This is my Godzilla post on amino acids; indeed Godzilla and Godzooky all rolled into one. In fact this post is so big that it is split into two parts. So, nice cup of tea/coffee/cocoa (or something stronger if you wish), feet up and read on.
Part 1. Schizophrenia
Metabolomics. The word just rolls off the tongue. The science of reading biological samples for clues to symptoms, diseases, conditions. Not particularly fussy about which medium to use: urine, blood, saliva. The technology is spectacular; the physics and chemistry complicated, and in the past few years, metabolomics has become quite a 'sexy' area of research - 'your mass spectrometer or mine'.
I recently chanced upon an article published on the website Internal Medicine News about the application of metabolomics to schizophrenia. Another conference presentation; this time given at the 2011 annual congress of the European College of Psychopharmacology in Paris by Dr Dan Rujescu. Rujescu is no stranger to schizophrenia research, displaying an impressive PubMed reference list including some work on a cats best rat-catching compadre Toxoplasma gondii.
The current findings: seven compounds were found to discriminate samples (not sure what kind of samples) of people with schizophrenia (n=265) from controls (n=216). The compounds were: ornithine, arginine, glutamine, histidine, phosphatidylcholine acyl-alkyl C38:2, dodecenoyl carnitine, and octenoyl carnitine. Only ornithine was 'down-regulated'; the others were elevated. There is some further text on the use of gene-metabolite networks but I will let you read more of that for yourselves.
Intriguing that a panel of seven compounds, including several amino acids, might carry some discriminatory power for determining schizophrenia from not-schizophrenia. This is of course not the first time that amino acid patterns have been discussed in relation to schizophrenia as witnessed by this paper; one of several hundred detailing a possible connection. Takes me back to a few findings suggesting similar things for autism.
Part 2. Autism
The second part of this entry has been on my 'to do' list for a few weeks now. The reason why I wanted to get to it is because amino acids and their presentation in the various biological fluids in autism represents a growing research area. Perhaps more than that they tie into some important things already covered on this blog in relation to in-born errors of metabolism (like PKU), the various dietary factors associated to autism spectrum conditions and research pertinent to our old friend homocysteine. This could turn out to be a very long post indeed if I were to go through all the research on amino acids in autism so I will put on my cherry-picking goggles on in order to present a condensed version.
What are amino acids I thought I heard you say? Well, I should have said this in part 1 but the way I tend to look at it is that proteins, those long chains of amino acids, are equivalent to sentences. Peptides, short chains of amino acids, are the words of the sentence. The individual amino acids are the letters. Indeed when talking about amino acids, single letters are often used to denote specific amino acids (also alongside their three letter abbreviations also).
The earliest report that I can find discussing amino acid metabolism in relation to autism is this paper from 1958. I was however nudged into this post by this paper* by Tirouvanziam and colleagues appearing quite recently reporting on a few interesting findings in relation to amino acids and autism. The team from Stanford University analysed levels of plasma amino acids in children with autism spectrum conditions (n=27) and asymptomatic controls (n=20) and found lower levels of most neutral amino acids as well as others in the autism group. Importantly the authors also noted that various excitatory amino acids such as glutamate did not follow the usual age-related changes. The findings mirrored those presented in earlier investigations including this one which again found higher levels of plasma glutamate as did this one from Jim Adams and colleagues.
Now an even more recent paper has emerged by Shimmura and colleagues* (open-access) has confirmed the glutamate findings in relation to autism, or in the case of this paper, high-functioning autism. Indeed out of all the amino acids assayed for, only glutamine and glutamate were significantly different from controls: glutamate higher, glutamine lower. I could go on to talk about glutamate and the hyperglutamatergic hypothesis of autism. How about the link between glutamine and the gastrointestinal (GI) tract instead? Glutamine the 'food of the gut' and what happens when there 'aint enough of it. Glutamine and glutathione connected even?
If there was a take home message from this mega post it would be something like amino acids are important (we know that already); amino acids might be very, very important to conditions like autism and schizophrenia.
* Tirouvanziam R. et al. Distinct plasma profile of polar neutral amino acids, leucine and glutamate in children with autism spectrum disorders. JADD. June 2011.
** Shimmura C. et al. Alteration of plasma glutamate and glutamine in children with high-functioning autism. PLoS ONE. October 2011.
