On World Autism Day: Why I Am Concerned About the Use of Antidepressants During Pregnancy

Adam Urato, MD
25
194

Autism rates are on the rise, with the latest report from the US Centers for Disease Control showing 1 in 50 children to be affected (1).  Prozac, the first of the SSRI (selective serotonin reuptake inhibitor) antidepressants, was launched in 1987 and sales have risen since then.  Women of childbearing age make up a large percentage of SSRI users so the issue of pregnancy exposure is important.  Estimates are that up to 13% of US pregnancies are exposed (2) (or around 500,000 US pregnancies per year.)  How the SSRIs affect pregnancy has been an area of increasing concern (3).  Current evidence suggests that use of antidepressants during pregnancy is associated with miscarriage (4), birth defects (5), preterm birth (6), and newborn behavioral syndrome (7) along with other pregnancy complications such as preeclampsia (8) and low birth weight (9).  We know the SSRIs are associated with pregnancy complications, but a major area of concern is what the effects are on the developing brain of embryos and fetuses exposed to these drugs.  Available scientific data from animal and human studies raise serious concerns that exposure to SSRIs during pregnancy damages the developing brain and may cause neurodevelopmental abnormalities, including autism.

Serotonin: a crucial neurotransmitter

Serotonin is the first neurotransmitter expressed in the developing embryo and it plays a crucial role in human brain formation.  Serotonin has been shown to be essential for the growth and development of certain areas of the brain.  It is involved in such basic processes as cell division, differentiation, migration, and synaptogenesis (10).  In short, proper functioning of the serotonin system is essential for the brain to form and function normally.  In the adult brain serotonin plays a key role in cognition, mood, anxiety, sleep, aggression, and sexual function.

But serotonin’s critical role in development doesn’t end with the brain.  Among other organ systems, serotonin is also found in the intestinal tract, the bone, the lungs, and in the platelets of the blood.  The SSRIs are believed to exert their effects by blocking the reuptake of serotonin into neurons (the nerve cells that are the “basic” cell of the brain).  For a developing baby, such blockade is occurring throughout the body (including the brain) and throughout pregnancy development.

It is now well-established scientifically that autism is characterized by changes in the serotonin system.  Hyperserotonemia is the most consistent neurochemical change in autism (11).

Animal studies of exposed pregnancies are concerning

Most of the data we have on developmental effects of the SSRIs on the brain comes from animal studies on small mammals (mice and rats.)  The majority of these studies show significant changes in the brains and behavior of exposed animals and these results are very concerning.

In 2004, in the journal Science (one of the world’s leading scientific publications), Mark Ansorge and his coauthors published their research showing that exposing mice to Prozac (fluoxetine) during development led to abnormal emotional behaviors when those mice were adults (12).

In 2011, Kimberly Simpson and her colleagues at the University of Mississippi showed that rats exposed to Celexa (citalopram) had changes in the structure and function of their brains and showed impaired social behavior.  Males were more severely affected than females.  This gender difference (with males being affected more than females) is well-established in human studies on autism (13).

These are just two examples of the many, many animal studies that show changes in the brain and behavior that result when the serotonin system is altered during development by the use of the SSRI antidepressants.  These animal studies have been published in some of the world’s leading scientific journals like Science and The Proceedings of the National Academy of Sciences.  At the end of every scientific paper there is a “Discussion” section.  In the Discussion of these animal studies, again and again, the authors warn us that their findings (of harmful effects on offspring from exposure to SSRIs during brain development) should make us concerned with using them in humans.

Human studies are also finding problems

Several human studies looking at the effects of SSRI exposure during pregnancy have shown brain and behavioral changes in exposed children.

In 2003 Regina Casper showed that SSRI exposure during pregnancy had effects on motor development and motor control in young children (14).  In 2010 Lars Pedersen demonstrated that SSRI-exposed children sat up and walked later than their unexposed peers and that they had behavioral changes (15).  In 2013 Gillian Hanley showed that children prenatally exposed to SSRIs scored lower on gross motor, social-emotional, and adaptive behavior testing (16).  And these are just 3 of many studies that show changes in exposed children.

The most important study regarding the SSRI antidepressants, pregnancy, and autism came out in 2011.  In this study, Lisa Croen and her colleagues showed that SSRI exposure during pregnancy was associated with a doubling of the risk of autism.  Even more importantly, for first trimester exposure to the SSRIs, the risk was almost quadrupled.  Very importantly, her study looked at depressed women who were not on SSRIs, and in this group there was no increased risk of autism.  It was the antidepressant use that was linked to the autism and not the depression (17).

Basic science: “Brain damage proteins”

It is not possible to examine the brains of exposed human children in the same way that researchers can study rat and mice brains to look for effects of the SSRI antidepressants.  But there is ongoing basic science research in humans looking at evidence of brain injury in exposed babies.

S100B is an important brain protein that has been found to be lowered in babies who were exposed to alcohol and cocaine in utero.  In 2009, Jodi Pawluski and her colleagues in Vancouver published a landmark study showing decreased S100B levels in human babies who were exposed to the SSRI antidepressants in utero (18).

Activin A is a brain protein that is increased in cases of brain injury.  It is known as a “brain damage marker.”  In 2011 Valentina Bellisima and her colleagues in Italy showed that babies who are exposed to SSRI antidepressants in utero have dramatically higher levels of this brain damage marker in their blood and amniotic fluid (19).  This study leaves us with the question, why is the brain damage marker protein (Activin A) so elevated in the SSRI-exposed children?

