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Autism and Prenatal Vitamins

Science has found no evidence that vaccines cause autism; but the true cause(s) of autism have not yet been determined. So far the available evidence has pointed towards a largely genetic cause with possible interaction with environmental factors. A new study supports that interpretation. It also supports previous evidence that autism is triggered prior to birth, rather than at the time of vaccinations.

Schmidt et al. published a study in Epidemiology on May 23, 2011, entitled “Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism.” It was a population-based case control study of 566 subjects comparing a group of autistic children to a matched control group of children with normal development. They looked at maternal intake of prenatal vitamins in the 3 months before conception and the first month of pregnancy, and they looked for genotypes associated with autism. They found that mothers who didn’t take prenatal vitamins were at greater risk of having an autistic child, and certain genetic markers markedly increased the risk. There was a dose/response relationship: the more prenatal vitamins a woman took, the less likely she would have an autistic child. There was no association with other types of multivitamins, and no association with prenatal vitamin intake during months 2-9 of pregnancy.

They had a large sample size, and they tried to eliminate confounders. They looked for these potential confounders of the association between prenatal vitamin intake and autism: child’s sex, birth year, parent-reported race/ethnicity, family history of mental health conditions, paternal age at child’s birth, maternal age at child’s birth, education, prepregnancy body mass index (BMI) category, cereal intake from 3 months before through the first month of pregnancy, cigarette smoking, alcohol consumption, and residence with a smoker during the period 3 months before pregnancy to delivery. Only maternal education and the child’s year of birth proved to be confounders. They adjusted for these two factors in their analyses. A weakness of their study is that it depends on patient recall long after the fact. Also, it did not attempt to gather any diet information.

Mothers of children with autism were less likely to report taking prenatal vitamins (odds ratio 0.62). Having certain genotypes increased the odds that a vitamin-omitting woman would have an autistic child. Children with the COMT 472 AA gene were at increased risk of autism. If their mothers took prenatal vitamins, the odds ratio for the risk of autism was 1.8; if their mothers didn’t, the odds ratio jumped to 7.2.  This suggests that the maternal-fetal environment can magnify the effects of a child susceptibility gene. There was an association with certain maternal genes as well: those odds ratios went as high as 4.5.

The association was robust. The authors think there are plausible biological explanations. Folate and other B vitamins are critical to neurodevelopment. Iron could be involved.  The gene variants were within one-carbon metabolism pathways; methylation mechanisms may be responsible.

The authors speculate as to why multivitamins did not have the same effect. Prenatal vitamins typically contain more iron, vitamins B6 and B12, and twice as much folic acid (800 mcg) as multivitamins (400 mcg).

In their summary, the authors say:

Our data suggest that supplementation with prenatal vitamins before pregnancy and during the first month of pregnancy might protect against autism, particularly in genetically susceptible individuals. Additionally, COMT genotype may contribute to an elevated risk for autism, especially in offspring of unsupplemented mothers. This evidence for gene-by- environment interaction effects in autism etiology could help explain variations in previous findings across genetic studies. Whether similar interactions exist for susceptibility genes in other pathways, particularly those epigenetically regulated through methylation, remains to be explored. More research is warranted to replicate the findings, explicate potential mechanisms, and explore interactions with other autism candidate genes.

This is fascinating stuff. It confirms that certain genotypes are associated with autism and that environmental factors can interact with genetics to increase risk. We still need to pin down what it is about prenatal vitamins that prevents autism better than other multivitamins. Is it the folic acid? Is it a subset of the ingredients, or the whole mixture?

We should never blindly accept the results of a first study. These findings will have to be confirmed by other studies. Meanwhile, should we take action? We already recommend folic acid supplements for women who might become pregnant, and we recommend prenatal vitamins during pregnancy. I can’t see any downside to recommending prenatal vitamins in the pre-conception period for any woman who is likely to become pregnant. Some advisors (for instance the Mayo Clinic) were already recommending this practice even before the new study came out.

How will the anti-vaccine contingent react to this new study? It was convenient and satisfying for parents to be able to blame vaccines and accuse the evil medical establishment of causing their children’s autism. Now will those parents accept that at least part of the responsibility lies with their own genetic contributions and the mother’s actions prior to pregnancy? That’s not as palatable a thought, but it’s more realistic.

 

Posted in: Neuroscience/Mental Health, Nutrition

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71 thoughts on “Autism and Prenatal Vitamins

  1. hat_eater says:

    Many parents who believe that vaccines gave their children autism are extremely unlikely to change their opinion based on this work, even if following studies confirm the findings. I’m thinking of those parents who are opposed to any generally accepted authority telling them what to do to their children; they make up a rather large part of the alt med community. Accepting the notion that they could have tipped the balance in favor of their children by doing what’s recommended by the doctors, ie taking prenatal vitamins, would constitute an about face for them.

  2. Jan Willem Nienhuys says:

    Epidemiology on May 23, 2001

    That should be 2011 not 2001.

    I am always somewhat wary when researchers report that one ‘effect’ in very many possibilities seems to be statistically significant.

  3. hat_eater says:

    ‘Somewhat wary’ is a very good default attitude I think. :)
    I came back because by a lucky coincidence I just stumbled upon a wonderful article about how contradicting evidence strenghtens deeply rooted beliefs.

  4. CC says:

    That’s why they search for confounders. There are some things they couldn’t correct for in this study (diet is mentioned) so this isn’t definitive, but it looks like they have grounds to do more in depth studies. Maybe one of those multi-year studies where they track people and see what the outcomes are. If there’s a maternal genetic component then they might even be able to pre-screen and get a sample group that they think is more likely to have children develop autism than the rate in the general population.

  5. hateater “Accepting the notion that they could have tipped the balance in favor of their children by doing what’s recommended by the doctors, ie taking prenatal vitamins, would constitute an about face for them.”

    Actually, if I’m not misreading HH’s article, the doctor’s recommendations would have to change slightly. I believe the current recommendation is that women who are trying to get pregnant start taking prenatal vitamin. In that case, women who got pregnant right away, would not have taken the prenatal vitamins for three months before conception. Also, I don’t believe that prenatal vitamins are recommended for all women of childbearing age, so that doesn’t cover women with unintended pregnancies.

    In other words, you could still be following current doctor recommendations* and not have been taking prenatal vitamins three months before conception.

    * I’m going by recollection of recommendations in 2001.

  6. roblindeman says:

    I don’t have the original article in front of me. What was the case-definition of autism? Are we talking anywhere on the spectrum, or only old-fashioned Kannerian Autism?

    I suspect that prenatal vitamin use has remained steady or increased over time in the face of an explosion of ASD diagnoses. Something doesn’t flush here. If absence of prenatal vitamin use were a major risk factor, we’d expect to see a dramatic drop in vitamin use. I doubt there was one.

  7. Manduca says:

    Roblindeman:

    The “explosion” of ASD diagnoses is most likely a result of better screening and diagnostic substitution. No need to look for decreases in vitamin intake.

  8. daedalus2u says:

    This is very interesting. (Harriet, there is a typo in the date of the study which made me think it was a 10 year old study). I haven’t seen the whole study but it is very interesting.

    A reason that folate is recommended for women trying to conceive is because it does prevent neural tube defects. Teratogens that cause neural tube defects can also cause autism, for example thalidomide and valproate. Other anti-epileptic drugs that are associated with neural tube defects are also associated with autism causation too.