Thursday, 6 October 2011
Wednesday, 5 October 2011
New life for beta-blockers
I approach this post with slight trepidation. A touch of anxiety because I do not want it to become some kind of advert for beta-blockers (or any approach for that matter, pharmaceutical or otherwise) for autism or anything else. This despite some interesting news on potential benefits outside of their primary purposes. I will also at this point reiterate my mantra: 'I am not a medical doctor and do not offer anything like medical advice or recommendation'. OK, got your pinch of salt ready?
I am sure that the board rooms of a few pharmaceutical companies were of a slightly more jubilant mood when they heard about this report picked up the BBC recently on the embarkation of a study to examine the potentially positive effect from the use of beta-blockers in stopping breast cancer from spreading (metastasis), based on some earlier research (full-text) findings. I can also imagine that quite a few people whose lives may have been touched by breast cancer also found the news to be important for a slightly different and perhaps more important set of reasons.
The exact process for the effect of beta-blockers on inhibiting the formation of secondary cancers is still the source of some speculation but attention seems to be focusing on the primary activity of such pharmaceutics acting on stress hormones and in particular how beta-blockers block adrenergic receptors so diminishing the effects of catecholamines. It must be added that this is not the first time that beta-blockers have shown activity against cancers either peripherally or directly.
The good news for beta-blockers did not stop there with another feel-good story in this study by Beversdorf and colleagues* on a potential role for propranolol on word fluency in autism. The main effects were that alongside what one would expect (lower blood pressure, stabilising heart rate) there were also some cognitive 'enhancing' effects to be had for the high-functioning participants with autism similar to other research undertaken by the authors. Improved functional connectivity between brain areas has been suggested as a primary effect from propranolol.
There are some potentially very interesting facets to both these stories on beta-blockers. The biochemistry of effect in both cases is bound to be complicated and indeed might (probably) not even be showing the same effect across the different findings. Beta-blockers are primarily used to address cardiac function and hypertension. Outside of what has already been detailed there is some evidence of other effects; for example including a potential anti-parasitic effect as detailed by this review of treatments for Giardia lamblia. Like many pharmaceutics (and nutraceutics), the effects are likely to be numerous.
Before both these reports of a potential effect of beta-blockers on autism and halting metastatic breast cancer came out, I had intended to cover the very delicate subject of any relationship between autism and cancer on this blog. Those that follow Donna Williams will know about her on-going treatment following her diagnosis with breast cancer. Many people will know Donna through her books, speaking engagements and her website (including her blog) about her experiences of autism. She has been very open about her cancer and continues to plot her treatment course and the associated emotions which accompany it. I wish her well. There was also the publication of this paper (open-access)** in the journal Autism Research by Crespi on autism and cancer risk following on from other reports of possible correlations between autism and specifically with breast cancer. I'm not even going to approach the PTEN findings and any onward suggestions from there.
I don't however want to make too much of any commonalities between autism and cancer with the beta-blocker connection because there might not be any. Beta-blockers are not for everyone with autism; that is for sure. One need only look at my post on the medicine cabinet and autism, and specifically the ARI parent survey of interventions to see that. For autism, if it is possible to identify best-responders to the reported cognitive effects however, there are potential openings which perhaps need further exploration bearing in mind the issues of side-effects and contra-indications. As to effect, if it is tied into the adrenergic receptors or functional connectivity, so be it. If it might be due to a more generalised 'anti-hypertensive' effect being witnessed, questions need to be asked about other classes of medication with similar functions such as the ACE inhibitors (e.g. enalapril) alongside their suggested neuroprotective effects are worthy of some autism research consideration also. The accompanying development of mice models of autism offer an ideal platform for examination.
The last words of this post should be given over to beta-blockers, as an example of the realisation that the quite startling array of pharmaceutics currently on the market seemingly offer wide and diverse effects outside of their original design. Some of these potentially therapeutic effects are only now beginning to be revealed.
* Beversdorf DQ. et al. Effect of propranolol on word fluency in autism. Cognitive & Behavioral Neurology 2011. 24: 11-17
** Crespi B. Autism and cancer risk. Autism Research. August 2011.
I am sure that the board rooms of a few pharmaceutical companies were of a slightly more jubilant mood when they heard about this report picked up the BBC recently on the embarkation of a study to examine the potentially positive effect from the use of beta-blockers in stopping breast cancer from spreading (metastasis), based on some earlier research (full-text) findings. I can also imagine that quite a few people whose lives may have been touched by breast cancer also found the news to be important for a slightly different and perhaps more important set of reasons.