Common Sense: Putting it all together

A developing embryo and fetus is loaded with serotonin receptors and serotonin plays an absolutely critical role in development.  Why wouldn’t chemically interfering with this system affect human development—particularly in the brain?  Why would we expect that the addition of such a chemical to human development would not cause significant and likely harmful effects?  The SSRI antidepressants have been shown to be linked to miscarriage, birth defects, preterm birth, preeclampsia, and other pregnancy complications that suggest that the drugs can cause injury to the developing baby/pregnancy.  It should come, then, as no surprise that such medications could injure the fetal brain.  Animal data shows brain injury from exposure to these drugs during development and human data shows altered brain damage proteins from such exposure.  Finally, human studies in child development show that exposed babies have worsened neurobehavioral outcomes and increased rates of autism.

Conclusion:  Autism Awareness Day and the importance of public awareness

Today is Autism Awareness Day and we are in the midst of a growing epidemic of autism.  While many factors are likely contributing to the epidemic, we can no longer ignore the role of the widespread use of the SSRI antidepressants by pregnant women.

The complications of SSRI use might be considered tolerable if there was solid evidence of benefit with the use of antidepressants by pregnant women.  Sadly, in 25 years of study, not a single study has ever shown improvements in pregnancy outcomes in the antidepressant-treated group.  And, in studies of nonpregnant populations, there is little evidence of clinically significant benefit with the use of antidepressants (when compared with placebo) by most patients with depression.

Today, on Autism Awareness Day, it is essential that we raise public awareness of the issues surrounding antidepressant exposure during pregnancy and the ever-growing evidence of harm that we see in the scientific studies.  At this point, we do not know with 100% certainty that the SSRI antidepressants are causing autism, but several lines of evidence point strongly in that direction, and the evidence that these drugs can injure the developing brain is clear and consistent.  Pregnant women suffering from depression need treatment and care.  But, with good evidence that non-drug therapies, such as psychotherapy and exercise, provide at least as much benefit in the treatment of depression (if not more), it makes sense to first use these approaches in women of childbearing age — approaches that have not been linked to autism.

References:

(1) Blumberg, Stephen J, et al.  Changes in Prevalence of Parent-reported Autism Spectrum Disorder in School-aged U.S. Children: 2007 to 2011–2012.  CDC National Health Statistics Reports.  March 20, 2013.

(2) Cooper WO, Willy ME, Pont SJ, Ray WA. Increasing use of antidepressants in pregnancy. Am J Obstet Gynecol 2007; 196: 544.e1-5.

(3) Domar AD, Moragianni VA, Ryley DA, Urato AC.  The risks of selective serotonin reuptake inhibitor use in infertile women: a review of the impact on fertility, pregnancy, neonatal health and beyond.  Hum Reprod. 2013 Jan;28(1):160-71.

(4) Nakhai-Pour HR, Broy P, Bérard A.  Use of antidepressants during pregnancy and the risk of spontaneous abortion.  CMAJ. 2010 Jul 13;182(10):1031-7.

(5) Pedersen, L. H., Henriksen, T. B., Vestergaard, M., Olsen, J., & Bech, B. H. (2009). Selective serotonin reuptake inhibitors in pregnancy and congenital malformations: population based cohort study. British Medical Journal, 339, b3569 .

(6) Roca A, Garcia-Esteve L, Imaz ML, Torres A, Hernández S, Botet F, Gelabert E, Subirà S, Plaza A, Valdés M, Martin-Santos R.  Obstetrical and neonatal outcomes after prenatal exposure to selective serotonin reuptake inhibitors: the relevance of dose.  J Affect Disord. 2011 Dec;135(1-3):208-15.

(7) Levinson-Castiel R, Merlob P, Linder N, Sirota L, Klinger G. Neonatal abstinence syndrome after in utero exposure to selective serotonin reuptake inhibitors in term infants. Arch Pediatr Adolesc Med 2006; 160:173-176.

(8) De Vera MA, Bérard A.  Antidepressant use during pregnancy and the risk of pregnancy-induced hypertension.  Br J Clin Pharmacol. 2012 Aug;74(2):362-9.

(9) Grzeskowiak LE, Gilbert AL, Morrison JL.  Neonatal outcomes after late-gestation exposure to selective serotonin reuptake inhibitors.  J Clin Psychopharmacol. 2012 Oct;32(5):615-21.

(10) Bonnin A, Levitt P. Fetal, maternal, and placental sources of serotonin and new implications for developmental programming of the brain.  Neuroscience. 2011 Dec 1;197:1-7.

(11) Hadjikhani N.  Serotonin, pregnancy and increased autism prevalence: is there a link?  Med Hypotheses. 2010 May;74(5):880-3.

(12) Ansorge MS, Zhou M, Lira A, Hen R, Gingrich JA.  Early-life blockade of the 5-HT transporter alters emotional behavior in adult mice.  Science. 2004 Oct 29;306(5697):879-81.

(13) Simpson KL, Weaver KJ, de Villers-Sidani E, Lu JY, Cai Z, Pang Y, Rodriguez-Porcel F, Paul IA, Merzenich M, Lin RC.  Perinatal antidepressant exposure alters cortical network function in rodents. Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18465-70.