    Nitric oxide is intimately involved in neural tube closure with too little and too much both causing neural tube defects.

    http://www.ncbi.nlm.nih.gov/pubmed/12412009

    Nitric oxide can cause neural tube defects and these can be rescued with folate.

    http://www.ncbi.nlm.nih.gov/pubmed/14685162

    Nitric oxide synthase is required for neural tube closure, but this requirement is not mediated through NO.

    http://www.ncbi.nlm.nih.gov/pubmed/16300634

    One of the most characteristic aspects of autism neuroanatomy is an increased number of minicolums with a larger total number of neurons. Proliferation of neurons is inhibited by NO, so low NO causes more neurons to occur. The number of minicolums is fixed at ~8 weeks post conception. The characteristic neuroanatomy of autism occurs mostly during the first trimester in utero.

  9. passionlessDrone says:

    Hello friends –

    These findings have left me with significant confusion. The fuzzy nature of diagnostic jumbling is a big problem in getting an accurate picture.

    My initial thoughts are similar to Roblindeman; we should be seeing lots less autism now than in previous decades when there weren’t any prenatal vitamins or widespread supplementation in food. Instead, we see the opposite. Consider the UK study of adults with autism that was (supposedly) strong evidence of a stable rate of autism (when expedient); those mothers of those adults weren’t getting prenatal vitamins, especially the older ones, shouldn’t they be exhibiting far greater rates of autism than children?

    I’d also be interested in anyones thoughts about how these findings might mesh, or conflict with, several recent studies on CNVs and autism.

    What a mess.

    - pD

  10. Scott says:

    When I heard about this study (on Science Friday) one of the first things I did was check whether AoA had covered it. Of course, they hadn’t.

    If any further proof were needed that they care about autism only to the extent that they can claim it’s caused by vaccines, that’s it.

  11. Sorry to post a half assed thought, but I don’t have time to be fully assed.

    Please, someone correct me if I’m entirely off base, wasn’t there something about genetic markers being more strongly associated with the type of autism that is regressive, more severely disabling and associated with seizures?

  12. Angora Rabbit says:

    Nice summary and thank you for bringing it to our attention!

    A minor typo:
    “Prenatal vitamins typically contain more iron, vitamins B6 and B12, and twice as much folic acid (800 g) as multivitamins (400 g).”
    That should read micrograms (dropped special character?)

    Passionless Drone raises some of the same questions I initially had. I definitely recommend reading the study’s discussion because it addresses this issue. Foremost AUSD probably don’t have a single cause but likely gene-environment interactions, methyl metabolism may be just one variable and perhaps just for those folks with a methyl allelism. Fortification raised serum folate in the general population, but the requirement for pregnancy is 50% higher again (600 vs 400 ug/d). So current fortification intakes may not have been sufficient to prevent AUSDs; it was targeted against spina bifida. And that’s why the perinatal vitamin finding is so interesting; it finds risk reduction with a further increase in intake. There’s agreement in the field that the fortification may not address the needs of those with genetic polymorphisms that increase folate requirement (many of which were only discovered after the policy change). So it’s especially exciting that risk is linked to several of these polymorphisms.

    Again, this is just one study and needs replication. But if it is, then I foresee an intervention trial for families who are already at risk with one AUSD child. That would be very interesting!

  13. passionlessDrone says:

    Hi MichelleInMichigan –

    Please, someone correct me if I’m entirely off base, wasn’t there something about genetic markers being more strongly associated with the type of autism that is regressive, more severely disabling and associated with seizures?

    I’ve never seen anything like that. I do know that the regressive phenotype is generally associated with poorer outcomes, but I do not believe I’ve seen anything specifically associating specific genetic markers.

    There is one small exception I can think of, Rhett syndrome is definitely genetically mediated and has documented regression. I say a ‘small’ exception because AFAIK Rhett comprises only a very tiny subset of autism cases.

    Maybe someone out there has more knowledge on this than me though.

    - pD

  14. Harriet Hall says:

    “That should be 2011 not 2001.”

    Corrected. Thanks.

  15. Harriet Hall says:

    “twice as much folic acid (800 g) as multivitamins (400 g).”
    That should read micrograms”

    Corrected. Thanks.

  16. Harriet Hall says:

    Case definition: “Families were recruited through the large, populationbased,
    case-control CHARGE (CHildhood Autism Risks
    from Genetics and Environment) study.13 Eligible children
    were between 24 and 60 months of age, living with at least
    one biologic parent who spoke English or Spanish, born in
    California, and residing in the catchment areas of a specified
    group of Regional Centers (primarily in Northern California)
    that coordinate services for persons with developmental disabilities.
    Children with autism or with intellectual disability
    or developmental delay were identified through the state’s
    Department of Developmental Services, provider and clinic
    referrals, general public outreach, and self referrals. General
    population controls were identified from state birth files and
    were frequency-matched to the projected age, sex, and catchment
    area distribution of the autism cases.
    All children were assessed for cognitive function using
    the Mullen Scales of Early Learning and for adaptive function
    using the Vineland Adaptive Behavior Scales, as described
    previously.13 Autism cases were assessed using the Autism
    Diagnostic Interview-Revised14 and the Autism Diagnostic
    Observation Schedule-Generic15 to confirm child’s diagnostic
    group. The children recruited from the general population
    or with developmental delays were screened for evidence of
    autism spectrum disorder using the Social Communication
    Questionnaire. Those who scored 15 or above were further
    evaluated for autism. Assessments were conducted in English
    or Spanish at the Medical Investigation of Neurodevelopmental
    Disorders (M.I.N.D.) Institute by trained clinical staff.
    Final autism case status was defined as meeting criteria on the
    Communication, Social, and Repetitive Behavior domains of
    the ADI–R and scoring at or above the total cut off for autistic
    disorder on the ADOS Module 1 or 2. Autism spectrum disorder
    was defined using the criteria of Risi et al.16″

  17. daedalus2u says:

    pD, folate is only one factor in an extremely complicated regulatory cascade. Increased folate may have prevented an even larger increase than what was observed.

    I don’t think there is enough specificity in the genetics of autism yet to say which genes are associated with regressive or non-regressive (other than single or few gene hits like MeCP2 in Rett Syndrome).

    I did find this very interesting paper on the effects of folate on methylation of DNA and epigenetic programming of IGF2.

    http://www.ncbi.nlm.nih.gov/pubmed/21636975

    I was at a talk yesterday, where IGF1 was talked about as a treatment for Rett Syndrome and IGF2 was shown to be an important growth factor in fetal rat CSF. The talk on fetal CSF was very interesting. Fetal rat brain tissue will grow in fetal rat CSF, but the CSF is highly variable between litermates and over time (day to day, perhaps even hour to hour). There are many proteins in it and these proteins are highly variable. I suspect this variability is part of the meta-programming of the brain anatomy and epigenetic programming in utero.

    Rett Syndrome is due to the loss of MeCP2 which is on the X chromosome. It is lethal in utero in males, females are “rescued” because they have two X chromosomes and the deletion only affects one. The presence of MeCP2 in some cells “rescues” the cells that don’t have it. The MeCP2 gene codes for a protein the binds to methylated DNA and regulates the readout of that DNA and DNA nearby.

    DNA methylation is one of the main pathways by which in utero epigenetic programming happens.

    In thalidomide caused autism, there is a very narrow window, only a day or so wide during which exposure to thalidomide causes autism. It is somewhat earlier than neural tube closure, about 21 days post conception. Thalidomide happens to be a nitric oxide synthase inhibitor.

  18. passionlessDrone says:

    Hi daedulus2u –

    pD, folate is only one factor in an extremely complicated regulatory cascade. Increased folate may have prevented an even larger increase than what was observed.

