and the glutamate-blocker, memantine. I have talked about acetylcholinesterase inhibitors previously in relation to autism (here). I note that memantine has also been trialled in cases of autism with some indications of positive symptom response.
A recent paper by Ray and colleagues* (open access copy available here) looked at some of the products of amyloid precursor protein (APP) in plasma from people with autism. The paper is a quite complicated one and not the easiest piece to follow, hence my use of bullet-points to break the methods and selected findings down:
- A total of 39 participants were included for study: 15 diagnosed with severe autism (CARS score of 37+), 6 with mild-moderate autism (CARS: 30-36.5) and 18 asymptomatic controls. There was no significant difference across the mean ages of the groups.
- Various measures of the residues and peptides derived from APP in plasma were analysed alongside levels of brain-derived neurotrophic factor (BDNF). The main reason seems to be the study's focus on BDNF and specific APP breakdown products being neurotrophic (related to neuronal growth or survival) on the back of the data looking at head circumference in autism.
- There was no significant difference across the groups in terms of the mean total of total secreted amyloid precursor protein (sAPP) (that is the combined species based on the actions of the various forms of the secretase on APP).
- Levels of sAPP-alpha, the residue of the non-plaque associated form of APP, were elevated in the more severely affected autism group compared with controls.
- Levels of sAPP-beta, the residue associated with plaques from APP, were reduced in the more severely affected autism group compared with controls.
- Levels of the beta-amyloid peptides involved in plaque formation, including the most insoluble and toxic peptide, beta-amyloid-42, were also reduced in the more severely affected autism group compared with controls.
These are interesting findings. Plasma levels of beta-amyloid peptides (particularly 42) are associated with cognitive decline and onset of AD. I would however caution before making too many statements about the study results and risk of AD based on things like the small participant numbers included in the current study, and also their young age.
This is not the first time that this particular research group have published in this area. Indeed in a previous study based on even smaller participant numbers, they reported increased total sAPP in severe autism relative to other groups and controls; contrasting with no overall difference in the current study. Perhaps more interesting however was the confirmation from the recent study of higher levels of non-plaque related sAPP combined with lower levels of plaque-related beta-amyloid-40 peptide in severe autism. Likewise another group has confirmed some of theses findings.
I would like to believe that there may be some good sense in conducting further, large-scale study of levels of sAPP-alpha in autism which some have suggested might be a potential biomarker for autism. There are also a few other potential tie-ins to sAPP-alpha which might also necessitate some further investigation including a peripheral nicotinic effect, the use of statins, and the effect of selected neuropeptides.
As per my initial caveat, I would perhaps advise interested readers to do a little confirmatory reading before taking my observations as any kind of truth. If on the other hand you need someone to name your Star Wars villains, well I'm yer man..
* Ray B. et al. Increased secreted amyloid precursor protein-α (sAPPα) in severe autism: proposal of a specific, anabolic pathway and putative biomarker. PLoS ONE. 2011: 6:6
Tuesday, 9 August 2011
Cup of green tea anyone?
Whilst the recent riots witnessed on the streets of London and other English cities are making all the headlines at the moment, normal British culture tends to be a far more relaxed affair. Think England and most people would traditionally think cricket, Wimbledon tennis and afternoon tea a la Hugh Grant style. Although we don't all go around quaffing our favourite brew in our best Etonian blazers, tea drinking is very widely practiced here and we continue to drink quite a lot of it.
As well as being a pleasant drink, quite a large body of evidence has suggested that drinking tea, various types of tea, might also confer some health benefits. Rather than me list them all, this page does quite a good job of demonstrating how tea might help. I would perhaps reiterate the well-used adage 'correlation does not imply causation' for your guidance when reading about the potential health benefits of tea.
Tea drinking in relation to autism is perhaps not something that I ever envisaged myself talking about but this recent article* by Banji and colleagues based in Andhra Pradesh State in India has appeared. The study described the effects of supplementation with green tea extract on mice exposed to valproate; valproate exposure in mice previously being used to model autistic-like behaviour. The outcomes reported by the authors suggest a few things; primarily that green tea extract might offer some ameliorative properties to the valproate-exposed animals in terms of behaviour and in particular a role for oxidative stress in the valproate model. Green tea extract carries some significant antioxidant (and pro-oxidant) capability although most likely this may not be its only beneficial effect.