(14) Casper RC, Fleisher BE, Lee-Ancajas JC, Gilles A, Gaylor E, DeBattista A, Hoyme HE.  Follow-up of children of depressed mothers exposed or not exposed to antidepressant drugs during pregnancy. JPediatr. 2003  Apr;142(4):402-8.

(15) Pedersen LH, Henriksen TB, Olsen J.  Fetal exposure to antidepressants and normal milestone development at 6 and 19 months of age. Pediatrics. 2010 Mar;125(3):e600-8.

(16) Hanley GE, Brain U, Oberlander TF.  Infant developmental outcomes following prenatal exposure to antidepressants, and maternal depressed mood and positive affect.  Early Hum Dev. 2013 Feb 2. doi:pii: S0378-3782(13)00015-7. 10.1016/j.earlhumdev.2012.12.012.

(17) Croen LA, Grether JK, Yoshida CK, Odouli R, Hendrick V.  Antidepressant use during pregnancy and childhood autism spectrum disorders.  Arch Gen Psychiatry. 2011 Nov;68(11):1104-12.

(18) Pawluski JL, Galea LA, Brain U, Papsdorf M, Oberlander TF.  Neonatal S100B protein levels after prenatal exposure to selective serotonin reuptake inhibitors.  Pediatrics. 2009 Oct;124(4):e662-70.

(19) Bellissima V, Visser GH, Ververs TF, van Bel F, Termote JU, van der Heide M, Florio P, Li Volti G, Gazzolo D.  Antenatal maternal antidepressants drugs affect Activin A concentrations in maternal blood, in amniotic fluid and in fetal cord blood.  J Matern Fetal Neonatal Med. 2011 Oct;24 Suppl 2:31-4.

 

25 COMMENTS

  1. This is one of the scariest articles I’ve read in a long time. I keep up with the research in general but have never heard this information. It seems likely it is being intentionally suppressed. If folks really knew the data on this, most pregnant moms or women intending to become pregnant would stop antidepressants immediately!

    Which also gives another reason why alternative approaches, which as you say are known to be as effective or moreso without the damaging adverse effects, should be the first line of approach for anyone who is feeling depressed.

    —-Steve

    • My son is 10 and was diagnosed with Aspergers and has been on 4 different medications for 3 years, just to keep him in society. I took 300mg of Welbutrin every day when I was pregnant with him. I have 2 other children that are older that I did not take Welbutrin with and they have no psychological issues. I wish these studies had been done before I had my son in 2004. Everything I read said it was ok. I am 100% that Welbutrin caused my son to have these emotional issues and think that all antidepressants should be marked with a pregnancy rating of C or higher. PLEASE IF YOUR PREGNANT DO NOT TAKE ANTIDEPRESSANTS. Find another way, anyway, to maintain without your antidepressants while pregnant. It’s not worth the emotional pain you and your child will have to endure the rest of your lives.

      • caligirl,

        I don’t mean to sound judgmental but psych meds usually cause big time long term damage to people who already have neurological issues as folks who have AS do. Even folks without AS have these issues as an FYI, particularly if they are taking 4 meds.

        Food for thought.

  2. Thank you so much for articulating the very real risks associated with exposure to SSRIs during gestation. Surely, those on psych meds should be warned against conceiving. (I believe the dermatologists were very direct in cautioning young women on systemic Accutane of the dangers of becoming pregnant.) While some would have us weigh the risks of SSRI withdrawal of the fetus with the risk of continued exposure, I wonder about a conversation about ending a pregnancy for those who conceive while on an SSRI. For older mothers who undergo amniocentesis, the purpose is to know when to end a pregnancy. We also have genetic counseling elsewhere as well (for example, those carrying the Huntington allele). While these are very controversial issues, seems to me women should at least know their options. For a woman on SSRIs to proceed in a sanguine fashion assuming that she is fit to carry a fetus is just not realistic. The ramifications will not only redound to the families involved but also to the public health care dollar.

  3. This is an important issue to broadcast, though I doubt impact on serotonin is the whole story. And because most mothers of the current exploding population of children with autism did not take antidepressants in pregnancy (or even before pregnancy), the drugs can’t be the cause of an epidemic of a very identifiable disorder which has gone from 1 in 10K to 1 in 50 within a generation. Nevertheless, SSRIs may be key to identifying the toxic mechanism.

    In 2007 I attended the ICSPP conference in Maryland and Senate presentation and heard Dr. Grace Jackson present a modest case study she’d done of a case of Depakote induced autism in a seven year-old boy. The paper, later published in the group’s newsletter (it may be available online in archives), was titled “Chemo Brain.”

    Apparently the subject of the paper had undergone chemotherapy at age two and had developed seizures, for which he’d been prescribed Depakote and an antipsychotic later in childhood and it seems the drugs, particularly valproic acid, had compounded the already existing damage wrought by chemotherapy in this typical but medically fragile child. He then developed symptoms of autism.

    I later got to know the mother of the child subject through mutual contacts and the paper only describes a sketch of autistic behaviors: in fact, according to his mother, the boy developed all the hallmark symptoms of severe, full-blown autism until he was removed from Depakote. Unfortunately, though the more severe autism symptoms abated, he continued to have seizures and severe dementia set in.

    This quiet little study of late-onset autism of course didn’t get the attention or recognition it deserved, particularly because the mechanisms of cellular damage Dr. Jackson identified in the overlap between chemo and known effects of Depakote, rather than displacing the mercury-induced autism theory (thimerosal, a mercury preservative in vaccines, has long been fingered as playing a role in the epidemic of autism), actually replicates some of the findings on thimerosal/mercury and identifies another overlap, namely a mitochondrial pathway.