    Haha! Interesting point; it just gets muddier and muddier.

    This paper is very similar to the one you posted.

    http://www.ncbi.nlm.nih.gov/pubmed/19924280

    - pD

  19. Rick says:

    I think when you look at all the factors of better screening tools, along with over diagnosis by as much as 20% that I’ve seen and studies coming out with aging parents being more likely to have autistic children (along with downs) we are probably getting close to answers for the overall increase.

  20. daedalus2u says:

    No pD, it has always been this muddy, it is only now being appreciated (by some) how muddy it actually is.

  21. thecardiffgiant says:

    Could this support the upcoming (July 2011) study in Epidemiology (Zerbo, et al.) which says that children conceived in winter months show an increased risk? It seems reasonable that the ‘environmental’ trigger could be lack of access to nutrients (like folate) in food during those months, which could help to explain why prenatal vitamins seem beneficial.

  22. aeauooo says:

    “one of the first things I did was check whether AoA had covered it. Of course, they hadn’t.”

    I’ll bet this one doesn’t go unnoticed by Joe Mercola and his ilk who can now advertise that their vitamin supplements are clinically proven to prevent autism

    – that is, until the FDA catches up with them.

  23. Enkidu says:

    Did anyone catch the article CNN wrote referencing this study? Is was titled Scientists Warn of Chemical-Autism Link. It was basically a list of every chemical thought to possibly maybe at one time cause autism, wrapped around this study on prenatal vitamins. It was one of the worst pieces of science journalism I have ever read.

  24. Amy says:

    “we’d expect to see a dramatic drop in vitamin use”

    only about 50% of pregnancy are planned, so quite a lot of women aren’t going to be taking prenatal until she finds out at about 1 month (which is really only about 2 weeks post-conception, depending on your cycle). So it isn’t a stretch to think many women aren’t taking prenatal in the first and 2nd month.

    Well, it’s somewhat disappointing as this puts a lot of blame on mom, but that’s my ideological standpoint which I will give up for science. The conclusion that prenatal is important to early on, does lead one to think taking a prenatal preconception is important, although I thought most doctors would recommend this to women trying to conceive, since you don’t know exactly when you get pregnant, and you don’t find out until 2 wks later (which is dated as a month).

  25. lilady says:

    Dr. Hall poses the question, “How will the anti-vaccine contingent react to this study”.

    I have it from the “highest authority” (I frequently visit anti-vax websites), that they are not too pleased; even less pleased with the SBM and RI blogs that analyze recent research into genetic causes and the preconception factors/prenatal environment impact on a developing fetus.

    Now that their theories about thimerisol causing autism have been thoroughly debunked, they grasp at other straws such as excipients and adjuvants in vaccine causing autism. And, they were really pinning their hopes on “environmental” studies…everything (and anything) to make their argument that their perfectly-normal-at-birth children were somehow affected in the postnatal period.

    I suspect that some anti-vaxers are finally “getting it” as many of the proposed studies environmentally causations are focusing on the prenatal (and preconception) environment.

    Yes, many OBs are recommending prenatal vitamins to women who are “planning” to become pregnant and that recommendation has been in place for a number of years, along with folate-enrichment in flours and baked goods for the benefit of a fetus and to decrease the chances of neural tube defects.

    A terrific analysis of this latest study, Dr. Hall.

  26. Geoff says:

    I have seen a number of case studies of ASD children having their diet switched up by their parents to a high fat, sometimes ketogenic, grain/legume/dairy free diet, resulting in dramatic and rapid improvements in ASD symptoms. As such, I find it pretty likely that there is a major nutritional component to ASD, likely related to gut health and blood-brain barrier health. While there may be a problem of micronutrient deficiencies, I think it is much more likely that the real problems are related to anti-predation proteins found in grains.
    http://www.psychologytoday.com/blog/evolutionary-psychiatry/201104/diet-and-autism
    http://www.psychologytoday.com/blog/evolutionary-psychiatry/201104/diet-and-autism-newer-studies-and-intriguing-links
    http://www.psychologytoday.com/blog/evolutionary-psychiatry/201104/autism-inflammation-speculation-and-nutrition

    Keep in mind that taking prenatal vitamins could be highly correlated with a lot of other health factors for a baby; breast feeding vs formula feeding, sugar intake during pregnancy and breast feeding, other supplementation like DHA, and countless other variables. Controlling for some of these variables during such a short portion of the pregnancy just doesn’t seem sufficient to conclude anything other than one or more of the lifestyle factors that differ between parents that take prenatal vitamins and parents that don’t probably matter. Of these lifestyle factors, I think that the vitamins themselves are pretty unlikely to be the cause.

  27. elburto says:

    CardiffGiant- WRT your winter theory, I’ve seen other tentative research claiming that religious Jewish and Muslim women who cover, and live in cool Northern places like Northern Europe and North America, are more likely to have autistic children.

    The reasoning is that these women (especially ultra orthodox Jews who are covered with only their faces and hands showing from age 3) lack the right amounts of vitamin D in pregnancy. Also, given that many of the orthodox Jewish women I’ve known won’t take non-hechshered (rabbinically approved as kosher) vitamins, and often have poor diets due to poverty, they have an increased risk of having autistic or otherwise developmentally delayed children. In places like New York, in OJ communities, virtually every family has at least one child under the care of the special educational services. The level of consanguinity in such communities would surely add to the issue of certain genotypes increasing risk.

  28. sam1am says:

    Check out this 1995 study linking folic acid intake and reduced neural tube defects in newborns: http://www.ncbi.nlm.nih.gov/pubmed/7619926

    Like this current study, this one saw the greatest effect for women taking vitamins before conception. My money is on Folic Acid being the key here.

  29. Axel says:

    Great article.

    Are the prenatal vitamins in the study regular multivitamins or formulas like explained here http://en.wikipedia.org/wiki/Prenatal_vitamins

    “Prenatal vitamins are similar to other multivitamins, but do contain different amounts of specific nutrients to better suit the needs of an expecting mother. Vitamins such as folic acid, calcium[2] and iron[3] are in higher concentrations while nutrients such as Vitamin A are reduced to reflect the current understanding of the role that these compounds play in fetal development.”

  30. Calli Arcale says:

    This is interesting but I’m with pD on this one — it’s muddy, and hard to know how to apply this information. It’s certainly a “needs more study” case. It’s entirely plausible for diet to have an effect, but diet is massively complex, so it’s difficult to answer precise questions about it. As another wrinkle, autism likely does not have a single cause.

    Random anecdote: I have two children, one of whom is on the autism spectrum. I used prenatal vitamins religiously while carrying the first, but was quite a bit sloppier while carrying the second. But the first is the one who is on the spectrum. So in this very small dataset of two pregnancies, we see the opposite effect, which only means this ain’t simple. ;-)

    Sometimes, I am glad I work with computers; even a fiendishly complex codebase is nothing compared to human beings living their day-to-day lives.

  31. Harriet Hall says:

    @Calli Arcale,

    No one is suggesting that autism has a single cause. In fact, this study suggests multiple causes and inter-relating causes.
    You say you took prenatal vitamins religiously: did you take them religiously for 3 months prior to conception and during the first month of pregnancy? Prenatal vitamins after the first month of pregnancy had no effect on the rate of autism.
    Of course it “ain’t simple” and the prenatal vitamin correlation only indicates a statistical risk, so counter-examples would not be meaningful.

