Tuesday, 13 October 2015

The neuropathology linking T. gondii infection and schizophrenia?

A quote to begin: "findings suggest that T gondii [Toxoplasma gondii] infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients."

So said the very interesting paper by Jakub Tomasik and colleagues [1] who set about comparing results from a mouse model of "chronic T gondii infection" looking for serum and brain signatures with those in postmortem "brain samples from 35 schizophrenia patients and 33 healthy controls." Researchers found that mice infected with T. gondii were pretty 'immune-stimulated' as a result; also manifesting with "neural damage and reactive tissue repair". Some of these immune consequences also seemingly 'overlapped' with what was observed in the very precious brain samples from those previously diagnosed with schizophrenia, particularly when it came to "C-reactive protein (CRP), interleukin-1 beta (IL-1β), interferon gamma (IFNγ), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1)." The authors conclude that any shared pathophysiology might be "a key step towards understanding their specific contributions to pathogenesis."

I'd like to think that the Tomasik paper is an important next step in the whole idea that T. gondii infection might show some important links with at least some schizophrenia (see here). Still a point of discussion in some quarters [2] insofar as the hows and whys of any association (see here), there is nevertheless, some quite reliable research appearing in the peer-reviewed domain to suggest that there may a link, correlation if you will, between this parasitic protozoan and the appearance of some schizophrenia or schizophrenia-linked symptoms. Putting some scientific flesh on the bones of 'mechanisms' through which infection might link to schizophrenia is important.

That being said, I do think we have to be slightly cautious when it comes to changes in immune function in relation to schizophrenia being solely pinned down to T. gondii infection. Given for example, the growing significance of something like CRP to schizophrenia in general (see here), I think you would be hard-pressed to say this is all down to T. gondii infection. Indeed, the maternal immune activation hypothesis may well play a role here (see here) as might the wider implications of something like inflammation when it comes to the wider arena of psychiatry (see here).


[1] Tomasik J. et al. Shared Immune and Repair Markers During Experimental Toxoplasma Chronic Brain Infection and Schizophrenia. Schizophr Bull. 2015 Sep 20. pii: sbv134.

[2] Wolf PJ. & Hamilton FE. Flawed analyses undermine proposed relationship between childhood cat ownership and schizophrenia. Schizophr Res. 2015 Aug 14. pii: S0920-9964(15)00427-2.


ResearchBlogging.org Tomasik J, Schultz TL, Kluge W, Yolken RH, Bahn S, & Carruthers VB (2015). Shared Immune and Repair Markers During Experimental Toxoplasma Chronic Brain Infection and Schizophrenia. Schizophrenia bulletin PMID: 26392628

Monday, 12 October 2015

Introducing 'cutaneous gluten sensitivity'

I'm always amazed that despite our many advances in science and medicine, new diagnoses and clinical entities still manage to pop up from time to time. Today I'm introducing one such occasion as detailed in the paper by Veronica Bonciolini and colleagues [1] (open-access available here) and the idea that 'cutaneous gluten sensitivity' (CGS) might be part and parcel of at least some presentation of non-coeliac gluten sensitivity (NCGS).

For those who might not know, NCGS describes part of a proposed spectrum of gluten-related conditions that lies outside of the classical 'gluten can affect health' autoimmune condition that is coeliac disease (CD). There is still some debate about the boundaries of NCGS and the precise diagnostic criteria (see here) but I'm of the opinion that there is something to see in this area and that, on occasion, there also may be psychological/behavioural issues associated with the label (see here) albeit with more research required.

Insofar as the relationship between cutaneous (skin) issues potentially associated with NCGS, well we have a precedent here with the link between dermatitis herpetiformis (DH) and CD, a skin condition manifesting as red raised patches of blisters often accompanied by severe itching. Treatment of DH normally involves a gluten-free diet (GFD) similar to the management of CD, although other preparations can also help soothe the itching and blistering.

The Bonciolini paper details the authors' efforts to document various cutaneous manifestations seemingly linked to NCGS and "to characterize the new pathologic entities known as CGS." To do this: "17 consecutive patients affected by NCGS after having considered gastroenterology and allergy in order to exclude other forms of gluten sensitivity such as CD and WA [wheat allergy]" were examined. The authors did a pretty good job of excluding conditions such as CD in their participant group as per their use of "serological assay with specific antibodies (anti-tissue transglutaminase antibodies (tTG) IgA and IgG, anti-endomysial antibodies (EMA), anti-gliadin antibodies (AGA), deamidated gliadin peptide (DGP) and total IgA) and esophagogastroduodenoscopy with multiple biopsies." Further researchers: "enrolled NCGS patients only after dietary elimination of gluten followed by DBPC [double-blind, placebo-controlled]" challenge. Skin samples were taken and various inspections of skin lesions carried out.