    Jackson identified several interweaving modes of damage along the lines of mitochondrial injury which, like every other toxic drug it seems, surely have an impact on serotonin, though this may only be one of a slew of effects. And the crucial thing is, the identical effects have been identified via SSRI antidepressants.

    1) Mercury, SSRIs and Depakote may all act as HDAC inhibitors to varying degrees- compounds which inhibit deacetylation of histone proteins within cell nuclei. All three can induce programmed cell death.
    2) All three can increase serum ammonia in the brain, replicating an effect of L-asperiganase. “Excessive ammonia levels deplete energy, impair neurotransmission, impair glial uptake of glutamate, increase the formation of glutamine and result in pathological tissue change” and swelling which Jackson likens to Alzheimer’s Type-II astrocytosis.
    3) All three disrupt the assembly of tubulin in the brain, replicating what Jackson identifies as the ototoxic and neurotoxic effects of vincristine, arresting mitosis in rapidly dividing cells (autism has resulted from chemotherapy treatment in some case studies).

    The argument I’ve heard from many researchers is that autism boils down to affected cellular pathways. The various causes of the specific damage which result in autism spectrum disorders in children may be more than one single cause but will not be limitless, since only a handful of substances to which children are commonly exposed (and even fewer to which children are ubiquitously exposed) can induce the critical overlaps which are likely to be key in producing the “right” kind of damage to the brain, nervous system and immune system (via mitochondrial damage).

    Epidemics are said to be pretty simple according to unconflicted epidemiologists, but here’s where the problem is: if we’re causing it, and because vaccine sales went from $6 billion in 2006 to $40 billion today and the $5+ billion “autism drug market” being driven by drug industry front groups like Autism Speaks, the NIMH and a slew of other astroturf collectives, (which help drive the overall $40 billion dollar psychopharm market largely on the growing sales of drugs like SSRIs) there’s a huge and growing disincentive to ever pinpoint the “hole in the bucket” and “fix it” (dear Abner). Like any form of disaster capitalism, drippy “Awareness” campaigns are only meant to raise funds for multi-million dollar front group board member salaries and sell more “autism drugs,” not to actually resolve the very profitable epidemic.

    In any case, the “jury” may not yet be in regarding the cause of the autism epidemic, but the evidence table is piled high and the rise in rate clearly represents a genuine epidemic despite all flimsy claims to the contrary. A population of 1 in 50 people under age 24, 60% of whom are low- to non-verbal, could not have been “hidden” in society in the past nor hidden within mental institutions or SSRI/SSI rosters which had past per capita mentally disabled populations that were far smaller than the current rate of autism.

    Any search of PubMed can bring up substantiations for Dr. Jackson’s case study and the overlaps with mercury and SSRIs, but here’s a few links and a cut and paste of a discussion on overlaps:

    Thimerosal/mercury and disruption of tubulin assembly: http://www.icnr.com/articles/autism2002.html

    SSRIs and the disruption of tubulin assembly:
    http://ukpmc.ac.uk/articles/PMC2928987//reload=0;jsessionid=9AD6FB232485184363EAFC4BF41B33C3.jvm1 “Here, in rats submitted to a behavioural test widely used to predict the efficacy of antidepressant drugs (forced swimming test: FST) a significant decrease of both cerebral tyrosinated α-tubulin expression and serotonin levels is monitored.”

    SSRI antidepressants can also cause or worsen hyperammonemic encephalopathy, aka hepatic encephalopathy, which is the same principle discussed below in a correspondence with a professor emeritus of toxicology. Since the SSRI in pregnancy/autism study didn’t control for vaccination, there’s no way to know if the drugs are a direct cause of autism or co-factor, though Depakote appears to be a cause and again shares mito/cellular damage overlaps with SSRIs. From the professor of toxicology (bear in mind that the discussion of Depakote also applies to the toxic mechanisms of SSRIs):

    “I finally had time to read your attachment on Chemo brain. There are two biochemical items that infer that Depakote mimics the biochemical toxicity of mercury. First, it causes the elevation of serum ammonia. Mercury inhibits the brain enzyme called ‘glutamine synthetase’ which combines glutamate (an excito-toxic amino acid) with toxic ammonia making the non-toxic amino acid glutamine. Inhibition by mercury of glutamine synthetase therefore increases levels of toxic ammonia and glutatmate.

    “Second, according to your attachment Depakote has a metabolite that inhibits the assembly of tubulin. Mercury not only does this but can also unravel previously formed normal microtublin into abnormally polymerized microtublin that does not disassemble at low temperatures as does normal brain tubulin. There are many compounds that disrupt microtubulin or prevents is polymerization, mercury is one of the best and it is found in the mouths of many older Americans at gram levels and exposes them to toxic levels of mercury every day. Other compounds, like Depakote, could add to this exacerbation of microtubulin. Tubulin, the protein that aggregates and makes microtubulin is the major brain protein as it is found in the major structures that coat the neurofibillary fibers that hold an axon in the proper position for nerve-nerve interaction. It is this synapse between nerve-nerve cells that is destroyed in AD brain… over 85% of microtubulin is abnormal in AD brain and that mercury could mimic this effect if added to normal brain. So can drugs like Depakote. Many drugs were developed first to interfere with tubulin polymerization which is also needed in the mitotic spindle for cell division. They were hoped to be treatments for rapidly dividing cancer cells but many also tested for other medical uses. Many compounds interfere with tubulin polymerization…”

    • “The argument I’ve heard from many researchers is that autism boils down to affected cellular pathways. The various causes of the specific damage which result in autism spectrum disorders in children may be more than one single cause but will not be limitless…”

      ATG,

      Your comment is important; it should be a blog post, not just a well-conceived addendum to Adam Urato’s blog. What you say here is quite true and penetrating. (Considering the general facts you present and the way in which you’ve presented them, together – adding that couple of paragraphs, at the end, from the professor emeritus of toxicology, I presume you must have science credentials.)

