Table 2.
Characteristic phenotypical changes of thyroid-stimulating hormone (TSH) and various classical and non-classical thyroid hormones in certain allostatic situations show nearly opposing changes in type 1 and type 2 allostatic load (61, 63, 111, 123, 170–182).
| TSH | FT4 | TT4 | FT3 | TT3 | rT3 | |
|---|---|---|---|---|---|---|
| Type 1 allostasis in fetal period, acute and chronic critical illness, and in deprivation of energy | ||||||
| Fetal life | ↓, → or ↑ | ↓ | ↓ | ↓ | ↓ | ↑ |
| Caloric deprivation | → or ↓ | → | ↓ | ↓ | ↓ | ↑ |
| Exhausting exercise | → or ↓ | → | ↓ | ↓ | ↓ | ↑ |
| Critical illness (general) | → or ↓ | → | → or ↓ | ↓ | ↓ | → or ↑ |
| Chronic heart failure | → or ↓ | → | → or ↓ | ↓ | ↓ | → or ↑ |
| Renal diseases | → | → or ↓ | → or ↓ | → | ↓ | → |
| Liver diseases | → | → or ↓ | ↑ | ↓ | → or ↑ | → or ↑ |
| Pulmonary diseases | → | → | → | ↓ | → | → or ↑ |
| Diabetes mellitus | → or ↓ | → or ↑ | ↓ | ↓ | ↓ | → or ↑ |
| Sepsis | ↓ | → | → or ↓ | ↓ | ↓ | → or ↑ |
| HIV infection | → | → or ↓ | → | → or ↓ | → | → or ↓ |
| Depression | → | → or ↑ | ↑ | ↓ | ↓ | → or ↑ |
| Type 2 allostasis-related conditions | ||||||
| Pregnancy | → or ↓ | → | ↑ | → | ↑ | → |
| Endurance training | ↓, → or ↑ | ↑ | ↑ | ↑ | → or ↓ | ↑ |
| Obesity | ↑ | → or ↓ | → or ↑ | ↑ | ↑ | → or ↓ |
| Adaptation to cold | ↓, → or ↑ | ↑ | ↓, → or ↑ | ↑ | ↑ | → or ↓ |
| Acute schizophrenia | → or ↑ | → or ↑ | ↑ | → or ↑ | ↑ | → |
| Post-traumatic stress disorder | → | → | ↑ | ↑ | ↑ | ? |
FT4 and FT3, free T4 and T3, respectively; TT4 and TT3, total (free + protein-bound) T4 and T3, respectively; rT3, reverse T3; TSH, thyroid-stimulating hormone.
Hormone concentration unchanged (→), increased (↑), decreased (↓), or not reported (?). Small studies also reported increased concentrations of 3,5-diiodothyronine (3,5-T2) (61–63), triiodothyroacetate and tetraiodothyroacetate (123, 124), and decreased concentrations of 3-monothyronamine (63) in critical illness and chronic heart failure (not shown in table). See text for definition of type 1 and type 2 allostasis in the context of pituitary–thyroid function.