The exact process for the effect of beta-blockers on inhibiting the formation of secondary cancers is still the source of some speculation but attention seems to be focusing on the primary activity of such pharmaceutics acting on stress hormones and in particular how beta-blockers block adrenergic receptors so diminishing the effects of catecholamines. It must be added that this is not the first time that beta-blockers have shown activity against cancers either peripherally or directly.
The good news for beta-blockers did not stop there with another feel-good story in this study by Beversdorf and colleagues* on a potential role for propranolol on word fluency in autism. The main effects were that alongside what one would expect (lower blood pressure, stabilising heart rate) there were also some cognitive 'enhancing' effects to be had for the high-functioning participants with autism similar to other research undertaken by the authors. Improved functional connectivity between brain areas has been suggested as a primary effect from propranolol.
There are some potentially very interesting facets to both these stories on beta-blockers. The biochemistry of effect in both cases is bound to be complicated and indeed might (probably) not even be showing the same effect across the different findings. Beta-blockers are primarily used to address cardiac function and hypertension. Outside of what has already been detailed there is some evidence of other effects; for example including a potential anti-parasitic effect as detailed by this review of treatments for Giardia lamblia. Like many pharmaceutics (and nutraceutics), the effects are likely to be numerous.
Before both these reports of a potential effect of beta-blockers on autism and halting metastatic breast cancer came out, I had intended to cover the very delicate subject of any relationship between autism and cancer on this blog. Those that follow Donna Williams will know about her on-going treatment following her diagnosis with breast cancer. Many people will know Donna through her books, speaking engagements and her website (including her blog) about her experiences of autism. She has been very open about her cancer and continues to plot her treatment course and the associated emotions which accompany it. I wish her well. There was also the publication of this paper (open-access)** in the journal Autism Research by Crespi on autism and cancer risk following on from other reports of possible correlations between autism and specifically with breast cancer. I'm not even going to approach the PTEN findings and any onward suggestions from there.
I don't however want to make too much of any commonalities between autism and cancer with the beta-blocker connection because there might not be any. Beta-blockers are not for everyone with autism; that is for sure. One need only look at my post on the medicine cabinet and autism, and specifically the ARI parent survey of interventions to see that. For autism, if it is possible to identify best-responders to the reported cognitive effects however, there are potential openings which perhaps need further exploration bearing in mind the issues of side-effects and contra-indications. As to effect, if it is tied into the adrenergic receptors or functional connectivity, so be it. If it might be due to a more generalised 'anti-hypertensive' effect being witnessed, questions need to be asked about other classes of medication with similar functions such as the ACE inhibitors (e.g. enalapril) alongside their suggested neuroprotective effects are worthy of some autism research consideration also. The accompanying development of mice models of autism offer an ideal platform for examination.
The last words of this post should be given over to beta-blockers, as an example of the realisation that the quite startling array of pharmaceutics currently on the market seemingly offer wide and diverse effects outside of their original design. Some of these potentially therapeutic effects are only now beginning to be revealed.
* Beversdorf DQ. et al. Effect of propranolol on word fluency in autism. Cognitive & Behavioral Neurology 2011. 24: 11-17
** Crespi B. Autism and cancer risk. Autism Research. August 2011.
Tuesday, 4 October 2011
As if to prove a point
I don't really like the phrase 'I told you so'. It always seems a little bit too smug. The kind of thing that Mums and Dads say to their children when they fall off the sofa whilst trying to copy surfers on the TV or indeed much admired superheros like the Silver Surfer (yes, that was me standing on the sofa doing my best Norrin Radd impression and failing). Much better to say something like 'as if to prove a point' so as not to come across as quite such a know-it-all mums and dads.
I say all this because a letter published in Nature today by Kerri Smith* reiterates a post a few days back on how our research focus really needs to start giving more to mental as well as physical ill-health. $1 trillion dollars a year is the price tag associated with the direct and indirect costs of 'brain disorders' in Europe alone to any health economists out there. Granted the words 'brain disorder' are not the best description that I would use (is a headache a brain disorder?) but you can't argue with the financials and the need for a lot more explanation of mental ill-health, at the same time trying to improve symptoms and quality of life whatever that is taken to mean.
There's very little more to say on this topic aside from 'as if to prove a point' and provide a link to some surfing dudes.. rad man!