      You’re uncovering a mystery, in a positively scientific search – with the punch of good journalism; just the slightest bit of added spit and polish, a byline and a few footnotes, this comment of yours could *easily* be published in any widely read ‘mainstream’ science periodical – no bull. (I am thinking Scientific American – or ScientificAmerican dot com’s ScientificMind…)

      Over the years, I’ve read so many reductive articles speculating upon the causes of this ‘epidemic’; your comment makes far more sense to me, than any one of them alone. Though, I do believe single factors could cause single cases, I believe there are a number of environmental toxins, which could be at cause, in any one given case.

      SSRIs alone will not account for many cases, but cumulative and synergistic dynamics…; were I you I’d consider how BPA and Phthalates may be added to the list of suspects. (Consider how many women began drinking water exclusively from plastic bottles, in the same period of time that the average number of neonatal vaccines went through the roof – and SSRI use exploded.)

      “Di-(2-ethylhexyl) phthalate and autism spectrum disorders”:

      http: //www.ncbi.nlm.nih.gov/pubmed/22537663

      “Bisphenol-A (BPA)”:

      http://health.westchestergov.com/bisphenol-a-and-phthalates

      Respectfully,

      ~Jonah

      P.S. — A general response to some of the other commenters: theories of presumed *brain* damage may be extremely misleading; if/when serotonin receptor sites are malfunctioning, improved ‘gut health’ may be key to any semblance of ‘recovery’ from the resulting syndromes.

      For more on that, check out…

      http://articles.mercola.com/sites/articles/archive/2011/07/31/dr-natasha-campbell-mcbride-on-gaps-nutritional-program.aspx?np=true

      • Jonah,

        Thanks for the response and the links. I’m involved in the media, not a scientist, and so far there’s been a pretty slow uptake in marrying these concepts in science but there is movement in that direction.

        Part of the problem is political and ideological: environmental autism researchers would have to take on the controversy ballast (and they have enough as it is) of psychopharm criticism; and then psychopharmaceutical critics would to stop fearing an admission that this one condition may, in fact, be the turf of medicine tacitly includes an admission that depression and the rest are as well. And I also sense that certain pharma watchdogs want to hang onto the few stray pediatricians among their supporters who are on board with psychopharm reform but yet make their living off vaccinations. Everyone would have to stop delegating opinions outside their own specialties to their buddies in those unfamiliar fields, generally get out of their respective comfort zones and dig into the science.

        Autism is medical the way a blow to the head with a brick is medical or alcohol-induced brain and physical damage. Anyone who’s spent time around it in real life can even see the evident physical manifestations of past encephalopathic and physical events. That doesn’t mean kiddy fidgeting or sadness is the territory of medicine or psychiatry or due to so-called brain chemical imbalance– and the “pathways” in question seem to have have as much or more to do with mitochondrial and immune systems than brain chemicals per se, or at least brain chemicals are secondary signs, not the immediate scene of the crime. But I’m afraid this area of research represents an intersection where all “angels” and potential whistleblowers fear to tread. The cooperative research is at last happening, but not at light speed.

        The SSRI in pregnancy/autism study followed an earlier study which found that SSRIs in the water supply were causing fish to act “autistic” (in fish terms, whatever that means. Then the pregnancy study was followed by a stealthy Harvard study which, though it actually largely measured the link between high rates of SSRI use among female abuse survivors (they’re prescribed the drugs at five-fold the already high 1 in 10 rate of the general pop) and their subsequent elevated rate of having children who were eventually diagnosed with autism, the media crowed that it was the abuse itself which was linked to increased risk.

        The cynical manipulation tells you someone already knows the mechanisms by which the meds are contributing to the condition and now they’re just figuring out how to spin it before the lid blows off, muddy the waters a bit. I’m sure we’ll be seeing more tobacco science making oblique correlations between highly drugged populations in studies which either don’t control for drugs or simply count on the media to highlight only the expedient, pharma-friendly results. The obvious goal is to quarantine the cause back to families of origin– their bad genes or bad lifestyles– in the minds of the public and consequently take the onus off pharma and other industrial culprits (big polluters, Big Ag, etc.)– the usual. Affected families and individuals will be further marginalized, stripped of services and support as a result of the quarantining spin (and worse), but no worries as long as everyone’s sacred cows, profits, reputations and ideology remain comfy.

        I agree about BPA by the way. It meshes with research on mercury and other metals as metallo-estrogens. These things coupled with hormones in milk and meat could go a long way towards explaining a generation of seven year-olds who are going into puberty. Mercury is also being found to change the sexual characteristics and behavior of wildlife, leading one crazy Italian journalist to suggest it was causing homosexuality (talk about reductive). Probably more to the point is that mercury is synergistic with testosterone and an excess of estrogen has been found to cause a backlash in the hormone feedback system, surprisingly causing a boost in androgens in some cases (something which is known in commercial fertility science). I have no idea what role this may play in autism, but it all certainly needs a harder look than it’s getting.