Whilst this is just a preliminary study carried out in one of the major tea exporting countries on mice with experimentally-induced autistic-like behaviours, I am intrigued by the findings. Experimental animal models of autism, whilst carrying certain ethical dilemmas, are providing some important clues about autism and its origins and biochemical course. Ideas about oxidative stress in relation to autism have been around for quite a while. Reducing that oxidative burden may potentially affect symptoms; even some of the medications commonly used in autism and other conditions can act as quite potent antioxidants.
So whilst there is panic on the streets of London, would anyone like a relaxing cup of tea?
* Banji D. et al. Amelioration of behavioral aberrations and oxidative markers by green tea extract in valproate induced autism in animals. Brain Research. July 2011.
As well as being a pleasant drink, quite a large body of evidence has suggested that drinking tea, various types of tea, might also confer some health benefits. Rather than me list them all, this page does quite a good job of demonstrating how tea might help. I would perhaps reiterate the well-used adage 'correlation does not imply causation' for your guidance when reading about the potential health benefits of tea.
Tea drinking in relation to autism is perhaps not something that I ever envisaged myself talking about but this recent article* by Banji and colleagues based in Andhra Pradesh State in India has appeared. The study described the effects of supplementation with green tea extract on mice exposed to valproate; valproate exposure in mice previously being used to model autistic-like behaviour. The outcomes reported by the authors suggest a few things; primarily that green tea extract might offer some ameliorative properties to the valproate-exposed animals in terms of behaviour and in particular a role for oxidative stress in the valproate model. Green tea extract carries some significant antioxidant (and pro-oxidant) capability although most likely this may not be its only beneficial effect.
Whilst this is just a preliminary study carried out in one of the major tea exporting countries on mice with experimentally-induced autistic-like behaviours, I am intrigued by the findings. Experimental animal models of autism, whilst carrying certain ethical dilemmas, are providing some important clues about autism and its origins and biochemical course. Ideas about oxidative stress in relation to autism have been around for quite a while. Reducing that oxidative burden may potentially affect symptoms; even some of the medications commonly used in autism and other conditions can act as quite potent antioxidants.
So whilst there is panic on the streets of London, would anyone like a relaxing cup of tea?
* Banji D. et al. Amelioration of behavioral aberrations and oxidative markers by green tea extract in valproate induced autism in animals. Brain Research. July 2011.
Sunday, 7 August 2011
Trends in autism and schizophrenia research
It is easy when writing a blog like this to become a little too focused on the object of your attention at the expense of the bigger picture. I assume there is some trendy name for such a psychological phenomenon - oh, yes 'not seeing the wood for the trees'. Over several years I (like many others) have become more and more convinced that whilst genetics is an important area of autism research, the various genetic models put forward so far have been sadly lacking in their appreciation of a contributory role for the environment in a kind of symbiotic relationship. I base such a view on the volumes of research that has passed through my humble PC over the years alongside the volumes of commentary which I have read about the research. One could perhaps argue that my view has become self-selecting and self-fulfilling as the years have gone by; that is, I see what I want to see, at the expense of any research which opposes my view.
One of the best remedies for this is to examine what is happening in other areas, in this case to have a look at other areas of research outside of autism or at least on the very periphery. I do try and do this as much as I can, to try and level my view and restore some degree of objectivity. One of the main areas of research that I try and keep tabs on is what is happening in the world of schizophrenia research.
Why schizophrenia you might ask? Well, schizophrenia and autism have some history, but more than that they are both spectrum conditions rather than one-presentation entities and both have some big question marks hanging over them about prevalence, aetiology and risk factors. I have blogged about schizophrenia previously.
So what is happening in the world of schizophrenia research and what might it tell us about autism research? There is quite a good review of all things schizophrenia here by NICE. This fairly recent, and quite hefty, document covers quite a few details and makes some interesting points:
I am sure that the discerning reader can see a few overlaps here with the autism spectrum conditions although not all features are the same. I might also add that schizophrenia has been tied into a few other overlapping areas related to autism; so things like a role for the immune system, a possible link with gluten (from Faith Dickerson and her research group), and issues with the hyperpermeability of the gastrointestinal tract. Indeed the 'second brain' seems to show more than a passing relationship with some cases of schizophrenia.