* Smith K. Trillion-dollar brain drain. Nature. 4 October 2011. doi:10.1038/478015a
I say all this because a letter published in Nature today by Kerri Smith* reiterates a post a few days back on how our research focus really needs to start giving more to mental as well as physical ill-health. $1 trillion dollars a year is the price tag associated with the direct and indirect costs of 'brain disorders' in Europe alone to any health economists out there. Granted the words 'brain disorder' are not the best description that I would use (is a headache a brain disorder?) but you can't argue with the financials and the need for a lot more explanation of mental ill-health, at the same time trying to improve symptoms and quality of life whatever that is taken to mean.
There's very little more to say on this topic aside from 'as if to prove a point' and provide a link to some surfing dudes.. rad man!
* Smith K. Trillion-dollar brain drain. Nature. 4 October 2011. doi:10.1038/478015a
Monday, 3 October 2011
Schizophrenia and epilepsy
Whilst few universal commonalities outside of overt clinical presentation are seemingly present in autism spectrum conditions, there are various co-morbidities which appear to be more strongly associated with a diagnosis. Learning or intellectual disability is perhaps the most frequently cited; but in terms of overall health (and risk of early mortality), the presence of epilepsy or seizure-type disorders is one of the most worrisome.
I have talked about epilepsy and autism on this blog previously. In this post however I turn my attention to a new piece of research which suggests that schizophrenia might also be a risk factor for epilepsy and likewise epilepsy might be a risk factor for schizophrenia. The study is this one by Yu-Tzu Chang and colleagues* published in the journal Epilepsia.
The details of this two-part study include:
Cumulatively what this data suggests is that the links, the bi-directional relationship, between schizophrenia and epilepsy might be quite strong. Given the information presented in my previous post on the use of EEGs and epilepsy (and autism) and the link between epilepsy and the electrical circuits of the brain, one can perhaps see how such a relationship might make sense. What we know about schizophrenia, the neurology, the neurochemistry, the biochemistry, the genetics is however the same as what we know about autism; that is, it is very, very complicated.
As the BBC report on this paper adds, psychosis has been previously linked to epilepsy exemplified by studies like this one. Whether there are shared genes, shared environmental factors between the conditions is at this moment unknown but I wouldn't be surprised if there were. I do wonder about the possible influence of things like diet in relation to this work. Dohan's hypothesis on schizophrenia and gluten and casein, the link between some cases of epilepsy and the use of a keotgenic / modified Atkins diet (low carbohydrate diet), what happens to epilepsy in some cases of autism where a gluten-free diet is implemented; all factors circling this important study and its important relationships.
* Yu-Tzu Chang et al. Bidirectional relation between schizophrenia and epilepsy: A population-based retrospective cohort study. Epilepsia. September 2011.
I have talked about epilepsy and autism on this blog previously. In this post however I turn my attention to a new piece of research which suggests that schizophrenia might also be a risk factor for epilepsy and likewise epilepsy might be a risk factor for schizophrenia. The study is this one by Yu-Tzu Chang and colleagues* published in the journal Epilepsia.
The details of this two-part study include:
- Based on Taiwanese health data, analysis 1 looked at over 5,000 people with an incidence of schizophrenia during the period 1999-2008 compared with over 20,000 asymptomatic controls. They reported that the incidence (note incidence not prevalence) of epilepsy in the schizophrenia group was some six times higher than the control group (6.99 vs. 1.19 per 1,000 person-years).
- Analysis 2 looked at over 11,000 patients newly diagnosed with epilepsy compared with over 46,000 age- and sex-matched controls. The incidence of schizophrenia was again much higher in the epilepsy group compared with controls (3.53 vs. 0.46 per 1,000 person-years).
- Gender seemed also to exert an effect: women with schizophrenia were more likely to present with epilepsy but men with epilepsy were at greater risk of presenting with schizophrenia.
Cumulatively what this data suggests is that the links, the bi-directional relationship, between schizophrenia and epilepsy might be quite strong. Given the information presented in my previous post on the use of EEGs and epilepsy (and autism) and the link between epilepsy and the electrical circuits of the brain, one can perhaps see how such a relationship might make sense. What we know about schizophrenia, the neurology, the neurochemistry, the biochemistry, the genetics is however the same as what we know about autism; that is, it is very, very complicated.
As the BBC report on this paper adds, psychosis has been previously linked to epilepsy exemplified by studies like this one. Whether there are shared genes, shared environmental factors between the conditions is at this moment unknown but I wouldn't be surprised if there were. I do wonder about the possible influence of things like diet in relation to this work. Dohan's hypothesis on schizophrenia and gluten and casein, the link between some cases of epilepsy and the use of a keotgenic / modified Atkins diet (low carbohydrate diet), what happens to epilepsy in some cases of autism where a gluten-free diet is implemented; all factors circling this important study and its important relationships.
