[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Physiology](https://durgical.com/en/physiology/) › [Reproduction, pregnancy and the fetus](https://durgical.com/en/physiology/areas/repro/) › Maternal hormones, metabolism and nutrition in pregnancy

# Maternal hormones, metabolism and nutrition in pregnancy

- Regulation
- Exam priority: medium

Pregnancy resets the mother's glands and metabolism to feed the fetus: more thyroid, cortisol and vitamin D activity, and planned insulin resistance.

Updated Nov 13, 2026

Also called: Gestational thyroid changes, Insulin resistance of pregnancy

## Key points

- First trimester: hCG weakly stimulates the TSH receptor, so free T4 rises a little and TSH falls; a low TSH alone is often physiological.
- Estrogen raises TBG: total T4 and T3 rise ≈ 50%, free hormone stays near normal; iodine needs and renal iodide loss rise.
- Calcitriol roughly doubles (renal and placental 1α-hydroxylase), doubling intestinal calcium absorption; PTH stays normal to low.
- Total calcium falls with albumin dilution, but ionized calcium is normal.
- CBG rises and placental CRH stimulates the axis: total and free cortisol rise, yet without Cushing features.
- Second half: hPL, placental GH, progesterone, cortisol and prolactin cause insulin resistance; if β cells cannot compensate, gestational diabetes appears.

## What it is

Placental hormones and high estrogen change nearly every maternal endocrine gland. Binding proteins rise, so total hormone levels go up while free levels stay near normal, and reference ranges change by trimester. Metabolism moves from storing fuel in the first half to releasing it in the second half, when insulin resistance diverts glucose to the fetus. Needs for energy, protein, iron, folate and iodine rise, and weight gain is expected within a range that depends on the starting BMI.

## Key facts

- Iron needs rise most in the second half; hemodilution lowers hemoglobin, so iron deficiency is common.
- Folate need rises early for DNA synthesis and neural tube closure, which happens before many women know they are pregnant.
- Iodine need rises because of more thyroid hormone production, renal iodide loss and fetal supply.
- Fetal skeleton takes about 25–30 g of calcium, mostly in the third trimester; maternal gut absorption, not bone, supplies most of it.

## How it works, step by step

- The anterior pituitary enlarges, mainly by lactotroph hyperplasia; prolactin rises about tenfold by term.
- Pituitary GH falls as placental GH takes over and drives IGF-1.
- Aldosterone, renin and angiotensin rise; progesterone partly blocks aldosterone at the kidney, so sodium is retained gradually.
- Early pregnancy is anabolic: normal insulin sensitivity and higher insulin store fat.
- Late pregnancy is catabolic for the mother: insulin resistance, lipolysis and quicker ketosis when fasting ('accelerated starvation').
- Glucose, amino acids and calcium are pulled toward the fetus while the mother burns more fat.

## Pregnancy reference points (approximate)

| Parameter | Value | Note |
| --- | --- | --- |
| Total weight gain, normal BMI | ≈ 11.5–16 kg | underweight 12.5–18; overweight 7–11.5; obese 5–9 kg |
| Extra energy need | ≈ +340 kcal/day (2nd), +450 kcal/day (3rd trimester) | almost none in the 1st |
| Total body water gain | ≈ 7–8 L | |
| Iron needed for the whole pregnancy | ≈ 1 g | fetus, placenta, larger maternal red cell mass |
| Prolactin at term | ≈ 10 times nonpregnant | |
| Total T4 | ≈ 1.5 times nonpregnant | free T4 near normal |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## Regulation

- *+* **hCG (first trimester)**: Stimulates TSH receptor: free T4 slightly up, TSH down.
- *+* **Estrogen**: Raises TBG, CBG and SHBG; stimulates lactotroph growth and prolactin.
- *+* **Placental CRH**: Drives ACTH and cortisol, rising toward term.
- *+* **hPL and placental GH**: Insulin resistance, lipolysis, more glucose and amino acids for the fetus; placental GH replaces pituitary GH.
- *+* **Relaxin (corpus luteum, placenta)**: Softens the cervix and pelvic ligaments, widens vessels and raises renal blood flow, peaking in the first trimester.
- *−* **High estrogen and progesterone**: Suppress LH and FSH: no ovulation or cycles during pregnancy.

## Clinical notes

- Gestational diabetes is the unmasking of limited β-cell reserve by the insulin resistance of late pregnancy; most cases resolve after delivery.
- Hyperemesis gravidarum and molar pregnancy have very high hCG and can cause transient biochemical hyperthyroidism.
- Untreated maternal hypothyroidism early in pregnancy harms fetal brain development, because the fetus relies on maternal T4 before its own thyroid works.
- Thyroid tests must be read against trimester-specific ranges; a nonpregnant TSH range misclassifies many women.

## Memory aid

'Bind more, free the same': in pregnancy, binding proteins rise, totals rise, and the free hormone hardly moves.

## Test yourself

Think of the answer, then tap the question to see it.

## At 10 weeks of pregnancy TSH is 0.2 mU/L and free T4 is at the upper limit of normal. What is the most likely explanation?

hCG, at its peak in the late first trimester, weakly stimulates the TSH receptor; free T4 rises slightly and TSH is suppressed. This is often physiological (gestational transient thyrotoxicosis).

## Why does total calcium fall in pregnancy while ionized calcium stays normal?

Plasma volume expansion dilutes albumin, which carries part of the calcium; the ionized fraction is held normal by higher calcitriol and intestinal absorption.

## Which placental hormones cause insulin resistance in late pregnancy?

Mainly hPL and placental GH, helped by progesterone, cortisol and prolactin. They spare glucose for the fetus and shift the mother to fat.

## What is the recommended total weight gain for a woman with a normal pre-pregnancy BMI?

About 11.5–16 kg; less for overweight (7–11.5 kg) and obese (5–9 kg) women, more for underweight women (12.5–18 kg).

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## Connections

## Related topics 4

- [Maternal physiological changes in pregnancy](https://durgical.com/en/physiology/maternal-physiological-changes-in-pregnancy/)
- [The placenta and pregnancy hormones](https://durgical.com/en/physiology/the-placenta-and-pregnancy-hormones/)
- [Thyroid hormone transport and deiodinases](https://durgical.com/en/physiology/thyroid-hormone-transport-and-deiodinases/)
- [Calcium regulation: PTH, vitamin D and calcitonin](https://durgical.com/en/physiology/calcium-regulation-pth-vitamin-d-and-calcitonin/)

## Related conditions 3

- [Gestational diabetes mellitus](https://durgical.com/en/conditions/gestational-diabetes-mellitus/)
- [Hyperemesis gravidarum](https://durgical.com/en/conditions/hyperemesis-gravidarum/)
- [Iron deficiency anaemia](https://durgical.com/en/conditions/iron-deficiency-anaemia/)

## In Biochemistry 1

- [Fed, fasting and starvation states](https://durgical.com/en/biochemistry/topics/fed-fasting-and-starvation-states/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [Pregnancy and Nutrition | MedlinePlus](https://medlineplus.gov/pregnancyandnutrition.html) (MedlinePlus, US National Library of Medicine, 2026); [Physiology, Placenta](https://www.ncbi.nlm.nih.gov/books/NBK538332/) (StatPearls (NCBI Bookshelf), 2023); [Hypothyroidism](https://www.ncbi.nlm.nih.gov/books/NBK519536/) (StatPearls (NCBI Bookshelf), 2023); [Iron Deficiency and Microcytic Hypochromic Anemia](https://www.ncbi.nlm.nih.gov/books/NBK560876/) (StatPearls (NCBI Bookshelf), 2023).

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