Results: "The common clinical feature of all the patients involved in this study, as well as the one detached from our clinical experience, was the severe itching." Researchers reported that the itching was difficult to treat with standard medications but "it showed prompt resolution when GFD was introduced" and "the reaction was faster than in DH patients." In terms of the skin lesions themselves, the authors describe them as "polymorphic" (I assume meaning that they took on various different shapes and sizes) and perhaps due to some pretty continual itching also took on a "psoriatic-like" appearance (as in similar to the plaques seen in psoriasis).

"The histological and immunopathological assays performed on skin samples exclude specific skin diseases of CD and the allergy skin tests exclude sensitization to gluten. Therefore, it is reasonable to assume that there may also appear skin manifestations among the extraintestinal manifestations of NCGS or that “cutaneous gluten sensitivity” (CGS) exists and needs to be characterized."

We await further investigations...


[1] Bonciolini V. et al. Cutaneous Manifestations of Non-Celiac Gluten Sensitivity: Clinical Histological and Immunopathological Features. Nutrients. 2015 Sep 15;7(9):7798-7805.


ResearchBlogging.org Bonciolini V, Bianchi B, Del Bianco E, Verdelli A, & Caproni M (2015). Cutaneous Manifestations of Non-Celiac Gluten Sensitivity: Clinical Histological and Immunopathological Features. Nutrients, 7 (9), 7798-7805 PMID: 26389946

Saturday, 10 October 2015

Views on autism from an "unaffected sibling"

It was a bit of a breath of fresh air to read the paper by Lauren Singer [1] (open-access) published in the journal Molecular Autism recently. Detailing the personal experiences of a sibling with a sister with autism who has "gone to walks, raised money via lemonade stands, volunteered in respite programs for families with kids with autism, and participated in autism research studies at the Yale Child Study Center", her very personal account is an important read in amongst the huge peer-reviewed science literature on the topic.

Focused specifically on the growing research interest on how autism manifests across the genders [2], the author discusses various themes that have emerged in this area including the idea of a female protective effect in light of the gender/sex disparity noted in rates of autism (see here). Although an interesting hypothesis [3] the suggestion that girls may be somehow "require greater etiologic load to manifest the same degree of impairment as males" is not however without its criticisms (see here).

Perhaps of greater importance are some valuable points raised by the author on a more personal level. So: "I have experienced firsthand the anguish autism inflicts on the entire family." I appreciate that that last sentence probably does not reflect every families experience of autism and might run counter to some viewpoints included in the debate about disability vs. difference and a focus on 'deficits over strengths', but it is an important sentence to highlight. Not least because Ms. Singer's experiences of growing up with a sister who by all accounts, is 'disabled' by autism and who was subsequently "moved into residential placement" on account of her behaviour posing a risk to her safety is a viewpoint that can sometimes get rather lost in the very heterogeneous chatter about autism. Similar things have also been mentioned in the popular press recently. Further: "Living with Jodie, and now having to live without her, has made me desperate for answers" similarly reflects the realities of living apart from a cherished loved one and the anguish that can bring.

"I also believe that scientists can enhance their careers by leaving the lab once in a while to interact with real people with autism." Without painting every autism researcher with the same brush, the idea that people with autism are people first (yes, I know this runs counter to some of the discussions on the ownership of the autism label) and that autism is very much more than just the sum of a triad/dyad of symptoms, is an important point made here. "Seeing people with autism challenged by daily living skills can make research designed to help them feel much more rewarding" likewise taps into growing calls for a focus on here-and-now research alongside the hows-and-whys research agenda that has prevailed over the years. As a side-note, intervention can mean lots of things, even comparatively simple things [4].

I close with another quote: "My experiences with Jodie and my hopes for her future have inspired me to want to be part of the cutting edge of discovery that will make a difference in the lives of thousands of people." Alongside the idea that families are the 'experts' on their various members, I'd like to think that Ms. Singer's article will be an important call for siblings, other family members and people with autism themselves to become much more engaged in the autism research landscape, and particularly, it's future shaping...