    I don’t think “it’s hard to know how to apply this information” – I think it raises legitimate concerns and I think it is a reasonable precaution to take prenatal vitamins starting 3 months prior to conception while we are waiting for better evidence.

  32. daedalus2u says:

    This study should (I hope) start to put a damper on the “genetics is everything” hype that many of the people studying genetics are trying to foster. The genetics is important, but development is extremely complicated. There are zillions of pathways and they are coupled to the environment at the level of noise. That is you can’t duplicate the in utero environment close enough that the differences does not matter no matter how much you try.

    That is what stochastic resonance in physiology does. It couples the non-linear behavior of physiology to the environment at the level of noise. That is why MZ twins are still different, and clones with a different in utero environment will be more different still.

    Dispersion in neurodevelopment (that is the same genotype supporting multiple neurological phenotypes) is a “feature”. It allows a relatively small gene pool (a tribe) to have a large diversity in neurological strengths. The tribe with dispersion in intellectual abilities, and the ability to draw on the strengths of each individual would do better than a tribe where everyone was the same. To get diversity from a limited gene pool, the differences can’t be due to genetics, they have to be due to differential effects of environment on development.

  33. Rick says:

    New article in the online version of Pediatrics suggests that not all children be screened for autism.

    Early Autism Detection: Are We Ready for Routine Screening?
    Mona Al-Qabandi, Jan Willem Gorter and Peter Rosenbaum
    http://pediatrics.aappublications.org/content/early/2011/06/08/peds.2010-1881

  34. I think, when we laymen hear about a diet interventions that may lower risks, we sometimes confuse that with a straight line to wholly preventing a condition.

    For instance my MIL once told me that the reason that Asian populations have a higher incident of cleft lip and palate is because they don’t have enough folic acid in their diet. To her, cleft lip and palate is completely or almost completely prevented by folic acid. But the research shows that Folic acid supplementation reduces the incident of clp by 1/3, in women in Norway. This is definitely significant and makes it worth supplementing, but it’s not the only factor. Race, family history, other environmental issues are also factors.

    It’s not water, it’s soup.

  35. Tell it like it is says:

    A traditional view is that science tests hypotheses by carrying out experiments that prove hypotheses true, but as Karl Popper points out, while an unsuccessful prediction can prove a hypothesis wrong, a successful prediction does not prove it right – right? So should we turn to the mediaeval monk William of Ockham and use his ‘Ockhams Razor’ (unless you are in Africa, when you hear the sound of equine hoof-beats think horses not zebras), to whom Newton, Lord Kelvin, and Einstein subscribed to and supported, to do our validations? Or should we turn to the work of Fisher and Taguchi to bring robustness into the tests – particularly on small sample environments containing lots of interactive factors.

    Certainly such glib statements as ‘gene-by- environment interaction’ I find amusing because genes are genes – the acorn contains the blueprint for the mighty oak it will eventually become; and, whilst I willingly accept that drugs such as thalidomide do cause genetic modification to take place (giving thalidomide to pregnant women alters the gene coding that instructs the foetus to grow limbs, which irreversibly stunts the child’s limb development), I cannot fathom out how the introduction or non-introduction of vitamins at any stage modifies the gene code into creating something else entirely that we claim wasn’t there in the first place.

    To me this begs the question – in looking for detection and ultimately prevention of autism through appropriate action using the right tools, in the right way, at the right time: are we wasting valuable analysis time barking up the wrong tree? And further: are we using the right tools to carry out the analysis – or sticking with flawed statistical ‘six sigma’ modelling that informs that there is a problem – but does not have the capability to provide any indication as to the root cause of that determination.

  36. lilady says:

    As Dr. Hall states, further studies are warranted. If folic acid supplementation in flour and baked goods has decreased the risk of neural tube defects and taking prenatal vitamins 3 months earlier than a planned pregnancy “may” decrease the risk of having a child with autism or any other developmentaI disability…I see no harm in that.

    I wouldn’t however assume the folic acid decreases the risk of having a child on the Autism Spectrum. Perhaps it is another mineral or vitamin contained in prenatal vitamins. And, perhaps there is a very subtle defect in the expectant mother’s ability to metabolize certain minerals or vitamins effectively.

    Considerable genetic research has been done on families with one or more children on the Spectrum and early reports after running genotypes on both parents and unaffected siblings have identified certain abnormal genetic (multiple genes/combinations of genes) that are present in the affected child and not in siblings. Also de nova genetic mutations have been identified. SFARI (Simons Foundation Autism Research Initiative) has issued reports about this research (SFARI All News and Commentary).

    The Foundation has the largest collection of gene patterns and de novo mutations that have been reported as implicated in causing autism and it is available to researchers. They have reached out to parents who have children with autism and are always seeking out more “volunteer” families to undergo genetic testing.

    Ironic, isn’t it, that the anti-vax sites rarely or never report any new studies that link genetic patterns to the incidence of autism. There is an editor on one of the more “notorious” anti-vax sites who states she has three children with ASD. I doubt whether she has volunteered to have her family undergo genetic testing.

  37. daedalus2u says:

    @Tell it like it is, if you think that thalidomide changes genes, you are mistaken. The effects of thalidomide occur without any change to the genome. The effects of thalidomide are not genetic, they are environmental. Environmental exposure to thalidomide during certain periods of development has effects on that development. Similarly the effects of folate outside the “normal” range (which we don’t know what that is) are also environmental.

    The effects of thalidomide are due to interference with the normal signaling that goes on during neurodevelopment. The genes only “know” to turn on when they are told to turn on by signals. When the genes are trying to construct a structure that is extended in size, the genes need signals from every part of that structure. If that signaling is interfered with, the structure that the genes construct will be interfered with too. To construct an extended structure like a brain, the developing cells need to communicate with each other over the whole of the extended structure, the cells that are developing into a brain need to communicate over the whole brain. If that communication is interfered with, the structure of the brain will be interfered with too.

    @ lilady, you not quite right on the research on autism genetics. The genetic causes of autism that you mention, the copy number variants, CNVs or the deletions and duplications that are observed to be associated with autism are virtually always de novo, only rarely do they occur in families. The type of autism that is familial has (so far) undecipherable genetics with no single gene accounting to even a factor of 2 in incidence.

    http://www.ncbi.nlm.nih.gov/pubmed/20663923

    It is easy to misinterpret the autism genetics research because it isn’t always well articulated how the different types and subtypes of autism are related to the genes. All the different types of autism are lumped together and when genetic causation is found for some, it is then assumed there will be genetic causation for the others. For de novo autism, which usually is also associated with dysmorphic features, I think that CNVs are the likely cause and there likely will be possible to find a genetic cause. For the familial autism, they have looked really hard for the genes and can’t find them.

  38. lilady says:

    @ Daedalus2U: Very interesting Pubmed citation you provided…with the added bonus of the “Free Article” attached.

    I have been viewing SFARI All News and Commentary and did locate an interesting synopsis of a recent family study of what appears to be familial autism, by keying in:

    SFARI Families Hint at Diverse Effects of Chromosome 16P Deletion

    (apologies for my profound lack of “linking skills”)

    I suppose I may have some bias here because of my extensive history of advocacy on behalf of the developmentally disabled and my affiliations with the Autism Society of America…going back more than 30 years. Long before Autism Spectrum Disorder was ever defined, I worked a lot with families who had children with (classic-type) severe autism. I know of one family whose only 3 children…all males…have classic autism, still another family where both boys have classic autism…one with profound mental retardation the other boy somewhat higher functioning intellectually…he had a savant skill to be able to identify the correct day of the week for a given date in the past hundreds of years. One family had (naturally conceived) triplets…2 girls and a boy…all with classic autism.