* Yu-Tzu Chang et al. Bidirectional relation between schizophrenia and epilepsy: A population-based retrospective cohort study. Epilepsia. September 2011.
Saturday, 1 October 2011
Is the entire human race destined for obesity?
I will readily admit that I am slightly outside of my comfort zone when talking about obesity and the research around it. Don't get me wrong, I am very interested in how our weight affects our health particularly when related to conditions like autism and the increasing interest in the physical health of people with autism. Moving away from just obsessing on the 'triad' of behavioural traits is in my view a point where we start making real progress in equality for people with autism in terms of things like appropriate access to healthcare and levelling the 'life opportunities' playing field. Outside of autism however, more general obesity and diet research is a little more of a learning curve for me.
The BBC News Magazine carries an interesting take on the various statistics collected over the years relating to levels of overweight and obese people in the UK titled 'Go Figure: will we really keep getting fatter?'.
Michael Blastland authors the piece, and by coincidence and completely unrelated to this post, is I think, the same Michael Blastland who wrote this article for the New Statesman a few years back about his very personal experience of autism as father to Joe. I think it is the same chap but don't take me word for it.
The BBC article is interesting one. It shows how the figures look according to official sources and how various soundbites have perhaps 'inflated' the issue in terms of the current and future prevalence of overweightedness (?) and obesity. One particular point caught my eye with regards to the use of prediction and where we were predicted to be in terms of the rate of obesity a few years back and what the current reality is. Stand by for a blog first as I attempt to paste in one of the tables presented in the article, fully referenced to Blastland M* and the BBC of course.
In my daydreaming moments, I often wondered whether anyone has (or would want to) go back through the ages and look at the various predictions made 20, 30 or 40 years ago about lots of things related to health, just to see how right (or wrong) we were. Lies, damn lies and statistics perhaps?
Without wishing to come across as some kind of 'agitator', I did post a while back about how Governments and other bodies deliver the health message, the evidence-based health message. Added to the lessons to be learned, I would perhaps echo the comments of Mr Blastland which amount to a request for people to look at the figures and make their own minds up rather than taking things at face value.
* Blastland M. Go Figure: will we really keep getting fatter? BBC Magazine http://www.bbc.co.uk/news/magazine-15108966 (29 September 2011)
The BBC News Magazine carries an interesting take on the various statistics collected over the years relating to levels of overweight and obese people in the UK titled 'Go Figure: will we really keep getting fatter?'.
Michael Blastland authors the piece, and by coincidence and completely unrelated to this post, is I think, the same Michael Blastland who wrote this article for the New Statesman a few years back about his very personal experience of autism as father to Joe. I think it is the same chap but don't take me word for it.
The BBC article is interesting one. It shows how the figures look according to official sources and how various soundbites have perhaps 'inflated' the issue in terms of the current and future prevalence of overweightedness (?) and obesity. One particular point caught my eye with regards to the use of prediction and where we were predicted to be in terms of the rate of obesity a few years back and what the current reality is. Stand by for a blog first as I attempt to paste in one of the tables presented in the article, fully referenced to Blastland M* and the BBC of course.
Without wishing to come across as some kind of 'agitator', I did post a while back about how Governments and other bodies deliver the health message, the evidence-based health message. Added to the lessons to be learned, I would perhaps echo the comments of Mr Blastland which amount to a request for people to look at the figures and make their own minds up rather than taking things at face value.
* Blastland M. Go Figure: will we really keep getting fatter? BBC Magazine http://www.bbc.co.uk/news/magazine-15108966 (29 September 2011)
Bah Ram Ewe, sheep be true
Babe, the sheep-pig, the hero/heroine of the novel (and films) by Dick King-Smith is always a family favourite. Babe's sheep-herding abilities are based in part on the revelation that there is a secret code among sheep 'Bah Ram Ewe, sheep be true'. As a user of this code, Babe earns a perfect sheep-herding round at the sheepdog trials; to be congratulated by Farmer Hoggett "That'll do Pig. That'll do" and satirised by Peter Griffin, everyone's favourite Family Guy.
Why oh why is he talking about Babe and sheep I thought I heard you ask? The reason is a new piece of research which suggests that even lambs can be picky eaters, and when fed monotonous diets, lambs become more stressed than lambs fed a diverse diet which is also reflected in their physiology and open-field behaviour.