[1] Singer L. Thoughts about sex and gender differences from the next generation of autism scientists. Mol Autism. 2015; 6:52.

[2] Jamison TR. & Schuttler JO. Examining social competence, self-perception, quality of life, and internalizing and externalizing symptoms in adolescent females with and without autism spectrum disorder: a quantitative design including between-groups and correlational analyses. Mol Autism. 2015 Sep 17;6:53.

[3] Robinson EB. et al. Examining and interpreting the female protective effect against autistic behavior. PNAS. 2013; 110: 5258-5262.

[4] Schmidt L. et al. Psychosocial Functioning and Life Satisfaction in Adults With Autism Spectrum Disorder Without Intellectual Impairment. J Clin Psychol. 2015 Sep 25.

ResearchBlogging.org Singer L (2015). Thoughts about sex and gender differences from the next generation of autism scientists. Molecular autism, 6 PMID: 26388981

Friday, 9 October 2015

ADHD and asthma (yet again)

"Children with ADHD [attention-deficit hyperactivity disorder] have a higher prevalence of asthma than the general Quebec pediatric population."

So said the findings of the study by Grizenko and colleagues [1] adding to quite a volume of research potentially connecting the two conditions. During this latest foray into this area of research, researchers also observed that: "Children with ADHD born prematurely and/or those whose mothers experienced stress during pregnancy have a significantly increased risk of developing asthma" so putting a little more scientific flesh on to the bones of any connection between ADHD and asthma.

This is a topic that interests me on this blog. Having talked about the possibility of a link between asthma and ADHD several times (see here and see here and see here) it is not new news that there may be quite a bit more to see in this area. That ADHD might be one of the more common diagnoses 'over-represented' when it comes to autism (see here) also provides an interesting 'correlation' to other subject matter too (see here) albeit with caveats (see here).

I don't really want to repeat myself over the possible hows and whys of any connection between ADHD and asthma (e.g. genetics, immune function, gut bacteria, medication and/or pollutants); suffice to say there are several hypotheses and any link is likely to be complicated and not necessarily generalisable to all cases. I will however reiterate the idea that preferential screening of either condition when the other is diagnosed might be a very good idea.


[1] Grizenko N. et al. Increased Risk of Asthma in Children with ADHD: Role of Prematurity and Maternal Stress during Pregnancy. J Can Acad Child Adolesc Psychiatry. 2015 Fall;24(2):109-115.

ResearchBlogging.org Grizenko N, Osmanlliu E, Fortier MÈ, & Joober R (2015). Increased Risk of Asthma in Children with ADHD: Role of Prematurity and Maternal Stress during Pregnancy. Journal of the Canadian Academy of Child and Adolescent Psychiatry = Journal de l'Academie canadienne de psychiatrie de l'enfant et de l'adolescent, 24 (2), 109-115 PMID: 26379722

Thursday, 8 October 2015

KPAX002 for Chronic Fatigue Syndrome?

My attention was grabbed recently by the paper published by Jon Kaiser [1] (open-access available here) detailing the results of a 'proof-of-concept investigation' examining the use of something called KPAX002 on a small number of participants diagnosed with Chronic Fatigue Syndrome (CFS).

Looking at how KPAX002 - "a combination of low-dose methylphenidate hydrochloride and mitochondrial support nutrients currently under development by K-PAX Pharmaceuticals" - impacted on fatigue symptoms and "concentration disturbance" symptoms, Kaiser reports that there may be more to see from this preparation.

Indeed, after 12 weeks of use: "Treatment with KPAX002 was well tolerated and significantly improved fatigue and concentration disturbance symptoms in greater than 50% of patients with CFS." Further information about the current (and future) trial results can be found here including details on the Synergy trial (see here and see here) representing the next step in the research process. I  might also draw your attention to an interview with Dr Kasier here (thanks to Russell for the link).

Before progressing further, I should perhaps comment on a few methodological issues to bear in mind. This was very much an observational 'pilot' study over and above a thorough clinical trial. Participants knew that they were taking KPAX002 and when it came to scoring behaviours over the trial period, this was done using subjective instruments without any objective representation. That no control group was employed (either asymptomatic nor CFS taking a placebo) should be noted. Also slightly unusually, in the section titled 'Disclosure of conflict of interest' on the paper, the words 'none' appears although in the discussion section, Dr Kasier elaborates that: "as a current employee of K-PAX Pharmaceuticals, the author may be viewed as biased toward the success of this treatment."

