Hormonal Influences on Fetal development

Fetal Development is Dependent on Hormones

Besides genetic potential and availability nutrition, optimal fetal development is influenced by number of hormones.

30 different hormones are secreted during pregnancy and are regulated by the complex interactions of mother’s, fetal and placental endocrine systems.

Placenta is the major control station for fetal hormones. It produces its own hormones and prevents the mother’s hormones to flood fetal circulation.

Alcohol consumption during pregnancy is disastrous for the intricate balance of hormones essential for its favourable outcome.

Thyroid Hormone is essential for normal fetal development

Pregnancy increases the demand on maternal thyroid gland to produce more thyroxin. High levels of estrogen during pregnancy influence mother’s thyroid gland to meet the requirements of thyroid hormone for both the mother and the fetus.

Mother’s thyroid hormone can easily cross placenta. Maternal thyroxin is crucial for normal development of fetal brain. It also contributes to growth and maturation of other fetal organs including the lungs. Babies of hypothyroid mothers are abnormal at birth.

Thyroid hormone from fetus itself becomes available only from gestational age of 12 weeks. Even with congenital absence of thyroid gland fetal development is normal till birth. Baby’s own thyroid hormone becomes essential for infant brain development only birth on wards. The real danger arises when a mother’s system cannot meet the demand.

Hypothyroidism in pregnancy occurs when a subclinical hypothyroid mother conceives. It is seen in 2 - 2.5 percent of expecting mothers by 15-18 weeks of gestation.

Mothers with sub-optimal thyroid hormone levels during pregnancy risk:

Pregnancy loss
Increased perinatal mortality due to eclampsia and abruption placenta
Low birth weight baby with immature lungs and marred brain development.

Alcohol consumption diminishes thyroid hormone secretion in a pregnant women.

Another cause of sub-clinical hypothyroidism is autoimmune disease, where the anti-thyroid antibodies cross the placenta and damage the fetal thyroid gland as well.

Women with undiagnosed clinical hypothyroid state cannot conceive. Hypothyroidism is associated with infertility.

Iodine supplementation

Pregnant women should take adequate iodine in their diet throughout the pregnancy for optimal fetal development.

The World Health Organization recommends an iodine intake of at least
200 micrograms per day during pregnancy to prevent intrauterine brain damage associated with low thyroid hormone levels.

Iodine is essential for normal production of thyroxin. Adequate intake of iodine supplements by an expectant mother helps maintain her and the fetus’ thyroid functions to the optimal.

Iodine deficiency in diet can result in inadequate thyroid hormone levels to support fetal brain development. The irreversible fetal brain damage that follows is seen in affected newborns as cretinism, mental retardation,
deaf-mutism and spasticity.

Insulin

Insulin plays a key role in stimulating fetal growth.
Fetal pancreas begins secreting insulin by the tenth week of gestational age.

Mother’s insulin does not cross placenta. Fetus has to meet its own needs. Insulin levels in fetal blood are controlled by its glucose concentration, which are directly proportional to mother’s blood glucose levels.

Fetal insulin activity attributes to fetal growth variations

Excessive weight gain is seen in infants of uncontrolled diabetic mother resulting in “Large for Date” babies.
If mother’s diabetes is well controlled through out the pregnancy, fetal development is normal.
A mother with severe uncontrolled diabetes could also have
“Small for date” baby. Fetal growth retardation occurs due to compromised uterine blood flow secondary to diabetes induced atherosclerosis (narrowing and hardening of the blood vessels).
Congenital absence of fetal pancreas or genetic deficiency of insulin receptors in the fetus are also characterised by severe intrauterine growth retardation.

Insulin like growth factor (IGF)

Insulin like growth factor is structurally related to insulin and also has some insulin like metabolic activities. It is involved in regulation of uterine and placental growth during pregnancy.

It is found in two active forms; IGF1 and IGF2. The structure and action of IGF2 in the fetus and placenta is determined by father’s genes.

Insulin like growth factors and their receptors are present almost in all fetal tissues except in fetal brain. In blood circulation, it is bound to IGF-binding proteins, which appear from 5 weeks of gestation.

Fetal growth, both somatic and that of its organs, is favourably influenced by IGF2, but the cord blood levels of IGF1 are found to be directly proportional to birth weight and length of the neonate. This is probably because IGF2 exerts most of its growth effects during the early phase of fetal development.

Provision of constant adequate nutrition is essential for regulating IGF production during fetal development.

This also holds true for the postnatal phase of child growth, when insulin like growth factor mediates the action of growth hormone.

Influences of Prostaglandins on fetal development:

Maturation of cardio-pulmonary system:

Prostaglandin E2 (PGE2) maintain the patency of Ductus Arteriorus during fetal life, which is crucial for survival of the fetus.

Leukotreines maintains pulmonary vasoconstriction during the intrauterine life.

Lung maturation

Prostaglandin D2 (PGD2) along with Prostacyclin promptly induces pulmonary vasodilatation soon after birth
Initiates childbirth process

Progestrone supports fetal development by:

Suppressing uterine activity
Decreasing mother’s immune response against fetal antigens

Glucocorticoids are essential for fetal development

Fetus’ own cortisol and cortisone are the most important hormones regulating fetal tissue maturation.

Cortisol levels increase continuously during the third trimester and are dramatically elevated in face of anxiety and in chronic stressful conditions.

Consumption of alcohol during pregnancy stimulates glucocorticoids secretion in the mother. Both alcohol and high levels of glucocorticoid cross the placenta and disturb fetal endocrine system, thereby restricting fetal development as seen in fetal alcohol syndrome.

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