Antidepressants in Pregnancy Tied to Autism Risk ;
Dr. Sarah A LoBisco, ND
originally published in NDNR.com
A recent Canadian study sought to examine whether there was an associate for autism spectrum disorder (ASD) in children whose mothers used antidepressants during pregnancy risk. 03.01 The researchers identified only 145.456 term deliveries a population-based cohort ongoing took place from 1998 to 2009, Québec pregnancy / child cohort. the antidepressant exposure was defined by quarter and class of antidepressants. 1 Assessment of drug use was based on mothers who had at least one prescription filled during their second or third trimester, a time of critical brain development. 3 one thousand fifty-four children were identified with ASD based on at least 1 diagnosis between your birth date and the last follow-up. Boys outnumbered girls in the diagnosis of 4 :. 1 1
According to Health Day
There were 4,724 infants exposed to antidepressants, while her mother was pregnant; about 89 percent were exposed during the first quarter and 54 percent during the second or third trimester.
The researchers found that the use of antidepressants in the second or third trimester appeared to increase the risk of autism by 87 percent. previous use of antidepressants do not seem to have an effect.
SSRI use, in particular, more than twice the risk of autism in a child, the study authors said. 2
The study concluded: “The use of antidepressants, selective reuptake inhibitors specifically selective serotonin during the second and / or third trimester increases the risk of TEA in children, even after accounting for maternal depression. ” 1
This is not the first study to examine the relationship between autism with the use of antidepressants in mothers-to-be. 05.06 Could it be that the increased use of antidepressants in mothers is affecting autism rates? 3.4 Perhaps, but it is likely that one of the many factors.
Autism is a multifactorial disease and epigenetic influences during pregnancy can have profound effects on cognition and brain development. Antidepressants are one such epigenetic influence. Several studies have examined this impact. 7-11
In a study in 2012 stated:
Until now, most studies investigated the genes within the hypothalamicpituitary- adrenal axis (HPA ) or neurotrophin system. Also of interest is that current psychopharmacological drugs including antidepressants, antipsychotics and mood stabilizers may exert some of their effects by inducing epigenetic changes is. In particular epigenetic alterations are potentially reversible and accessible drug treatment, leading to the development of new classes of antidepressant drugs. 8
antidepressants In 2014, an effect on DNA methylation was found:
Amitriptyline and imipramine tricyclic antidepressants, but also the SSRI paroxetine was shown to reduce the promoter DNA methylation in rat primary astrocytes, possibly by reducing DNA methyltransferase 1 activity.57,58 The mood stabilizer and the anticonvulsant valproate can induce an overall reduction in the levels of DNA methylation observed in human embryonic kidney cells and rat liver cells.59,60 Furthermore, the antipsychotic sulpiride and clozapine could activate demethyiation DNA in the frontal cortex and striatum. 9
Moreover, a 2008 study reported:
modifications of chromatin in specific promoters BDNF determine the differential expression of variants BDNF splice discrete. Such modifications have been observed in Alzheimer’s disease 128 and can also be caused by particular antidepressant drugs73.1-
However, it is important to remember other factors mother and baby environment can alter risk of autism and could be synergistic with the modifications of antidepressants. For example, it was found that environmental stress can affect DNA methylation of CpG rich promoter region of the serotonin transporter gene ( SLC6A4) a nurse cohort. 11
Another epigenetic modulator is diet 13 Certain nutrients are important for brain development and antidepressants reduce their availability 14 a study examining the role of “brain foods” reported:
These studies represent a starting point for understanding how intracellular signaling triggered by factors of lifestyle can promote lasting changes in the function of DNA in the brain and cognitive ability. regulator information silent 2 (SIRT2), a member of the sirtuin protein family, has become an important modulator of genomic stability and cellular homeostasis that appears to act silencing function of specific genes. A diet that is high in saturated fats reduces the expression of SIRT2 in the rat hippocampus 90 , whereas a diet that is high in omega-3 has the opposite effect2.13
Therefore, a mother who is depressed with a poor diet and taking antidepressants may have three strikes against her baby epigenetic modification of his / her brain development. This could modulate the risk of health problems in children.
Moreover, antidepressants can not address the root cause of depression, so that epigenetic changes a factor in the top of the underlying problems. 14-19 For example, the theory of depression cytokine binds uncontrolled oxidative stress or depression inflammation. 15 Immunotoxicity 15 genetic variations 16 alterations in the gut microbiome and 18-19 exposure to pesticides 19-20 changes in hormonal responses (which neurotransmitters impact) 21 and mitochondrial dysfunction 24 are also considerations to address brain and cognitive health the mother and baby. Taking into account these factors, epigenetic factors on top of them can increase the risk of autism even more.
In summary may be a link with antidepressants and autism risk due to the effect of medication on this interaction epigenetics and many other factors.
Interestingly, I just read another study linking antidepressant use with the risk of bipolar manic episodes and later users. 25-26 cycle address a symptom only look at a possible mechanism and manipulating one via continue to create other symptoms. That is why, as professional naturopathic and functional medicine, we can help stop the cycle by finding all the factors involved and address the underlying cause.
Sarah Lobisco, ND , is a graduate of the University of the University of Bridgeport naturopathic medicine (UBCNM). She is licensed in Vermont as a naturopath and has a degree in psychology from the State University of New York at Geneseo. Dr. LoBisco is a comprehensive health speaker, has several publications, and is a candidate for certification in functional medicine. Dr. LoBisco now incorporates her training as a naturopathic doctor and practitioner of functional medicine through writing, research, private practice, and through independent contract work for companies regarding supplements, nutraceuticals, essential oils and food medical. She has a small, private practice wellness consultation via phone and Skype. Dr. LoBisco also enjoys continuing to educate and train their readers through their blogs and social media.
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