TSH and cortisol secretion profiles are circadian, so why are their levels not parallel through the night and day?
The difference in these two hormone profiles is attributable to the extent that each is influenced by either process-C or process-S. However, this question is not straightforward. The difference demonstrates nicely the primary process-C contribution to cortisol secretion versus the influence of a combination of process-S plus process-C on TSH secretion. In general, the day-to-night pattern for both hormones is not parallel, but they are similar. The patterns of both reveal the highest hormone levels during sleep and the lowest levels during the day, but the 24-hour highest level for TSH occurs as a person goes to sleep, whereas the cortisol peak occurs as the person wakes up. The cortisol profile is nearly all circadian governed (process-C), so it does not show significant variation with acute sleep deprivation. In contrast, nocturnal TSH will increase with acute sleep loss and decrease with daytime-recovery sleep. Thus, the evening TSH increase before sleep onset reveals process-C influence, whereas the decrease of TSH during sleep reflects an influence of process-S. To continue a description of the excursion of these hormones during a normal 24-hour cycle, TSH fluctuations precede those of cortisol, with TSH starting its rise before sleep onset and before the cortisol rise and starting its descent also before the cortisol descent. Cortisol peaks in the last third of the night, and, as mentioned, TSH begins to rise before sleep onset. Then, with sleep achieved, TSH hits its peak between 10 pm and midnight followed by a slow during-the-day TSH decline with a nadir by mid-afternoon. Given that corticotrophin (ACTH) release is primarily influenced by the time of day (process-C), the normal 24-hour cortisol profile does not have a significant change in shape with total sleep deprivation or during daytime recovery sleep. Cortisol will hit its 24-hour nadir after the transition to sleep, between 10 pm and midnight; then, as though someone rattles its cage, cortisol rises abruptly after midnight and peaks at 6 to 9 am (by the second third of sleep, the cortisol rise is underway regardless of sleep–wake state). Normal awakening is the herald of the cortisol decline, progressing over the entire waking period with a nadir after sleep transition in the successive night of sleep. But, as is well known, cortisol is a stress response hormone and will increase with stress (e.g., someone cuts in front in traffic, or there is a morning dental appointment); with such events, this end-of-the-night/start-of-the-day surge of cortisol pattern will change. This stress-sensitive trigger is not seen with TSH. Therefore, a change to one’s sleep-wake cycle influences the release of both hormones but to different extents. In a study of healthy young men during nocturnal sleep deprivation from 10 pm to 6 am, with the lack of TSH suppression by sleep, TSH more than doubled. That is, TSH rose from its afternoon nadir of approximately 1.5 mU/L to a new peak of approximately 3.8 mU/L at 2 am and, in the follow-on recovery sleep (10 am–6 pm), TSH returned to a mean of 1.25 mU/L; but there was no effect on cortisol. It is well documented that interruptions to nocturnal sleep are associated with short-term TSH elevations. TSH levels normalize when normal nocturnal sleep is resumed. In contrast to the absence of acute sleep deprivation effects on cortisol, repeated and prolonged nocturnal sleep interruptions do result in cortisol elevations.
Primary Influence on 24 Hour Variation
GH, Growth hormone; PRL, prolactin; TSH, thyroid-stimulating hormone.