One of the bigger questions in schizophrenia surrounds what factors might influence the initial 'vulnerability' to schizophrenia and what does this tell us about our potential risk. I say this because of this paper recently released in Nature Genetics by Girard and colleagues. The paper suggests that de novo mutations in various genes were more commonly detected in cases of schizophrenia than controls, and said mutations might account for the increase in cases of the condition being observed. When I saw this paper, the first thought to cross my mind was how strikingly similar these findings were to those recently reported in relation to autism (see here) in terms of the meaning of the findings: de novo = not inherited from parents. Indeed this paper out today also in Nature Genetics picked up by the BBC says pretty much the same thing.
Coupled with various other failures to detect consistent genetic markers, this paper actually summarises quite well the current state of play with regards to genes and schizophrenia; the initial promise (and hefty research price tag) of a 'schizophrenia gene' with classical genetic transmission pattern being unmet and more likely now down to various gene-environment interactions. Spontaneous mutation, perhaps suggesting some interesting environmental connections (see my recent post on our chemical romance, and no not 'my chemical romance'), is a research line which seems to be going places. Please do not assume from this that I am saying that traditional genetics are defunct when it comes to schizophrenia because I am not. There is still evidence to suggest that risk of schizophrenia is increased in families with a history of the condition alongside ethnicity also being a factor. The sum total of the research so far does however mean that the vulnerability basis for schizophrenia is not solely genetic.
I would like to think that schizophrenia research or research in other areas is a good balance to that of autism research. The trends being picked up in autism are being mirrored in schizophrenia and other areas and vice-versa. Our rigid models of such conditions being somehow the result of consistent single or multiple genes are slowly being overturned and the concept of genetic diversity is beginning to shine through, influenced in part by the environment around us.
If you need more evidence of some interesting environmental overlaps, consider this paper on birth spacing in schizophrenia and compare it with the similar findings in autism (even mentioning our old friends folate metabolism and pre- and peri-natal nutrients). Interesting.
One of the best remedies for this is to examine what is happening in other areas, in this case to have a look at other areas of research outside of autism or at least on the very periphery. I do try and do this as much as I can, to try and level my view and restore some degree of objectivity. One of the main areas of research that I try and keep tabs on is what is happening in the world of schizophrenia research.
Why schizophrenia you might ask? Well, schizophrenia and autism have some history, but more than that they are both spectrum conditions rather than one-presentation entities and both have some big question marks hanging over them about prevalence, aetiology and risk factors. I have blogged about schizophrenia previously.
So what is happening in the world of schizophrenia research and what might it tell us about autism research? There is quite a good review of all things schizophrenia here by NICE. This fairly recent, and quite hefty, document covers quite a few details and makes some interesting points:
- Diagnosis remains solely on the analysis of 'behavioural' history.
- Although the topic of some debate, prevalence of schizophrenia, core schizophrenia, is round about 1% over a lifetime.
- Various co-morbidities both psychiatric and somatic can surround a diagnosis; schizophrenia is not protective against the development of other conditions.
- Although no one model for the aetiology of schizophrenia exists, a 'vulnerability-stress' model has been proposed whereby genes and biochemistry act as 'risk' factors modified by psychological and social factors.
I am sure that the discerning reader can see a few overlaps here with the autism spectrum conditions although not all features are the same. I might also add that schizophrenia has been tied into a few other overlapping areas related to autism; so things like a role for the immune system, a possible link with gluten (from Faith Dickerson and her research group), and issues with the hyperpermeability of the gastrointestinal tract. Indeed the 'second brain' seems to show more than a passing relationship with some cases of schizophrenia.
One of the bigger questions in schizophrenia surrounds what factors might influence the initial 'vulnerability' to schizophrenia and what does this tell us about our potential risk. I say this because of this paper recently released in Nature Genetics by Girard and colleagues. The paper suggests that de novo mutations in various genes were more commonly detected in cases of schizophrenia than controls, and said mutations might account for the increase in cases of the condition being observed. When I saw this paper, the first thought to cross my mind was how strikingly similar these findings were to those recently reported in relation to autism (see here) in terms of the meaning of the findings: de novo = not inherited from parents. Indeed this paper out today also in Nature Genetics picked up by the BBC says pretty much the same thing.
