The “Bad Father”: Paternal Role in Biology of Pregnancy and in Birth Outcome

Abstract

Pregnancy is generally studied as a biological interaction between a mother and a fetus; however, the father, with his characteristics, lifestyle, genetics, and living environment, is by no means unrelated to the outcome of pregnancy. The half of the fetal genetic heritage of paternal derivation can be decisive in cases of inherited chromosomal disorders, and can be the result of de novo genetic alterations. In addition to the strictly pathological aspects, paternal genetics may transmit thrombophilic traits that affect the implantation and vascular construction of the feto-placental unit, lead to placenta-mediated diseases such as pre-eclampsia and fetal growth retardation, and contribute to the multifactorial genesis of preterm delivery. Biological aspects of immunological tolerance to paternal antigens also appear to be crucial for these pathologies. Finally, this review describes the biological findings by which the environment, exposure to pathogens, lifestyle, and nutritional style of the father affect fetal pathophysiological and epigenetic definition.

Paradoxes: Cholesterol and Hypoxia in Preeclampsia

“…Several factors are widely recognized as increasing the risk of developing preeclampsia, including previous preeclampsia, chronic hypertension, pregestational diabetes, multiple gestation, pre-pregnancy BMI > 30, and antiphospholipid syndrome, with a lesser increased relative risk associated with a history of lupus erythematosus, stillbirth, pre-pregnancy BMI > 25, nulliparity, prior placental abruption, assisted reproductive technology, paternal factors [ 164 ], chronic kidney disease, advanced maternal age, and genetic susceptibility [ 1 ]. Although less generally noted, abnormal maternal serum lipids also convey an increased risk of preeclampsia, with reduced maternal serum omega-3 fatty acids increasing the relative risk 7.6 times, [ 5 , 165 , 166 ] elevated maternal red blood cell (RBC) TUFAs increasing the relative risk 3–7.4 times [ 3 , 167 ], and a high dietary intake of total PUFAs increasing the relative risk 2.6 to 5 times [ 4 , 14 ].…”