Vitamin A and oxytocin pathway dysfunction in autism spectrum disorder

¶ … Vitamin a for Autism Spectrum Disorder

The Theory of Using Vitamin a as Treatment for Autism Spectrum Disorders

There is widespread linkage of Autism Spectrum Disorders (ASD) and Oxytoxin. There are reports that any decrease in the pathway of Oxytocin, is a possible causative factor to the development of autistic situation (Munese-et-al., 2008). Decrease in Oxytocin comes about because of mutations in its receptors, which lead to a reduction on the amount of Oxytocin released to the body posing possible chances for the development of autistic conditions (Lerer et-al., 2008). There is partial dependency of Oxytocin secretion to a protein found, in the cellular membranes of certain red blood cells. The scientific reference of these proteins is CD38, and whenever they mutate there develops a risk of Autism. Mice engineered without the oxytocin receptor gene have been shown to display socially anomalous behavior such as a deficiency of maternal behavior in females and increased aggression in males (Nishimori et al., 2008). However, it has been theorized that administrating Trans Retionic Acid, treats autistic spectrum disorders. This is a treatment derived from Vitamin A and it helps in creating an increase in CD38 expression.

Relationship between oxytocin and CD38

There are several studies conducted by past researchers, to prove the relationship of the theory of using Vitamin A as treatment for autism spectrum disorders through animal experiments (Riebold et al., 2011). This may be a way forward towards ensuring that the situation stays under control and no longer becomes a life-threatening factor like in the past scenarios.)It is increasingly becoming common using animal studies; in substantiate the role neuropeptide Oxytocin plays in regulating social affiliation and attachments (Riebold et al., 2011). There is further evidence that of reduction of stress and anxiety affected by use of oxytocins. The results derived from animal studies are evidential enough to prove the role Oxytocin plays in the social human behavioral attachments within settings of social interactions (Munese-et-al., 2008).

This is possible proof that Oxytocin may be involved in the social interaction impairment of social attachments and interactions in cases of ASD (Autism Spectrum Disorders) (Wermter et al., 2010). In ASD etiology, the crucial gene in the human oxytocin is the receptor gene. There are reports of established relationships of ASD and oxytocin, and that CD38 is a major player in ASD etiology and overall availability or secretion of OT. This may be represented by phenotypic behavior differences correlating to ASD probands basal expressions (Wemter et al., 2010). There is also evidence that when CD38 reduces, there may be a chance of correction through its treatment with ATRA, which induces the secretion of Oxytocin (Riebold et al., 2011). There is also an evident association between oxytocin receptor (OCTR) and autism.

The determination of these claims have come from past experimental researches through mouse CD38 gene knockout demonstrations for studying the role of ADP-ribosyl cyclase with glycoprotein activity through the assistance of release of OT in the brain (Riebold et al., 2011). There are also reports that there is a lifetime influence, and there is no pathognomonic influence of reduction in CD38 transcriptions for ASD. CD38 may play a role in the causes of autism by modulating the central availability of oxytocin (Riebold et al., 2011). However, there may be some clinical values of diagnosis of disorders on the sole basis of behavioural assessments at 3 years of age. Furthermore, the CD38 expressions dependent of circulation on lymphocytes present potential foundation, for diagnostic indication of ASD (Riebold et al., 2011). However, it is reported that crucial need in ASD is within the early years of perinatal and prenatal diagnosis tools is the most effective. This may be better done through study of the levels of CD38 mRNA in the amniotic fluid and cord blood.

Administration of OXT for the treatment of ASD

As Higashida et al. (2012) states, some subjects of ASD subgroups having R140W SNP as well as intelligence disorder impairments. Research claims that the effective treatment of these conditions may be effective by using OXT. There exists evidence based ASD treatment using OXT as stated in Munesue et al., (2010), and some subgroups of ASD patients having reduced OXT plasma levels could be a potential contributor to benefits of replacement therapy of OXT.

Administration of all Trans retinoic acid (ATRA), which is a derivative of Vit A, increases CD38 expression, and may therefore be a useful treatment for autistic spectrum disorders (Munesue et al., 2010).

Given that Trans renoic acid, which is a derivative of Vit A, may have viable treatment capacity for autism, there is also the possibility that low levels of OXT are not just contributed by low CD38 SNP (Campbell et al., 2010). There are other factors, which influence its capacity, though there are no known reasons currently reported. Through studies on the neuroendocrinological relationships of CD38 and ADPR on secretions of OXT of human and mouse Hypothalamus, there exists a social role on human and mice behaviors dependent on CD38. Therefore, there may be OXT signal system defects involvement in ASD pathophysiology (Campbell et al., 2010).

Therefore, despite the growing interest in the use of vitamin A treatment for autism disorders, the practice still faces a number of challenges and requires further research. There is inadequate knowledge on the effect of the activity of CB38 resultant from social and environmental sensitive contexts (Campbell et al., 2010). From resent research, it is possible that CD38 contributes to the overall OXT secretion, though in may not have any relationship with the secretion of OXT upon empathetic psychological stimulation. Also, unknown are the other molecules, which interact with CD38 in the OXT secretion regulation. Campbell et al., (2010) states that, there is evidence indicating that oxytocin receptor (OXTR) is essential in a variety of social behaviors. There is an attempt for the determination of the relationship of genetic differences in the signaling system of oxytocin and ASD. Through sample sizes of 57-436 families, there was no identification of any associations between social behaviors of ASD subjects and OXTR polymorphism.