Coupled with various other failures to detect consistent genetic markers, this paper actually summarises quite well the current state of play with regards to genes and schizophrenia; the initial promise (and hefty research price tag) of a 'schizophrenia gene' with classical genetic transmission pattern being unmet and more likely now down to various gene-environment interactions. Spontaneous mutation, perhaps suggesting some interesting environmental connections (see my recent post on our chemical romance, and no not 'my chemical romance'), is a research line which seems to be going places. Please do not assume from this that I am saying that traditional genetics are defunct when it comes to schizophrenia because I am not. There is still evidence to suggest that risk of schizophrenia is increased in families with a history of the condition alongside ethnicity also being a factor. The sum total of the research so far does however mean that the vulnerability basis for schizophrenia is not solely genetic.
I would like to think that schizophrenia research or research in other areas is a good balance to that of autism research. The trends being picked up in autism are being mirrored in schizophrenia and other areas and vice-versa. Our rigid models of such conditions being somehow the result of consistent single or multiple genes are slowly being overturned and the concept of genetic diversity is beginning to shine through, influenced in part by the environment around us.
If you need more evidence of some interesting environmental overlaps, consider this paper on birth spacing in schizophrenia and compare it with the similar findings in autism (even mentioning our old friends folate metabolism and pre- and peri-natal nutrients). Interesting.
Saturday, 6 August 2011
Coughs and sneezes and omega-3 fatty acids
A quick post on this cold and rainy Saturday evening. Our summer weather here in the North-East of England has vanished it seems, although the garden is as green as ever as a result of the downpours.
The journal Pediatrics includes details of a new study suggesting a beneficial effect from pre-natal supplementation with docosahexaenoic acid (DHA) - an omega-3 fatty acid - on the duration and severity of coughs and sneezes in young infants. The paper* by Imhoff-Kunsch and colleagues reports on a double-blind, randomised-controlled, placebo-controlled study of over 1000 pregnant women and their 800 or so infants. Mums-to-be were given either 400mg of DHA or placebo during the second and third trimesters of pregnancy. The results suggested that those infants in the DHA supplement group still got coughs and sneezes but generally speaking the episodes at 1, 3 and 6 months were fewer and shorter in duration compared with the placebo group.
The study design and number of participants included in the study are impressive and make for quite a powerful study. The evidence continues to mount for the value of fatty acids for body and brain.
* Imhoff-Kunsch B. et al. Prenatal docosahexaenoic acid supplementation and infant morbidity: randomized controlled trial. Pediatrics. August 2011.
The journal Pediatrics includes details of a new study suggesting a beneficial effect from pre-natal supplementation with docosahexaenoic acid (DHA) - an omega-3 fatty acid - on the duration and severity of coughs and sneezes in young infants. The paper* by Imhoff-Kunsch and colleagues reports on a double-blind, randomised-controlled, placebo-controlled study of over 1000 pregnant women and their 800 or so infants. Mums-to-be were given either 400mg of DHA or placebo during the second and third trimesters of pregnancy. The results suggested that those infants in the DHA supplement group still got coughs and sneezes but generally speaking the episodes at 1, 3 and 6 months were fewer and shorter in duration compared with the placebo group.
The study design and number of participants included in the study are impressive and make for quite a powerful study. The evidence continues to mount for the value of fatty acids for body and brain.
* Imhoff-Kunsch B. et al. Prenatal docosahexaenoic acid supplementation and infant morbidity: randomized controlled trial. Pediatrics. August 2011.
Friday, 5 August 2011
Stability of autistic traits in the general population
In a post a few weeks back, I discussed the relative stability, or instability, of autistic traits from a diagnostic point of view. The take-home message from that post was that autism taken as a population whole, can be a fairly unstable concept in terms of symptom presentation both in the short- and long-term as a function of lots of different factors. Much like everyone else, people with autism and their symptoms change with maturity and experience.
