oxytocin and Diseases-in-Twins

Serotonin and vitamin D have been proposed to play a role in autism; however, no causal mechanism has been established. Here, we present evidence that vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues outside the blood-brain barrier at a distinct VDRE. The proposed mechanism explains 4 major characteristics associated with autism: the low concentrations of serotonin in the brain and its elevated concentrations in tissues outside the blood-brain barrier; the low concentrations of the vitamin D hormone precursor 25-hydroxyvitamin D [25(OH)D3]; the high male prevalence of autism; and the presence of maternal antibodies against fetal brain tissue. Two peptide hormones, oxytocin and vasopressin, are also associated with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and the arginine vasopressin receptor contain VDREs for activation. Supplementation with vitamin D and tryptophan is a practical and affordable solution to help prevent autism and possibly ameliorate some symptoms of the disorder.

Topics: Animals; Autistic Disorder; Autoimmunity; Black People; Blood-Brain Barrier; Brain; Brain Chemistry; Calcitriol; Digestive System Abnormalities; Diseases in Twins; Estrogens; Female; Fetus; Humans; Incidence; Inflammation; Male; Maternal-Fetal Exchange; Models, Biological; Mothers; Oxytocin; Pregnancy; Receptors, Calcitriol; Serotonin; Tryptophan Hydroxylase; Vitamin D; Vitamin D Deficiency; Vitamin D Response Element

Oxytocin (OT) is becoming increasingly established as a prosocial neuropeptide in humans with therapeutic potential in treatment of social, cognitive, and mood disorders. However, the potential of OT as a general facilitator of human learning and empathy is unclear. The current double-blind experiments on healthy adult male volunteers investigated first whether treatment with intranasal OT enhanced learning performance on a feedback-guided item-category association task where either social (smiling and angry faces) or nonsocial (green and red lights) reinforcers were used, and second whether it increased either cognitive or emotional empathy measured by the Multifaceted Empathy Test. Further experiments investigated whether OT-sensitive behavioral components required a normal functional amygdala. Results in control groups showed that learning performance was improved when social rather than nonsocial reinforcement was used. Intranasal OT potentiated this social reinforcement advantage and greatly increased emotional, but not cognitive, empathy in response to both positive and negative valence stimuli. Interestingly, after OT treatment, emotional empathy responses in men were raised to levels similar to those found in untreated women. Two patients with selective bilateral damage to the amygdala (monozygotic twins with congenital Urbach-Wiethe disease) were impaired on both OT-sensitive aspects of these learning and empathy tasks, but performed normally on nonsocially reinforced learning and cognitive empathy. Overall these findings provide the first demonstration that OT can facilitate amygdala-dependent, socially reinforced learning and emotional empathy in men.

Topics: Administration, Intranasal; Adult; Amygdala; Diseases in Twins; Double-Blind Method; Emotions; Empathy; Facial Expression; Female; Humans; Lipoid Proteinosis of Urbach and Wiethe; Male; Oxytocin; Photic Stimulation; Reinforcement, Psychology; Social Behavior; Young Adult

Topics: Adult; Anencephaly; Diseases in Twins; Female; Fetal Death; Humans; Infant, Newborn; Labor, Induced; Oxytocin; Pregnancy