Such issues aside, I'm interested in this formulation and findings reported. I was not aware that methylphenidate, more typically indicated as a management option for attention-deficit hyperactivity disorder (ADHD), was something 'suggested' for CFS. Kaiser does make reference to the findings reported by Blockmans and colleagues [2] who reported that under placebo-controlled conditions: "Methylphenidate at a dose of 2 x 10 mg/day is significantly better than placebo in relieving fatigue and concentration disturbances in a minority of chronic fatigue syndrome patients." Various other studies looking at the issue of 'fatigue' attached to various other diagnoses have utilised methylphenidate with varying degrees of clinical success.

The 'mitochondrial support nutrients' included in the KPAX002 preparation are a little more familiar to me. Covering 30+ additional vitamins, minerals and other nutrients including acetyl L-carnitine and N-acetylcysteine, I was interested in the possibilities here. Mitochondria and CFS is a topic that has cropped up on this blog before (see here) in light of the findings from Sarah Myhill and colleagues [2]. As a point of note, Dr Myhill's book 'Mitochondria, Not Hypochondria' received something of an accolade at the recent British Medical Association (BMA) book awards suggesting that views might be changing in this area of the CFS landscape. Although quite a bit more research is required on the topic, mitochondrial issues in relation to CFS is something of a research growth area [3].

Reiterating that the current Kasier results should be viewed with methodological caution, it will be interesting to see what becomes of KPAX002 in relation to [some] CFS. As a point of note, Kaiser also has another entry on the US ClinicalTrials.gov database for KPAX002 in relation to an equally mystifying condition: Gulf War Syndrome (GWS) on the basis of a "high degree of symptom overlap" between CFS and GWS. No doubt KPAX002 will be gracing this blog again in future...

Music: Semisonic - Secret Smile.


[1] Kaiser JD. A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. Int J Clin Exp Med. 2015 Jul 15;8(7):11064-11074.

[2] Blockmans D. et al. Does methylphenidate reduce the symptoms of chronic fatigue syndrome? Am J Med. 2006 Feb;119(2):167.e23-30.

[3] Morris G. & Maes M. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways. Metab Brain Dis. 2014 Mar;29(1):19-36.


ResearchBlogging.org Kaiser JD (2015). A prospective, proof-of-concept investigation of KPAX002 in chronic fatigue syndrome. International journal of clinical and experimental medicine, 8 (7), 11064-74 PMID: 26379906

Wednesday, 7 October 2015

On glyphosate and autism (without scaremongering)

Glyphosate use and autism rates - should I blog about it?

Well, after some deliberation I decided it was a topic worthy of an entry. There is some peer-reviewed science discussions behind it and, as per other areas of controversy on the autism research landscape, the idea that 'science is about debate' (why else does everyone keep going on about open-access and transparency) should always prevail.

I'm assuming most people have heard of the organophosphonate (that's phosphonate not phosphate) herbicide glyphosate - N-phosphonomethylglycine - over the course of its discovery and use under the trade name Roundup. First patented as a chelating agent (another area of 'discussion' with autism in mind) glyphosate has been successfully killing weeds for quite a few years by interfering with some of the chemistry of the aromatic amino acids tryptophan, tyrosine and phenylalanine via its actions on the shikimate pathway. As per many other herbicides, such formulations always require a degree of care in their use given the possibility of side-effects following accidental over-exposure. Indeed, government agencies are cottoning on to this fact (see here).

The debate on glyphosate and its potential effects on human and animal health has been a hot one in recent times. Partly overlapping with the introduction of genetically modified (GM) crops that are glyphosate-tolerant (Roundup Ready) by the company who initially brought glyphosate to the market, the safety angle of glyphosate has been scrutinised and debated. Only this year (2015), an arm of the World Health Organisation (WHO) described glyphosate (and several organophosphate pesticides I might add) as "probably carcinogenic to humans". Following such an announcement, quite a few media column inches were produced as one might expect.

Set within that context, discussions have turned to whether there may be other 'effects' following the fairly widespread use of glyphosate. Perhaps inevitably, autism, and particularly the quite phenomenal increase in cases of autism, has been suggested to be 'linked' to the use of glyphosate. One might say that in this respect, glyphosate is a victim of its own success insofar as how widely it has been and is currently used.

