Monozygotic twins split into two zygotes at some time very early in the pregnancy. The timing of this separation determines the chorionicity (the number of placentae) and amniocity (the number of sacs) of the pregnancy. Dichorionic twins either never divided (i.e. : were dizygotic) or they divided within the first 4 days. Monoamnionic twins divide after the first week. In very rare cases, twins become conjoined twins. Non-conjoined monozygotic twins form up to day 14 of embryonic development, but when twinning occurs after 14 days, the twins will likely be conjoined. Furthermore, there can be various degrees of shared environment of twins in the womb, potentially leading to pregnancy complications. It is a common misconception that two placentas automatically implies dizygotic twins, but if monozygotic twins separate early enough, the arrangement of sacs and placentas in utero is in fact indistinguishable from that of dizygotic twins. Demographics
A 2006 study has found that insulin-like growth factor present in dairy products may increase the chance of dizygotic twinning. Specifically, the study found that vegan mothers (who exclude dairy from their diets) are one-fifth as likely to have twins as vegetarian or omnivore mothers, and concluded that "Genotypes favoring elevated IGF and diets including dairy products, especially in areas where growth hormone is given to cattle, appear to enhance the chances of multiple pregnancies due to ovarian stimulation. "From 1980 to 1997, the number of twin births in the United States rose 52%.
Miller syndrome, also known as Genée–Wiedemann syndrome, Wildervanck–Smith syndrome or postaxial acrofacial dystosis, is an extremely rare genetic condition that manifests as craniofacial, limb and eye deformities. It is caused by a mutation in the DHODH gene. The incidence of the condition is not known, and nothing is known of its pathogenesis. Presentation
The syndrome consists of severe micrognathia, cleft lip and/or palate, hypoplasia or aplasia of the postaxial elements of the limbs, coloboma of the eyelids and supernumerary nipples. Additional features of the syndrome include downward-slanting palpebral fissures, malar hypoplasia, malformed ears, and a broad nasal ridge. Other features include supernumerary vertebrae and other vertebral segmentation and rib defects, heart defects (patent ductus arteriosus, ventricular septal defect and ostium primum atrial septal defect), lung disease from chronic infection, single umbilical artery, absence of the hemidiaphragm, hypoplasia of the femora, ossification defects of the ischium and pubis, bilobed tongue, lung hypoplasia, and renal reflux. Cause
The gene responsible for this disorder is DHODH located at chromosome 16q22. This gene encodes an enzyme – dihydroorotate dehydrogenase – which catalyses the ubiquinone-mediated oxidation of dihydroorotate to orotate, the fourth enzymatic step in de novo pyrimidine biosynthesis. The protein is normally located on the outer surface of the inner mitochondrial membrane. Genetics
A mutation in this gene was reported by Morgan in 1910 in the fruit fly Drosophila melanogaster. In the fly this mutation is characterized by wing anomalies, defective oogenesis, and malformed posterior legs. In humans Miller syndrome is due to recessive mutation in the DHODH gene.