    I hope that I didn’t mislead anyone with my posting above about prenatal vitamins…taking them does not impact on the genetic makeup of a developing fetus. Again, I feel that early prenatal vitamin intake, including the period of time before a “planned pregnancy” seems protective against neural tube defects and may have a protective effect for a fetus for other developmental disabilities.

  39. Calli Arcale says:

    Harriet:

    No one is suggesting that autism has a single cause. In fact, this study suggests multiple causes and inter-relating causes.

    I didn’t mean to imply that anyone suggested that; I was just mentioning it to illustrate how complex the problem is. There are doubtless confounders that we don’t know about. Some cases of autism may be provoked/aggravated by insufficient maternal nutrition; some may not. Obviously cases in the latter group won’t be as revealing in a study like this, which can cloud the issue.

    You say you took prenatal vitamins religiously: did you take them religiously for 3 months prior to conception and during the first month of pregnancy?

    Yes. Both of my pregnancies were planned. In fact, my doctor put me prescription supplements the first time around just in case, which I think was overkill; within a few months, I had switched to OTC prenatal vitamins. I was less religious about everything for the second pregnancy; that’s not unusual, since on the second pregnancy, one obviously already has a small child running around, with all that entails. ;-)

    I don’t think “it’s hard to know how to apply this information” – I think it raises legitimate concerns and I think it is a reasonable precaution to take prenatal vitamins starting 3 months prior to conception while we are waiting for better evidence.

    It’s *always* been a reasonable precaution, and for far more reasons than just autism. However, I do get concerned that mothers may fret too much over unplanned pregnancies, and blame themselves if they end up only starting prenatal vitamins at 3 months gestation (since it is entirely reasonable for a woman to not realize she is pregnant for that much time) and then the child winds up with autism. The flip side of this study is that the effect, if real, is not large. That was why I brought up my own family’s example: there will be outliers, probably quite a few, and there’s no way to know whether a particular child’s autism was influenced by maternal nutrition or not. Mothers get beat up enough for making the wrong choices while pregnant; I don’t think the data in this study would be sufficient to justify adding “you gave your child autism with your crappy diet” to that. That’s where my concern lies. And it’s not a trivial concern, in my opinion; I’ve seen mothers get seriously stressed out about doing the right thing for their child, and getting so obsessed about it that they wind up seriously stressed, and that might actually be worse for the child.

    Either this study is not finding a real effect, or my children are outliers. Both are entirely possible. I understand this. Others may not; that’s where it becomes difficult for people to apply this data.

  40. Calli – would you be an outlier? I’m sorry I’m am completely hopeless with numbers. The report that HH shows says that the prenatal vitamins lower risk, but since I don’t understand all the number stuff, I don’t get by how much.

    Perhaps someone could put the lower risk that was found in simple language for me (and possibly other non-math parents)?

  41. Angora Rabbit says:

    @Calli:
    “Either this study is not finding a real effect, or my children are outliers. Both are entirely possible. I understand this. Others may not; that’s where it becomes difficult for people to apply this data.”

    Or the third possibility (if I understand you correctly and maybe I’m not so apologies in advance) is that the effect is real but only for those pregnancies where mother or fetus are heterozygotic for loci that affect nutrient metabolism and requirement. For example, MTHFR in folate metabolism where 677C to T increases folate need; I mention this locus because it popped up as risk factor in this study. So not outliers, just another mechanism in the complex soup. :)

    And for Tell it like it is, MTHFR is a perfect example of a gene-environment interaction. People inherit allelisms that may or not produce a phenotype depending on the environment that person experiences. This is what we researchers often mean by a gene-environment interaction. The literature is rife with examples and it is a hot research topic in a number of biomedical fields ranging from cardiovascular disease to obesity to birth defects to neurosciences.

    For a more “direct” example of gene-environment interaction, take a look at the literature on epigenetics, where environment “rewrites” DNA and histone methylation at each generation to alter gene expression. Search PubMed for Michael Skinner, Randy Jirtle and colleagues for some really amazing research. For a lay description, search the internet for the Nova tv program “The Ghost in Your Genes” (Not the Horizon version, too dumbed down IMO)

  42. Angora Rabbit says:

    “Perhaps someone could put the lower risk that was found in simple language for me (and possibly other non-math parents)?”

    Hey Michele. For prenatal vitamins in the total population, it lowered risk (OR 0.62, 95% confidence interval 0.42-0.93). Put another way, for 100 autism births without prenatal vitamins, 62 predicted for prenatal vitamin use with an uncertainty range of 42-93.

    For regular multivitamins the OR was 1.1 (0.57-2.3) or 110 for every 100, so no influence.

    Hope this helps!

  43. Tell it like it is says:

    @daedialus2u Thank you for your clarification. I stand corrected on using the words ‘genetic’ modifications’ to take place … when I was describing the mutant effects that occur when the coding or ‘instructions’ get screwed up by environmental factors – using the effects of thalidomide on the foetus as my qualifier. As you state, such deformities are not ‘genetic’ mutations, there is simply a screw-up in the software caused by external interference.

    In a way, we are tinkering with the building blocks of our own construction in an ever seeking quest to either fix our abnormalities, or (better) prevent them from occurring in the first place. We still have some way to go. Perhaps the solar eclipse signals an imminent breakthrough?

    Kindest regards

  44. Tell it like it is says:

    @ micheleinmitchigan At the risk of sounding risky, risk is all about ‘probability’, a word here which means ‘is this event likely to happen’. Most events can be grouped under five categories of risk: certain; highly likely; likely; unlikely; and uncertain.

    All risks are dependent upon something associated with that risk – hazards – a word here which means exposure to harm.

    An event that has a risk classification as ‘certain’ WILL happen. Day will follow night, and memento mori are two examples of ‘certain’. To the second, I risk the quote of Robert Herrick. Gather ye rosebuds while ye may; Old Time is still a-flying: And this same flower that smiles to-day; To-morrow will be dying.

    An event that has a risk category of ‘highly likely’ is one where you must expect the event to happen unless due care and attention is adhered to and ‘control measures’ are put in place. If you step into busy traffic without looking both ways (the control measure) it is highly likely that you will get injured through lack of due care and attention.

    An event with a risk category of ‘likely’ is one where ‘exposure to the risk’ is considered – a term which here means ‘the more you expose yourself to harm, the more likely you are of harming yourself; and also appropriate ‘preventative measures’ are implemented.

    To illustrate, if you smoke cigarettes it is likely that you will damage your organs. The more you smoke, the more harm you will inflict on yourself and others. If you are visiting a country such as Egypt during the malaria season then you should either have a malaria vaccination prior to your visit (the preventative measure), or go to an area where there isn’t any malaria (reduce your chance of exposure). In any event, you should visit Egypt, start at Luxor and do a Nile cruise towards the Aswan dam. On the way, you will see some of the worlds best kept and marvellous temples and structures – many built over five thousand years ago.

    If you base yourself in Luxor and take the coach each day, you will risk having to set off at some unearthly hour of the night to arrive at your destination. It is likely that you will miss the splendid ‘sun spectacles’ that occur every morning in each temple as the sun rises, and it is highly likely that you will have a long boring journey to return to your base – getting longer with each passing day. Whereas, if you elect for the much less risky cruise option, you will sail through the night in affordable luxury that belies belief, and will wake up right outside of the ancient monument ready to absorb its spectacle. One thing is certain – you will LOVE it!