        In the meantime, it’s great to see that some are starting to question the spin.

      • Probably, most psychiatrists would read “autism boils down to affected cellular pathways” as a variation on the “diseased brain circuit” theories.

        After all, most psychiatrists tend to be obsessed with the brain; most make a fetish of it – even as they abuse it, endlessly, with psychopharmceuticals…

        Regarding almost any seemingly ‘mysterious’ suffering, psychiatrists are notorious for *presuming* (and/or, pretending) to ‘know’ that the brain is, ultimately, at fault; that’s their way to ‘justify’ tampering with the brain.

        In their endless attempts to ‘treat’ supposed “mental illness,” they strike wildly at the brain, they create nothing but misery.

        Of course, unlike so many theoretical “mental illness,” ‘autism’ can be considered a ‘neurological disorder’; though, I don’t believe one must accept that definition, one can — in which case, one may care to consult a neurologist for advice.

        But, why take any child who’s apparently affected by autism, to a psychiatrist? I’d avoid psychiatrists altogether.

        (Personally, I would *not* take this group of kids – nor any other kids – to a psychiatrist… unless, maybe if it was the extremely rare psychiatrist sort of psychiatrist who is strictly opposed to drugging kids… and strictly opposed to forcing ‘treatments’ on anyone.)

        Moreover, in the case of apparent autism, I’d avoid neurologists — because, in my opinion, no good comes of ‘medically treating’ autism.

        To me, “autism boils down to affected cellular pathways” means exactly what it says (i.e., it seems quite plain to me, that no focus upon the brain is necessary); I say this not to deny any possibilities of brain injury existing.

        Simply, I know that the nervous system is spread throughout the body; and, imho, toxic chemicals (of various kinds, including but not limited to psychopharmaceuticals) are harming many, countless persons’ nervous systems – including the nervous systems of countless, as yet, unborn infants…

        Such chemicals are causing the epidemic being addressed on this Web page…

        In my humble opinion, good ‘gut health'(including good nutrition) is key to ‘recovering’ from such damages.

        (But, “recovering” may not be the best word to employ here; “healing” may be better – but even that word may be somewhat misleading, as I am suggesting a kind of ‘healing,’ which, in many instances, requires, ultimately, an acceptance of some *seeming* ‘handicaps’.)

        In any case, I feel, it is best to avoid drugging these kids…

        _________________________

        “Hope For Autism & Asperger’s Syndrome: My Story”

        http://www.youtube.com/watch?v=OV_CcmLlaw4&feature=related

        “Forget What You Know: Jacob Barnett at TEDxTeen”

        http://www.youtube.com/watch?v=Uq-FOOQ1TpE

  4. You should be concerned whenever anyone takes an SSRI. SSRI’s are arguably the greatest medical scam ever. Has anyone here read our very own Carl Elliott’s White Coat Black Hat or Toxic Psychiatry? It seems like no one has or else you would realize this. Getting into the intricacies of SSRI efficacy is like getting into the intricacies of Bernie Madoff’s ponzi scheme. It’s all fraud.

  5. As I commented on Dr. Kelly Brogan’s post regarding medicating pregnant women https://www.madinamerica.com/2013/03/to-medicate-or-not-to-medicate-that-is-not-the-question/ :

    Neonatal withdrawal syndrome is well documented. Like adult withdrawal syndrome, it is assumed to last only a few weeks. In neonates, this is when the baby stops continually crying and spasming.

    However, in adults, withdrawal syndrome may last quite a bit longer than a few weeks, sometimes into a lengthy post-acute withdrawal syndrome (PAWS) phase, as with other drugs of dependency — see https://www.madinamerica.com/2013/03/alarming-report-on-antidepressant-side-effects/ .

    The authors of the above-referenced paper, based on anecdotal patient reports, refer to a “postwithdrawal phase, consisting of tardive receptor supersensitivity disorders.”

    We really don’t know what’s going on with neonatal withdrawal syndrome. The baby might stop crying and twitching, but may be suffering the newborn version of depersonalization (for example) for months or years, as adults do.

    Let us hope that neonatal neuroplasticity compensates and accelerates recovery from the supersensitivity disorders, and does not devolve into, say, autism.

    Allow me to add: Hypersensitivity to various stimuli and neuroactive drugs, supplements, and even foods is a very, very common withdrawal symptom when adults go off antidepressants too precipitously. Who knows what these tiny babies are experiencing?

    • Yes, my OB/GYN is much more aware of adverse effects of psychiatric drugs on women than most psychiatrists. She said she’s seen lots of adult withdrawal syndrome and neonatal withdrawal syndrome.

      She’s totally anti-psych drug now, a pharma skeptic among the best of them! She loved the copy of Anatomy of an Epidemic I gave her.

