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In pregnancy, subclinical hypothyroidism is defined as a TSH between 2.5 and 10 mIU/L with a normal thyroxine level, while those with TSH above 10 mIU/L are considered to be overtly hypothyroid even if the thyroxine level is normal. [44]
Thyroid hormones, T4 and TSH, diffuse across the placenta traveling from the mother to fetus for 10–12 weeks before the fetus’s own thyroid gland can begin synthesizing its own thyroid hormones. [2] The mother continues to supply some T4 to the fetus even after he/she is able to synthesize his/her own.
Thyroid hormone concentrations in blood are increased in pregnancy, partly due to the high levels of estrogen and due to the weak thyroid stimulating effects of human chorionic gonadotropin (hCG) that acts like TSH. Thyroxine (T4) levels rise from about 6–12 weeks, and peak by mid-gestation; reverse changes are seen with TSH.
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T 4), and then triiodothyronine (T 3) which stimulates the metabolism of almost every tissue in the body. [1]
According to a study conducted by Whitcome, et al., lumbar lordosis can increase from an angle of 32 degrees at 0% fetal mass (i.e. non-pregnant women or very early in pregnancy) to 50 degrees at 100% fetal mass (very late in pregnancy). Postpartum, the angle of the lordosis declines and can reach the angle prior to pregnancy.
This is because ovulation stops during menopause and slows down during breastfeeding.
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