    An event with a risk category of ‘unlikely’ is one were all practicable precautions have been taken (the preventative measures), you have implemented all the necessary control measures, and you have also taken ‘precautions’ a word which here means sought advice, acted upon it, and sent someone else instead.

    An event with a risk category of ‘uncertain’ is where sufficient evidence has not been gathered to be able to make a value judgement; or we are unsure of the source of harm; or we are unsure of what causes the harm in the first place. My illustrative example is for you to obtain a DVD of the film (movie) ‘Lorenzo’s Oil’ starring Nick Nolte and Susan Sarandon. Be prepared for tears and take all precautions! I am sorry to have to tell you that there are no ‘preventative measures’, but that is how it is.

    One last thing. Prevention is better than cure – but – we must also have ‘recovery systems’ in place for when things go wrong – which is highly likely.

    One thing is certain, it is highly likely that humans will continue to push the boundaries in medicine and space; it is likely that greed will dictate what cures we seek and which we ignore; it is unlikely that we will give up our quest; and how well we succeed is uncertain.

    Kindest regards

  45. Angora Rabbit, Thanks!

    So if my reading of your post is correct, we are looking at the possibility that prenatal vitamin use 3 months before conception and 1 month after conception prevent about 1/3 of the cases of autism. (?)

    Somewhat similar to what I’ve read on cleft lip and palate and folic acid, although I don’t know when the folic acid was taken (if three months before conception or not).

    Thanks again.

  46. @Tell it like it is…

    I generally enjoy an off the wall comment, but sadly today I have a headache, didn’t sleep, the kids just got off school for the summer, and I’m really behind on my at-home work benchmark, so you lost me more than a bit.

    I hope to try again when I’m in a better place. :)

    I always wanted to go to Egypt and Israel…

  47. Angora Rabbit says:

    Hi Michele, hope you’re feeling better.
    “So if my reading of your post is correct, we are looking at the possibility that prenatal vitamin use 3 months before conception and 1 month after conception prevent about 1/3 of the cases of autism. (?)”

    Almost. :) A better way to say it is that, *all other things being equal* between the two groups, the prenatal vitamins would have between 42-93 cases (the confidence interval) instead of 100. But all things are never equal and there are many other risk factors so the reduction would very likely be less than 1/3.

    You can see where this pops out when they stratified the groups based on their genetics of folate and methyl group metabolism (these two things are very related). When they did that, mothers having two copies of one particular folate gene (MTHFR 377TT) meant that the autism risk shot up between 1.4-14.6-fold (OR 4.5) in the absence of perinatal vitamins. That’s what really got my attention with this paper, that it wasn’t just perinatal vit use but its even stronger association with certain maternal and child genotypes that we can definitely link to folate/methyl usage. A loverly gene-environment interaction. :)

  48. daedalus2u says:

    I have a very complex view of autism, I have Asperger’s, my mother did, and essentially all of my 5 siblings are on the spectrum.

    Autism is a property of a phenotype, not a genotype. All emergent behaviors (everything that takes multiple cells to instantiate, like a neural tube, a nervous system or a brain) is a property of a phenotype, not a genotype.

    How a genotype makes a phenotype is 99.9999% unknown. We know it happens, so there is a process, but the details of that process are essentially completely unknown. Neurodevelopment is an ongoing process. Neurodevelopment only stops at death.

    It is a wrong conceptualization to think of a “genetic” component and an “environmental” component, or any fixed percentage compartmentalization or fixed degree of interaction. Both genetics and environment are 100% important.

    @ Angora, I have not seen the actual paper, but I would be concerned about the size of the cohorts used to make these determinations. How big was the group that didn’t take prenatal vitamins and also had a child with autism and also had the genetic variation? Prenatal vitamin status was determined retrospectively. That is a very wide confidence limit.

  49. angora rabbit, tomorrow is much likely to be a better day.

    Thanks for the second pass. That gives me a clearer picture.

  50. Venna says:

    I’m not entirely sure I buy the prenatal vitamin link myself. Having had six children, all of them ‘surprises’ so prenatal vitamins weren’t taken prior to getting pregnant and in some cases I wasn’t supposed to be able to get pregnant (based on what doctor had told me per a condition I had developed after using a particular form of birth control), Typically most women don’t know they are pregnant until they miss their first period (which usually occurs two to three weeks into the actual date of conception) and it can take another two or three weeks after missing before a woman gets confirmation that she is pregnant. By that time, the first month of pregnancy is over. At that point, unless she takes prenatals as her daily supplement anyway, it would be too late to begin taking prenatal vitamins in the first month.

    Also, prenatal vitamins are a fairly new addition to the recommended activities of pregnant women. I can’t seem to find anywhere that gives a history of prenatal vitamins or a date when they were invented but taking into consideration that they are fairly recently added and autism rates have dramatically increased over the past decade or so, It may be a bit of a stretch to say that prenatal vitamins alone will make an impact.

    With my children, I began taking prenatal vitamins as soon as I learned I was pregnant and could afford to buy them (let’s face it, they are expensive and I’ve not always *never* been financially well off). My first child, I was four months along before I was able to begin taking them. With my second, I didn’t take them at all. With my third, I didn’t even know I was pregnant until 25 weeks into my pregnancy and still didn’t begin taking them right away so it was really just the last trimester with my third that I took prenatal vitamins. With my forth, I began taking them sooner, but didn’t take them regularly because with his pregnancy, my mind was well, I found myself much more forgetful. With my fifth, I began taking them right away after getting the pregnancy confirmation (I was about 9 weeks along) and I also included extra folic acid, calcium and iron per my doctor’s recommendations (I have a family history of spina bifida). With my sixth, I began taking prenatals, along with the extra folic acid and calcium, about 12 weeks into it.

    Of my six children, the first five are neurotypical, and all born before my 29th birthday. My sixth has autism and I was going on 37 when he was born. I mention my age because I believe, in my case at least, that has much more to do with his autism then anything else. I personally believe there are a lot of factors that contribute to autism for the child. Parental age I believe is a huge factor (how many of these children are born to women in their 30′s or older?) Spontaneous mutation is another factor that may contribute which would make it genetic but not hereditary in the case of only one sibling having autism and the rest do not.

    I don’t believe anyone should put all their eggs in one basket. Until the whistle blows and all votes are in and we know for certain what it is that causes it, we need to keep an open mind and allow for all possibilities. Is it possible that pre and early pregnancy intake of prenatal vitamins may be a factor in some situations, but I don’t buy it for all situations.

  51. lilady says:

    Actually prenatal vitamins have been prescribed for pregnant women for 40 or more years by OBs here in the United States. It was common practice to prescribe them as soon as the expectant mother had her first encounter with an obstetrician. When I was pregnant 41 and 36 years ago, pregnancy tests were not done until after the second missed period…no drugstore early pregnancy tests were available back then. So, none of the infants had the benefit of the vitamins taken by women either before or in their early stages of fetal development. There also was no “epidemic” of autism/autism spectrum disorders for that generation’s children.

    Of course Venna is correct with a correlation for a small number of children diagnosed with autistic disorders and other developmental disabilities associated with older maternal and paternal ages at time of conception. There are certain co-morbid conditions such as gestational diabetes and hypertension that are more prevalent in the older pregnant woman.

    The best health care insurance plans only cover a small number of IVF procedures. Consequently women who delay pregnancy or need fertility treatments and procedures usually have 2 or 3 embryos implanted to increase the chance of producing a single infant. Problems arise when all three embryos are implanted successfully, resulting in high order births… the chances of very premature twin and triplet births increase dramatically. These babies are all at risk for developmental disabilities.

