Nearly every cell in the body requires the thyroid hormones to function. Thyroid hormones are involved in almost all phases of reproduction and the thyroid gland continuously interacts with the ovaries. Thyroid dysfunctions are common among women of reproductive age and can affect fertility in various ways. If the woman is even marginally hypothyroid, she can’t produce and regulate the sex hormones oestrogen and progesterone necessary for ovulation of a mature egg and provide the endometrium with the mucus necessary to accept and hold the implanted embryo. Altered thyroid hormone levels are associated with disturbed folliculogenesis, a lower fertilization rate, and lower embryo quality. High prolactin level and PCOS are also associated with thyroid deficiency. Undiagnosed and untreated thyroid disease can be a cause of subfertility.
Therefore, screening for thyroid function should be performed as part of a preconception assessment for anyone trying to conceive.
If any of the following is applicable, a full thyroid assessment should be done as soon as possible.
Many cases of thyroid problems are missed because a comprehensive test has not been performed. Thyroid blood tests should include the following:
The TSH range is set statistically, with the lowest 2.5% of readings being defined as hypothyroidism and the top 2.5% being defined as hyperthyroidism. The broad “normal” range results in many people suffering symptoms of hypothyroidism without the benefit of diagnosis or treatment. Many people with Hashimoto’s autoimmune thyroid disease may have a normal TSH reading so this test alone cannot rule out the presence of thyroid disease.
The TSH range for fertility differs from that for the general population. Ideally, TSH levels should be monitored and lowered prior to fertility treatment and conception to reduce the risk of harm to the development of the baby and complications during pregnancy.
It is suggested that for optimal fertility, TSH should be at the lower end of the reference range, in the 1.0 – 2.0 mIU/L range. In general, TSH should not rise above 2.5 mIU/L during pregnancy. Hypothyroid patients undergoing treatment (receiving thyroid hormone replacement medication) who are planning a pregnancy should have their dose adjusted to optimize serum TSH values. Lower preconception TSH values reduce the risk of TSH elevation during the first trimester.
T4 and T3:
These are actual thyroid hormones acting at cellular and subcellular levels (nucleus and mitochondria) regulating the basal metabolic rate. A low level of T4 or T3 can produce symptoms arising from low cellular energy production. One should ensure that the T4 and T3 readings are in the middle of the normal range as that normal range is set so broad. The thyroid gland excretes 85% of T4 and only 15% of T3. T4, which persists in the blood for several days, acts as a reservoir, providing the body with a continual supply of the much shorter-lived T3. T3 is four times more potent than T4 and it controls the metabolic rate at the cellular level by modulating the rate of energy consumption in virtually every tissue in the body. The body tissues convert the low potency thyroid hormone T4 into the high potency thyroid hormone T3. So, this tissue-level control of T4-to-T3 conversion is potentially a huge determinant of the basal metabolic rate. The prescribed thyroid replacement medications (T4) such as Synthroid (levothyroxine) assume that it will convert into T3 but patients need to be tested to check if that is occurring as it is not a given. The enzyme that converts T4 into T3 is selenium-dependent.
Reverse T3 (rT3):
T4 can be converted into reverse T3 (rT3), which has no thyroid hormone activity at all, and which undercuts the basal metabolic rate. If no measurements are taken of T3 and rT3 levels, we have no idea of the relative contribution of activation and deactivation of the thyroid hormone.
Thyroid antibody is discussed in a separate article.