A recent paper appearing in PLoS ONE offers some further insight into this process, long-term. The paper (open-text here) by Whitehouse and colleagues* sought to measure autistic traits among typically-developing toddlers and the degree to which such traits were predictive of things a couple of decades later. It is important to realise that this was not a study looking at children with a diagnosis of autism, but rather the overlap of traits in the general population. Longitudinal research to the extreme!
Without repeating the paper rote fashion, here's a summary of what they did and found:
Although there are elements to this study which might raise an eyebrow of many scientific sorts out there, I have to say that I do like this study. I like it because it was prospective and it had a large participant group. I also like the fact after so many years a good percentage of the original group were still willing to volunteer, albeit perhaps from a higher socio-economically advantaged group. Of course we are 'almost' dealing with apples and oranges in terms of the different scales used over the study period and the different informants (parents vs. participants), so these need to be kept in mind.
The gender differences are interesting. Interesting because of the various debates around diagnosis of autism in males and females. The current results hinting that autistic traits in typically-developing young girls were not the same or predictive of the same group in early adulthood may imply either different biological mechanisms or different social factors are at work in modifying such behaviours compared with boys. How this might translate into autism and presentation by gender, I don't know.
The authors are quite reserved in their interpretation of their findings despite the significance values obtained. 'Modest' is a word used quite a bit throughout the article, and to me, that sounds about right. Kudos to them for the work they have put it and the results obtained.
* Whitehouse AJO. et al. Are autistic traits in the general population stable across development? PLoS ONE. August 2011.
A recent paper appearing in PLoS ONE offers some further insight into this process, long-term. The paper (open-text here) by Whitehouse and colleagues* sought to measure autistic traits among typically-developing toddlers and the degree to which such traits were predictive of things a couple of decades later. It is important to realise that this was not a study looking at children with a diagnosis of autism, but rather the overlap of traits in the general population. Longitudinal research to the extreme!
Without repeating the paper rote fashion, here's a summary of what they did and found:
- 2900 mums-to-be were recruited for a study looking at the repeated effects of ultra-sound during gestation. 2868 children were invited to take part in a follow-up study involving various assessments during their childhood and young adult years.
- When children were aged approximately 2 years, their parents completed the pervasive developmental problem sub-scale derived from the Childhood Behaviour Checklist (CBCL) on behalf of their child. The scale looks at social and non-social autistic traits. Participants were followed-up some 17-18 years later and completed the self-report Autism Spectrum Quotient. The scoring schedules whilst not exactly the same, were compared and various potential sources of bias taken into account (most of which occurred during gestation).
- The results from participants (males: 360, females: 400) are presented with correlations between the two instrument scores. A significance value of p<0.006 was used as a result of some statistical adjustment made for the multiple comparisons used.
- Males showed the greatest positive correlations between the testing sessions with several associations surpassing the significance boundaries set in areas of total score and social autistic trait score combinations. Having said that the R-squared values (measure of predictive correlation) were not exactly brilliant (0.16-0.17), where 0 is no predictive value and 1 is absolutely predictive. Non-social autistic traits in males showed nothing in particular across the study. Females scores across social and non-social autistic traits over the study period again showed nothing in particular.
Although there are elements to this study which might raise an eyebrow of many scientific sorts out there, I have to say that I do like this study. I like it because it was prospective and it had a large participant group. I also like the fact after so many years a good percentage of the original group were still willing to volunteer, albeit perhaps from a higher socio-economically advantaged group. Of course we are 'almost' dealing with apples and oranges in terms of the different scales used over the study period and the different informants (parents vs. participants), so these need to be kept in mind.
The gender differences are interesting. Interesting because of the various debates around diagnosis of autism in males and females. The current results hinting that autistic traits in typically-developing young girls were not the same or predictive of the same group in early adulthood may imply either different biological mechanisms or different social factors are at work in modifying such behaviours compared with boys. How this might translate into autism and presentation by gender, I don't know.
The authors are quite reserved in their interpretation of their findings despite the significance values obtained. 'Modest' is a word used quite a bit throughout the article, and to me, that sounds about right. Kudos to them for the work they have put it and the results obtained.
* Whitehouse AJO. et al. Are autistic traits in the general population stable across development? PLoS ONE. August 2011.
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