  6. The primary reason for the rising rates lies in nothing more than overdiagnosis. The vast majority of that diagnosis has been in Aspergers for people who are simply shy and nothing else. Since when has shyness been a brain disease. Well everything is to psychiatry – I’m waiting for breathing to become a brain disease, but when it comes to the community at large nothing suprises me. Any child who throws a temper tamptrum due to never having been told no at any time in there life is labelled as Autistic. Children who have pacifiers stuck in there mouths, as parents never take them from them, are labelled as autistic when there speech is delayed, as they can’t speak they have plastic permanently in there mouths. Teenagers who move from remote communities to massive inner city schools and are overwhelmed on the first day are diagnosed as Autistic. Children who have no consistent caregiving and have major attachment issues are labelled as Autistic. The average child now experiences less than one hour a day of quality time with there parents. The average family dog gets more. Then we wonder they children have problems. Everything is Autism today.

    I agree fully that SSRI’s and a million other things all contribute to a child’s development. Of course if a mother is taking SSRI’s they are usually doped up and hence less attentive to the child to begin with and while not abusive, children in that situation require more nurturing contact with parents. Much easier to believe that Autism is a real brain disease than to admit that we are now labelling everything as Autism, much the same as we label any sad feeling as depression.

    Lets also not forget the research that shows that parents who massage there babies every day have significantly lower levels of Autism, even when other risk factors are accounted for, and for those that are diagnosed, they show much better prospects for living fuller and healthier lives, and not being as locked into the behaviour. But this does not fit with brain disease theories, so we can’t let is have any role.

    • “The primary reason for the rising rates lies in nothing more than overdiagnosis. The vast majority of that diagnosis has been in Aspergers for people who are simply shy and nothing else.”

      Belinda,

      It may be true that a major reason for the rising rates lies in overdiagnosis; but, I’m not sure if it’s the primary reason.

      Certainly, overdiagnosis is occurring; but, I believe claims of an ‘epidemic’ of autism may be due to far more than just diagnostic inflation; significantly increased rates of *undisputable* cases of “autism” are a proven reality, I believe; and, I do believe the identification of “autism” can be scientifically validated — making it a legitimate diagnosis.

      (In fact, ‘autism’ is a diagnosis with relatively solid scientific validity — if and when carefully observed; that’s why, personally, I am careful to *avoid* placing ‘autism’ in the realm of so-called “mental disorders” — which is, of course, the territory of psychiatrists; the ‘diagnosing’ of so-called “mental disorders” is pseudoscience; those ‘diagnoses’ are highly subjective judgment calls.)

      Here’s a link to a study abstract regarding, “Diagnostic Observation Scale for Autistic Disorders: initial results of reliability and validity” http://www.ncbi.nlm.nih.gov/pubmed/14992047 It’s not easy for a layman to interpret such a study; but, I encourage people who may be interested in this issue to Google (and learn about) “kappa” scores for ‘autism’ in comparison to such scores for so-called “depression” or “bipolar” or “childhood bipolar”.

      In fact, the seeming ‘epidemic’ of so-called “childhood bipolar” is, beyond any shadow of a doubt, a complete fabrication of psychiatric myth-making (driven by the machinations of Big Pharma).

      The seeming ‘epidempic’ of “depression” is very largely a fabrication, too.

      The same is not true (at least, not to nearly the same extent) when it comes to autism.

      At least, such is my conclusion — based on my study of these issues.

      Thus, I must disagree with you, when you say, “we are now labelling everything as Autism, much the same as we label any sad feeling as depression.”

      The diagnosis of “autism” is placed on a ‘spectrum’ — from mild to severe, and the incidence of ‘severe autism’ is very much on the rise.

      Autism that’s not mild, when properly identified, is nothing like mere ‘shyness’ (not by a long-shot).

      So…

      RE your statement, that, “The vast majority of that diagnosis has been in Aspergers for people who are simply shy and nothing else,” I believe the DSM-5 is eliminating the “Asperger’s” label.

      You may be aware of that, and you may not appreciate that first Youtube I’ve offered, above (“Hope For Autism & Asperger’s Syndrome: My Story”), because it’s focus is upon a young woman who was diagnosed with “Asperger’s”; and, so, you may feel she was just ‘shy’ to begin.

      However, the second Youtube recommendation (“Forget What You Know: Jacob Barnett at TEDxTeen”) could be of interest to anyone who’s intrigued by this subject — as the young man giving the talk describes what he’d experienced, early on, as effects of autism. (If you watch it, you’ll see that he’s describing something quite different from mere shyness.)

      Here’s a link to an article titled, “Autism as a Disorder of Complex Information Processing”: http://www.lavc.edu/child_development/Autism%20as%20a%20disorder%20of%20complex%20information%20processing.pdf

      Respectfully,

      ~Jonah

      • “…The surge in autism is similar to the rise in childhood asthma, which has reached epidemic proportions for unexplained reasons. Medical officials originally thought that, too, might be due to increased reporting of the disease, but now they acknowledge that many more children are asthmatic than in the past. Experts suspect that environmental pollutants or immune changes could be responsible…”

        That’s from a very readable article titled, “New Study: Autism Linked to Environment” (dated January 9, 2009)

          • Jared— some good links, thanks.

            It’s not necessary to even partly concede to the better diagnosis explanation– it does not explain and doesn’t hold water.

            http://www.ucdmc.ucdavis.edu/welcome/features/20090218_autism_environment/

            The only solid epidemiology on prevalence changes states the rise in autism cannot be “better diagnosis/increased recognition.” “Better diagnosis” not only doesn’t account for a majority of cases but a bare single digit percentage of cases. There is absolutely no peer reviewed science to back the “better diagnosis/increased recognition” claim– this is merely mainstream spin, a bit like the claim of SSRI “brain chemical imbalance correction” that everyone spouted for years (and some still do).