    I suspect in the next few years, researchers will be more able to define what genetic factors and prenatal environments may impact on the developing infant.

    Imagine how far along the research would be, if we didn’t waste tax dollars on research to debunk the many vaccine-autism links theories.

  52. Harriet Hall says:

    @ Venna,

    I’m puzzled by your comments “I don’t believe anyone should put all their eggs in one basket” and “we need to keep an open mind and allow for all possibilities.” Perhaps you can explain what you meant. I didn’t think there was anything in the study or in my post to suggest one basket or closed minds.

  53. Venna says:

    I apologize if I was disrespectful, that wasn’t my intention. I suppose this particular issue could be similar to the vaccine autism issue where a select few may jump on it and run and forget about everything else that’s out there being researched.

    New evidence as to circumstances that exist in the individual with autism are being revealed all the time. All these studies will eventually come together to create a cohesive whole I’m sure, but since each study is being done separately it can sometimes be a little confusing. So until all the facts are in and we know, beyond a doubt what the cause is, we need to make sure we aren’t getting stuck on one thing and forgetting everything else.

    In my case, I don’t believe lack of prenatal vitamins prior to or early in my pregnancy played a part in my son. Perhaps they may have in someone else, but it can be difficult to know for certain who actually did take prenatal vitamins and who didn’t. I know I had to wrack my brain to remember and I’m not certain I remember correctly.

    I’ve been shunned, with very violent language by the anti-vaccine community when I tried to reach out to them as fellow parents of children with autism (before I knew they were anti-vaccine). It was specifically Age of Autism. My son developed autism without the vaccines so I don’t buy their line, never have, but just was looking for support and advice. The blog posted something about an anti-vaccine rally they held and I posted a comment explaining how I don’t believe vaccines cause autism, science tells us otherwise. If we had been in the same room, I would have been beaten to death. It was quite scary, the insults, the verbal assaults, even threats of physical violence and death (fortunately they don’t know where I live), being called a liar and being told my son doesn’t matter then because he wasn’t vaccine injured. I tried to defend myself and I got banned from posting. I don’t consider anti-vaccine parents advocates for autism, otherwise they would accept anyone, regardless of whether or not they follow their line or not.

    It would be sad to see others take the hard line against others regarding the prenatal vitamin link, if that happened. So what I said was really for anyone kind of sitting on the fence, not sure what to believe, because at this point in time, there’s a lot of evidence, but nothing really conclusive, so we need to keep an open mind about it.

  54. lilady says:

    @ Venna: Most people who post here are not fixated on any one answer to the complexities of autism…so unlike the folks at Age of Autism.

    Don’t feel bad that Age of Autism “moderated” your comment…they do it all the time. I also wouldn’t attempt to post at that site even if I found I agreed with an article, as I don’t trust them. They have a terrible record of pursuing people at their place of employment (Dr. David Gorski and others) who dare blog or post anything that is not in lockstep with their peculiar theories.

    A case in point. One of their editor’s daughters had a terrible experience (abuse) aboard a school bus. I did want to reach out to the editor, as I was able to…along with a group of other parents…pass meaningful legislation in my state for fingerprinting and criminal records checks for personnel aboard school buses. I didn’t reach out as I know their history of hunting down people who ever have deviated from their fixations/theories.

    We are just at the very beginning of understanding factors that may impact on autism and other genetic diseases.

    After my son was born in 1976 and underwent chromosomal studies, we were still uncertain what genetic disorder he had. We knew he had multiple and severe problems, but his chromosomal study was normal…obviously “it’ was in the genes. I financially supported the foundation begun by parents of children with his rare genetic disorder, that in turn supported research, once the human genome was mapped.

    Three months before he died the NIH determined most of the genetic patterns of his disorder…autosomal dominant with the vast majority with de novo mutations.

    I suspect that autism in all its forms will have many genetic causes identified in the future, but in the meantime we all love our children and deal with their problems and support real scientific research, not the bogus nonsense that is the proverbial dead end street.

  55. SarahAnn says:

    We have additional evidence that points to a nutritional deficiency as a potential factor in autism, that children of women that have little time between pregnancies have higher levels of ASD:

    http://www.abc2news.com/dpp/news/health/time-between-pregnancies-could-be-linked-to-autism

    Could be vitamin D as previously mentioned as there is lots of observational evidence. (northern migrants from southerly latitudes have more autistic children)

    Science moves so goddamn slowly, I wonder are there any interventional trials for vitamin D underway?

  56. lilady says:

    I located the original study that SarahAnn referred to, on the internet:

    Pediatrics: Closely Spaced Pregnancies are Associated with Increased Odds of Autism in California Siblings

    I also located an interview that explains some of the increases in autism diagnoses in the school setting for the period covered (1992-2002) in the Television reported referred to by SarahAnn:

    Autism “Epidemic?” A newsmaker interviews with Morton An Gernschacher, Ph.D and Craig J. Newschaffer Ph.D. (Medscape Medical News July 15, 2005)

    The interview points out the wide differences between the DSM III autism diagnostic criteria and the DSM IV autism diagnostic criteria, which greatly expanded the diagnostic criteria. There is now a virtual “Chinese Menu”-type of Diagnostic criteria (16 versus 8 criteria as contained in the DSM III Manual and a much lower threshold for diagnoses on the ASD hierarchy.

    “We have additional evidence that points to a nutritional deficiency as a potential factor in autism…..” (Citations, please)

    When I keyed in “Vitamin D deficiency Autism” what came up was slew of Alt/Cam sites. Persistence paid off, however and I located a report from a reliable research site:

    SFARI Scientists Probe Reports of Somali Autism “Cluster”

    Yes, there was a study done in Sweden that determined that Somali children had a higher incidence of an autism diagnosis versus children born to white Swedish parents. (Somali parents living in Sweden labeled autism as the “Swedish Disease”.

    Recently, after Andrew Wakefield visited the Somali community in Minneapolis three times to drum up support for his latest “theory” of an alarming increase of autism diagnoses in Somali children attending Minneapolis Schools, there has been a dramatic decrease in Somali Children who are unimmunized against measles…which precipitated the start of, and the extension of, a 21 case outbreak of measles. Interesting to note here that Somali people residing in Minneapolis label autism as the “American Disease.”

    There are other factors at play here as well. Somalis frequently intermarry…first cousin marriages are very common.
    Somalians in America are very much an enclosed society and most speak the “native tongue” (Somalian an East Cushtic branch of the Afro-Asiatic language group) within the home and within “their group”. Their is also a financial incentive to have a special needs child with English language deficits classified as autistic for the SSI benefits and for Medicaid coverage, as well.

    I recall only too well, the theory advanced by J. B. Handley and others at Age of Autism “linking” low immunization rates with the junk science of “no autism incidence within the Amish community”.

    Before I plug into Vitamin D deficiency in Somali Children in northern climes causing increased autism rates, I think I will await the study being conducted by the IACC (NIH Interagency Autism Coordinating Council) that is studying the Minneapolis Somalian Community.

  57. “native tongue” (Somalian an East Cushtic branch of the Afro-Asiatic language group) within the home and within “their group”. Their is also a financial incentive to have a special needs child with English language deficits classified as autistic for the SSI benefits and for Medicaid coverage, as well.”

    I would think that if the children were tested in the language that they are competent in, then there shouldn’t be a concern about language differences showing up as language deficits.

  58. lilady says:

    Children should be tested prior to school entry in the “native tongue” and if questions arise about their developmental stage, then psychologists/social workers who are trained in testing modalities and fluent in the foreign language can administer further tests.