The paper is this one by Villalba and colleagues* published in the journal Physiology & Behaviour. I appreciate that this might be pushing the boundaries of what this blog was originally supposed to do but what this and other research suggests is that we might be able to learn something from our wool-bound friends. Stay with me on this.
I will at this point add that I am in no way suggesting any person, any group of people, or any condition is in anyway related to sheep or any other animal. Some people may have heard that 'All cats have Asperger Syndrome' but not from me.
Back to sheep. The Villalba study looked at 3 diets: (i) a monotonous yet suitably nutritious diet, (ii) a diverse diet changing at set periods with various combinations of foods, (iii) a diverse diet similar to group (ii) also including supplementary phytochemicals. The results. When shown a more diverse diet, the monotonous diet sheep group got more stressed than the other groups as demonstrated by increased plasma cortisol levels and changes to rectal temperature when exposed to the open field test. Stress can be a learned response.
Whilst making generalisations from sheep behaviour to human behaviour is fraught with difficulties, I do feel as though there could be something in such research as this. The implication is that early dietary restrictiveness as a 'norm' might invoke a heightened stress response when a greater number of foods is presented to a person. So when a toddler who eats only pizza and chips (link to BBC3 programme 'Fast food baby') is presented with vegetables or fruit not normally included in the diet, the refusal side of things might not just bring about a tantrum but also some learned physiological stress? The flipside to such observations is that reducing the physiological stress response might make for a more varied diet, as per the recent presentation at the BPS conference on carrot not stick to get children to eat new foods.
Studying mammals like sheep perhaps removes some of the various social and cultural 'baggage' which would accompany similar human research. That and the fact that most human volunteers probably would not like their rectal temperature taken for any kind of experimental study; at least not without some significant reward. I will perhaps return to our mammalian friends at later points in this blog and how, as models of humans, they may offer some special insights into our very human behaviours e.g. autistic mice**?
* Villalba JJ.et al. Relationships between early experience to dietary diversity, acceptance of novel flavors, and open field behavior in sheep. Physiology & Behaviour. August 2011.
** Penagarikano O. et al. Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits. Cell. September 2011.
Why oh why is he talking about Babe and sheep I thought I heard you ask? The reason is a new piece of research which suggests that even lambs can be picky eaters, and when fed monotonous diets, lambs become more stressed than lambs fed a diverse diet which is also reflected in their physiology and open-field behaviour.
The paper is this one by Villalba and colleagues* published in the journal Physiology & Behaviour. I appreciate that this might be pushing the boundaries of what this blog was originally supposed to do but what this and other research suggests is that we might be able to learn something from our wool-bound friends. Stay with me on this.
I will at this point add that I am in no way suggesting any person, any group of people, or any condition is in anyway related to sheep or any other animal. Some people may have heard that 'All cats have Asperger Syndrome' but not from me.
Back to sheep. The Villalba study looked at 3 diets: (i) a monotonous yet suitably nutritious diet, (ii) a diverse diet changing at set periods with various combinations of foods, (iii) a diverse diet similar to group (ii) also including supplementary phytochemicals. The results. When shown a more diverse diet, the monotonous diet sheep group got more stressed than the other groups as demonstrated by increased plasma cortisol levels and changes to rectal temperature when exposed to the open field test. Stress can be a learned response.
Whilst making generalisations from sheep behaviour to human behaviour is fraught with difficulties, I do feel as though there could be something in such research as this. The implication is that early dietary restrictiveness as a 'norm' might invoke a heightened stress response when a greater number of foods is presented to a person. So when a toddler who eats only pizza and chips (link to BBC3 programme 'Fast food baby') is presented with vegetables or fruit not normally included in the diet, the refusal side of things might not just bring about a tantrum but also some learned physiological stress? The flipside to such observations is that reducing the physiological stress response might make for a more varied diet, as per the recent presentation at the BPS conference on carrot not stick to get children to eat new foods.
Studying mammals like sheep perhaps removes some of the various social and cultural 'baggage' which would accompany similar human research. That and the fact that most human volunteers probably would not like their rectal temperature taken for any kind of experimental study; at least not without some significant reward. I will perhaps return to our mammalian friends at later points in this blog and how, as models of humans, they may offer some special insights into our very human behaviours e.g. autistic mice**?
* Villalba JJ.et al. Relationships between early experience to dietary diversity, acceptance of novel flavors, and open field behavior in sheep. Physiology & Behaviour. August 2011.
** Penagarikano O. et al. Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits. Cell. September 2011.
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