The paper that seems to have started the ball rolling suggesting a link between glyphosate and autism is that from Anthony Samsel and Stephanie Seneff [1]. A review paper focussing specifically on the proposed inhibitory actions of glyphosate on CYP enzymes, mention of autism in the text and particularly that "glyphosate may be the most significant environmental toxin contributing to autism" was bound to stir up debate. With added soundbites about how half of children will be born with autism in the United States by 2025 and graphs correlating autism prevalence and glyphosate use, such observations were ripe for speculation and discussion.

Further papers from Samsel & Seneff [2] have continued the theme that autism may be one of many conditions/labels where glyphosate might be implicated. Drawing on animal and plant studies implicating glyphosate use with specific depletion of manganese (Mn), a whirlwind of research studies and references have been used to link such depletions to autism (and associated aspects such as anxiety) among various other conditions. To quote: "Many diseases and conditions are currently on the rise in step with glyphosate usage in agriculture, particularly on GM crops of corn and soy. These include autism, AD [Alzheimer's disease], PD [Parkinson's disease], anxiety disorder, osteoporosis, inflammatory bowel disease, renal lithiasis, osteomalacia, cholestasis, thyroid dysfunction, and infertility. All of these conditions can be substantially explained by the dysregulation of Mn utilization in the body due to glyphosate." Just in case you thought that Samsel / Seneff are the sole research team talking about glyphosate use and autism rates, I'll also refer you to the paper by Cynthia Nevison [3] that has been previously discussed on this blog (see here).

As other commentators have noted, there are a few considerations to mention about the discussions so far on any relationship between glyphosate use and autism. That 'correlation is not the same as causation' is perhaps the most important element to the data as they currently stand given that, to my knowledge, no-one has actually published any peer-reviewed results on levels of glyphosate and/or metabolites in people with autism and/or other family members compared to asymptomatic controls for example. It's not as if such a feat is too complicated given the various means and methods already published on this topic [4].

'Correlation is not the same as causation' is one of the themes also discussed in the review paper by Miguel Faria [5] who provides an important discussion to some of the points raised by Samsel & Seneff. I don't want to head too much into this quite long commentary on the Samsel / Seneff paper (complete with author replies) but it does strike me as providing something of a counter-balance to the very hypothesis-based writings of the original authors. That glyphosate is one of a multitude of herbicides and insecticides in use is an important point made in terms of the difficulties in disentangling it from the 'chemical soup' (not to demonise) that we live our lives in these days. The only other thing that I might mention is my much-used notion about the continued pluralisation of autism (see here) and its varied comorbidity as being something to bear in mind when it comes to any discussions about aetiology.

Where next, or is there even 'a next' for looking at any possible relationship between glyphosate use and autism rates? Well, I'd like to think that autism research can learn a lesson or two about not throwing out baby and bathwater when it comes to theories about [some] autism as per what seems to have happened to something like methylmalonic acid (MMA) and autism (see here) for example. It's not beyond the realms of possibility that certain chemicals or mixtures might be linked to autism risk and/or onset as per preliminary research talk about dioxin exposure being potentially linked to [some] autism or autistic traits (see here) albeit with a lot more follow-up research required.

But such research needs to be done with care and assiduity; mindful that this is a topic that will inevitably garner significant attention (as per the editorial sentence on the original Samsel / Seneff paper: "Note added by the Publisher: This paper attracts great attention.") and knowing what can happen sometimes when science and media mix (see here).

Perhaps a little less focus on soundbites and more on cold, objective science is the best way forward in this area?

Music: Fleetwood Mac- Dreams.


[1] Samsel A. & Seneff S. Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. Entropy 2013. 15; 1416-1463.

[2] Samsel A. & Seneff S. Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies. Surgical Neurology International. 2015;6:45.

[3] Nevison CD. A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors. Environ Health. 2014 Sep 5;13:73.

[4] Yoshioka N. et al. Rapid determination of glyphosate, glufosinate, bialaphos, and their major metabolites in serum by liquid chromatography-tandem mass spectrometry using hydrophilic interaction chromatography. J Chromatogr A. 2011 Jun 10;1218(23):3675-80.

[5] Faria MA. Glyphosate, neurological diseases – and the scientific method. Surgical Neurology International. 2015;6:132. doi:10.4103/2152-7806.162550.