            Furthermore, the vast majority with autism are not high functioning and could not, even if they had existed at these rates in the past, have fallen under the diagnostic radar. Only distant bystanders to autism– those who idly believe or convince themselves the bulk of the affected population is “just a little quirky”– or invested spin doctors even attempt to make this argument.

            What’s more, since the general rate of mental disability has skyrocketed in the pharma/industrial age, there’s the question of WHERE such an enormous, severely disabled population would have been hidden. The common claim is that they were hidden either under other mental illness diagnoses like schizophrenia or hidden within the ranks of the “intellectually impaired” (aka, the non-PC term, “mentally retarded”).

            As for the latter, attempting to argue that individuals with autism in the past were hidden within a “mentally retarded” population is tantamount to admitting that most were and are severely disabled– not the shiny genius version of autism promoted by front groups who want to lull the public into believing the rise is “no big deal” (even as the cost of care is exploding with the rate).

            To even entertain the idea that the current rate of autism was hidden within the ranks of the simply intellectually impaired for a moment, the big problem with this theory is that the rate of mental retardation has remained very stable over the past and previous century. The population with intellectual challenges is the same as far as rate… and now there’s the autism population beside it. So either autism has risen while intellectual impairment has gone down or vice-versa– somewhere there’s an epidemic which again points to environment. In any case, the above theory is impossible, the numbers simply don’t work. Fortunately those who try to spin autism as just “quirky” rarely visit that theory because it makes the case the population can’t fall “under the radar” and were not all Danial Tammets.

            As for the second idea, that individuals with autism were “hidden” under other diagnoses, the question is, hidden where? Here’s a table from Robert Whitaker’s “Anatomy of an Epidemic” derived from SSI/SSRI, NIMH and Census Bureau stats for mental disability:

            Year Mental Disability per 1000
            1850——- .2
            1903——- 1.86
            1955——- 3.38
            1987——- 13.75
            2003——- 26.2

            And here’s the rate of autism overlapping some of the same years only for those under 18:

            1850—— no reported cases
            1903—— no reported cases
            1955—— not statistically significant
            1970—— 1 in 14,500
            1987—— 1 per 10,000
            2003—— 1 in 166
            2004—— 1 in 150
            2011—— 1 in 110
            2012—— 1 in 88
            2013—— 1 in 50

            Try to do the math on these figures and then remember the UC-Davis study is the only standing, solid research on change in prevalence. The rest is media myth. Even if every other type of mental illness within any age group were supplanted in 1987, the disabled mentally ill population from just 26 years ago could never “hide” the current rate of young people with severe autism. The rate of autism would still overflow it.

            It’s simply wishful thinking to try to make this “increased recognition” theory fit or worse– a totally faith-based adherence to industry spin which has a serious investment in casting autism as genetic (to the tune of $5 billion in “autism drug” sales coupled with increasing evidence of culpability for the epidemic).

            Some try to argue again that most with autism are so high functioning that they once evaded diagnoses. If this is true, then there should be serious alarm that autism has become so much more severe that 40% are nonverbal and 70% will never be independent. Try to fit 40% or 70% of the current 1 in 50 children (1 in 31 boys) into the stats for 1955.

            There is no evidence of similar current numbers of affected people over age 24. There was one pharma funded study in the UK which purported to find 1/100 adults with the condition but a colleague of Brugha blew the whistle on the research, demonstrating that the methods were unsound– tiny sample diagnosed over phone interview and without using any of the standard tools to screen for childhood onset. It was concluded the study may have been cynically measuring instead adult onset prescription drug injury, precisely because, as Breggin warned and as the SSRI-pregnancy-autism study may hint, SSRIs and other drug classes are known to produce in children and adults very similar symptoms to autism such as social withdrawal, speech and memory issues, OCD, etc.

            It’s curious to see who falls for the “increased recognition/better diagnosis” malarkey– people who usually pride themselves on reading between the lines of media or who claim to be critical of industry spin. The “increased recognition” is the most in-the-box, conformist view– on top of simply being demonstrably wrong and in service to an extremely evident agenda.

            Autism is not grab-bag like ADHD. We’ve all heard NPR (J&J) and Slate (Bill and Melinda Gates/pharma) trying to cast autism as something only a hair away from typical, just kind of pleasant and quirky. But this is autism for most: https://www.youtube.com/watch?v=PzYREX0jrY4

            All the spin does is leave the majority of severe children like this without medical support for the actually physical injuries involved with the etymology of the condition. The video is from the UK and, due to the genes/gut-brain-injury debate, many children there are literally left to die of GI disorders when they come in tow with autism.

            I’m sure those in a time warp who never heard that the “refrigerator mother” theorist faked his credentials, was repeatedly accused of child molestation and committed suicide will comment that the child is this way because of parental abuse or whatever, but it hardly explains how parenting became so much worse in the past twenty years (since eras of slavery? Since eras of legal child thrashing? Since legal domestic violence??) that there are 70% of 1.5 million children who are arguably this severely impaired in the US (give or take a few more words in a very limited vocabulary)– more than 1 million, 50 thousand– or why so many terrible cases of trauma are seen in children without any autism symptoms.

            Lies kill, even PC-sounding I’m-so-evolved-I-embrace-disability kind of lies. No need to give them any credence or parse the difference for the sake of diplomacy. It’s very tragic.