    Children may speak a wide variety of foreign languages, but they usually are not taught in their “native tongue” in regular classrooms, but rather enrolled in special services or dedicated classrooms taught by ESL teachers…as I am sure the Somali children not diagnosed with autism are taught.

    Nevertheless, there is a rather high spike in autism diagnoses in children with Somalian heritage…not seen in other groups whose first or second language is not English.

    There is a study specifically directed at the Somalian community in Minneapolis to investigate the causes of this higher incidence of diagnoses of autism in the school population, funded jointly through the NIMH and Autism Speaks and under the auspices of the IACC. I presume that the research will be impeccable without the assistance of Andrew Wakefield…and with the full cooperation of the parents whose children have been diagnosed with autism.

  59. passionlessDrone says:

    Hi Lilady & Michelleinmichigan –

    FYI – There is also an investigation into clusters of Somali autism in Sweden. Vitamin D in this group has been evaluated and looks to have trended towards an association.

    http://www.ncbi.nlm.nih.gov/pubmed/18754897
    http://www.ncbi.nlm.nih.gov/pubmed/20219032
    http://www.ncbi.nlm.nih.gov/pubmed/20964674

    There are also some other epidemiological reviews that tend to support the idea of vitamin D deficiency as a possible problem; i.e.,

    http://www.ncbi.nlm.nih.gov/pubmed/20592795

    - pD

  60. lilady – When my child was being evaluated for speech delays through Early Intervention, several times, from EI therapists/testers, I heard the speculations that immigrant parents who only speak their native language at home then seek evaluation through EI are just trying to get free services/preschool from special education.

    And, surprisingly, they also didn’t have the personnal to test my son in his native tongue. (It was much easier to pretend his articulation was fine in his native tongue and only severally delayed in English).

    Maybe it’s good to add that if some of the people who are designated to evaluated child are bias against diagnosing a delay or condition based immigration status, this could result in an under diagnoses of autism (or other conditions) in the immigrant population.

    This is not to be critical of the IACC study. I would think that they would have thought of such considerations.

  61. lilady says:

    Well it seems I started a conversation here about possible Vitamin D deficiency during pregnancy and a possible link to autism. As I stated above, I look forward to the report from the IACC to either confirm lesser abilities to absorb Vitamin D during pregnancy in northern climes and a link to increased rates of autism diagnoses, or to find other factors to explain the increased rate of autism among Somali immigrants.

    I believe that other factors may come into play here such as totally unreliable actual incidence rates of autism from the Somalian government, due to the civil unrest and destructive wars for the past 30 plus years in Somalia, vast cultural and language differences experienced by Somalis residing in the United States and the innate inability of any school system to bridge those gaps, for immigrant groups.

    We have had a very large group of immigrants who have migrated to the United States and to Canada from the Caribbean and from Central and South America who have darker complexions along with varying abilities to absorb Vitamin D, yet I haven’t seen any alarming numbers of increased autism diagnoses.

    Guyanese population in the United States is estimated at 350,000, half as much as those who presently resided in Guyana. But, the difference in these immigrant populations who are 30 % black and 51 % Indian (mainly from Madras) is that 99 % of the Guyanese population speak English (beautiful Queens English, I might add) and literacy is 97.1 %. Other Caribbean populations with varying skin tones and varying abilities to absorb Vitamin D have also immigrated to northern climes, but again they are highly literate in the English language. And, all these English speaking immigrants come from countries with highly established health systems and school systems not disrupted by civil wars, where incidence of autism and other developmental disabilities are more reliable.

    Again, I am delighted that the IACC has embarked on this study…although I wish that the study was begun earlier…before Andrew Wakefield had an opportunity to poison the well with his fraudulent vaccine-autism link. At a minimum, these Somali parents will have some questions answered and perhaps, more importantly, have services for their children enhanced. I am “all in” on providing children with special needs each and every service to enhance their abilities.

  62. KGelling says:

    Epidemiological evidence shows that autism is linked to season, skin colour and latitude (1) – all hallmarks of vitamin D as a causal factor (2).

    There is also anecdotal evidence that pharmaceutical doses of vitamin D can improve the behaviour of autistic children.

    ——-
    1. Grant, W. B. & Soles, C. M. Epidemiologic evidence supporting the role of maternal vitamin d deficiency as a risk factor for the development of infantile autism. Dermato-endocrinology 1, 223-228 (2009). URL http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835879/.
    2. Cannell, J. J. J. Autism and vitamin d. Medical hypotheses 70, 750-759 (2008). URL http://dx.doi.org/10.1016/j.mehy.2007.08.016.

  63. Chris says:

    Kgelling, cites to Medical Hypotheses are usually not considered relevant. To understand why, just look up what “hypotheses” means.

  64. lilady says:

    KGelling: Thank you for the references to the two articles. At the beginning of the first article, there is this statement

    “This article has been corrected” and linked to the second article your provided.

    The link led me to the Cannell article, but at that link I was led to the Vitamin D Council.org.

    At the Vitamin D Council.org I see commercial advertisements from Dr. Mercola, special laboratories that test for Vitamin D deficiencies and for companies that sell supplements.

    I echo what Chris states above “Medical Hypotheses are usually not considered relevant” and I would add that the author of the second article Mr. Cannell has commercial ties to (what I deem) alternative medicine, Vitamin D marketers and labs that do “specialized”/possibly unorthodox testing for vitamin deficiencies.

  65. lilady says:

    As a follow-up to my posting above I have checked further into the Vitamin D Council.org.

    I mistakenly identified the co-author of the study referenced by Kgelling as “Mr.” Cannell…he is Dr. Cannell, MD.

    I also stated that Dr. Cannell has “commercial ties” to the Vitamin D Council; he is the founder and president of the Board of Directors of the Vitamin D Council.

    Dr Cannell is also the owner of one the advertisers on the website of the Vitamin D Council, “may” be the owner or partial owner of another advertiser on the website…both are vitamin and supplement dealers on the internet.

    Dr. Cannell is also very much involved in the specialized laboratory that offers “home tests” for vitamin D deficiencies…also an advertiser on the Vitamin D Council’s website. He is also the doctor who signs off for ordering the vitamin D special testing…all through the internet…only qualification for the doctor to order the test without evaluating the patient face to face…would be paying for the test beforehand, charged to a credit card.

    Dr. Mercola’s advertisement on the website is for tanning Vitamin D devices…also sorts of tanning beds.

    So much for the Vitamin D. Council as a resource for sound medical advice for vitamin deficiencies. Just another alt/cam web page to hawk their wares.

  66. KGelling says:

    Chris: “cites to Medical Hypotheses are usually not considered relevant. To understand why, just look up what “hypotheses” means.”

    Science starts with hypotheses. To understand why, just look up what “scientific method” means!

    For example:

    1. Observe – pre-natal vitamins reduce autism, causal factors of autism match those of vitamin D deficiency, pre-natal vitamins contain vitamin D
    2. Hypothesise – vitamin D reduces autism
    3. Predict – Pregnant women taking vitamin D supplements will have fewer austistic children
    4. Test – To do

  67. Chris says:

    It starts with a hypothesis, which is a guess. The problem with that journal is that the papers usually end there, giving all sorts of rationalizations for the guess but no data and it is not peer reviewed. That particular journal is infamous for publishing bad papers, including AIDS denialism and one that explained “mongoloid” really was an appropriate term for people with Down syndrome, plus other dodgy guesses.

    So give us the results of the test and its replication published in a peer reviewed paper.

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