ResearchBlogging.org Faria MA (2015). Glyphosate, neurological diseases - and the scientific method. Surgical neurology international, 6 PMID: 26322242

Tuesday, 6 October 2015

Prenatal hormone involvement in autism risk?

The findings reported by Gayle Windham and colleagues [1] caught my eye recently and their observations based on the examination of mid-pregnancy serum hormone and protein markers for some 2500 mothers of children diagnosed with an autism spectrum disorder (ASD) compared with 600,000 controls.

Detailing results based on: "Second trimester levels of unconjugated estriol (uE3), human chorionic gonadotropin (hCG), and maternal serum alpha-fetoprotein (MSAFP)", researchers reported that their results: "further support prenatal hormone involvement in ASD risk."

I perhaps need to do a little 'defining' before progressing any further with this post. Unconjugated estriol (uE3) refers to an estrogen. It becomes the dominant oestrogen during pregnancy; produced by the baby's liver and placenta. Measured levels of uE3 during the 2nd trimester of pregnancy have been linked to various 'outcomes' including the possibility of Down's syndrome and neural tube defects.

Human chorionic gonadotropin (hCG) is another hormone; one that is normally used to confirm pregnancy. During pregnancy, levels of hCG can also be used to determine Down's syndrome. Serum alpha-fetoprotein (MSAFP) is the most abundant plasma protein found in the developing foetus. During pregnancy, extremes in levels of MSAFP can indicate issues in pregnancy. Combined together, these various hormones/proteins make up the so-called triple test, that when added to information such as maternal age and stage of pregnancy, can classify a pregnancy as being high or low risk for chromosomal abnormalities. That being said, the test is by no means perfect.

Windham et al report some rather complicated results based on adjusted odds ratios (AOR) when it came to autism vs control samples. So: "Lower uE3 (AOR for < 10th percentile vs. 25th-74th percentiles = 1.21, 95 % CI 1.06-1.37), and higher MSAFP (AOR = 1.21, 95 % CI 1.07-1.37 for > 90th percentile) were significantly associated with ASD. A U-shaped relationship was seen for hCG (AOR = 1.16, 95 % CI 1.02-1.32 for < 10th percentile; AOR = 1.19, 95 % CI 1.05-1.36 for > 90th percentile)." Lower uE3 is a trend found in relation to Down's syndrome. Higher MSAFP however runs slightly counter to what has been discussed in relation to Down's syndrome. By contrast, elevations in MSAFP tend to be more readily linked to pregnancies where neural tube defects may be present. What this all means is that yes, these results could indicate the involvement of prenatal hormones and chromosomal issues in relation to 'some' autism, but science still needs to go a little way before anyone talks about a triple test being applied to autism (and the ethical issues that this might bring).

I think it's also worthwhile briefly bringing in a few caveats to such pregnancy testing that could be pertinent to other autism research findings. As per other information, a mother's weight during pregnancy can affect what results you get - "Serum marker levels tend to be decreased in heavier women, and increased in lighter women." If you map this on to the research talking about maternal obesity linked to some autism (being careful not to generalise here), you can see how adjustments might have been / have to be made. Ethnicity is another factor that needs to be kept in mind. Also: "AFP and uE3 levels tend to be low (about 8% and 6% respectively) in women with insulin dependent diabetes mellitus." This is particularly interesting in view of the quite consistent literature detailing how gestational diabetes seems to show a connection to risk of offspring autism (see here). Various other factors (vaginal bleeding) can similarly affect results.

The Windham results are nevertheless interesting and are strengthened somewhat by the large participant numbers included for study. That other groups have similarly talked about elevations in MSAFP in relation to autism [2] increases the confidence that there may something further to see in this area, at least for some autism.

Music: Al Green - Tired of Being Alone.


[1] Windham GC. et al. Autism Spectrum Disorder Risk in Relation to Maternal Mid-Pregnancy Serum Hormone and Protein Markers from Prenatal Screening in California. J Autism Dev Disord. 2015 Sep 14.

[2] Abdallah MW. et al. Autism spectrum disorders and maternal serum α-fetoprotein levels during pregnancy. Can J Psychiatry. 2011 Dec;56(12):727-34.


ResearchBlogging.org Windham GC, Lyall K, Anderson M, & Kharrazi M (2015). Autism Spectrum Disorder Risk in Relation to Maternal Mid-Pregnancy Serum Hormone and Protein Markers from Prenatal Screening in California. Journal of autism and developmental disorders PMID: 26370672