What is Endocrinology - How does obstructive sleep apnea (OSA) differ from sleep disordered breathing (SDB) and what does it mean?
The interchangeable use of the words sleep-related breathing disorders (SRBD), SDB, and OSA in the literature and in sleep laboratory results causes confusion. Similar to how chronic obstructive pulmonary disease (COPD) serves as a generic heading for various distinct disease entities, SRBD and SDB are diseases under which other disorders are grouped. SRBD includes OSA syndromes as well as adult and paediatric central apnea syndromes. In contrast, polysomnography is used to diagnose OSA, a specific condition (PSG). On the basis of complaints made by the patient or their bed mate, OSA may be suspected. Unintentional sleep episodes when awake, daytime tiredness, unrefreshing sleep, exhaustion or sleeplessness, waking from sleep with gasping or choking, loud snoring, and breathing disturbances are a few examples of these problems. If there are complaints from the patient or bed partner, the PSG requirements are less strict. The PSG must have five or more respiratory episodes per hour of sleep associated with increased respiratory effort in addition to complaints. The PSG must instead contain 15 or more of these respiratory episodes in the absence of a history of complaints. In either situation, a diagnosis of OSA must rule out any underlying medical, neurological, and/or substance addiction conditions. The risk of OSA can also be raised by several prescription drugs.
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What is Endocrinology - How does hormone release change as we age?
Hormonal alterations are hypothesised to be the result of changes in sleep architecture with ageing. Loss of SWS and REM sleep, as well as increased sleep fragmentation, are both symptoms of normal ageing. TSH, cortisol, and testosterone increase predominantly on the basis of the circadian cycle, whereas GH and PRL rise primarily in connection to the SWS of NREM sleep. SWS and GH secretion have a dosage response association in younger males. For instance, SWS accounts for approximately 20% of the sleep time in males and boys aged 16 to 25 and declines to 5% to 10% after age 40. This is linked to a 350 mg GH release during sleep in people between the ages of 16 and 25, but not more than 100 mg in people over the age of 35. Regardless of gender, the majority of the PRL released throughout a 24-hour period occurs when you're asleep. With age, nocturnal PRL release declines by over 50%. With age, the magnitude of the circadian fluctuations in cortisol and TSH is less pronounced. Age also dampens day-night TSH oscillations. What is Endocrinology -How do circadian rhythms and sleep-wake cycles affect insulin and glucose levels?
Both Process-C and SWH have an impact on insulin and glucose levels. Studies on healthy persons showed that during nocturnal sleep, glucose levels rose by 30% and insulin levels by 60%. A finding that suggests circadian modulation is that during sleep deprivation, glucose and insulin secretion rates rise at habitual sleep time, but to a much smaller extent. However, secretion rates of both insulin and glucose significantly rise during recovery sleep, indicating that sleep itself may be modulating these processes. What is Endocrinology - Being jet lagged is frequent. How are some of its symptoms related to the cortisol and TSH variations that have been noticed?
A sleep problem called jet lag results from rapidly changing time zones. In essence, the circadian cycle drifts away from the desired time zone. This is especially true while travelling east, as it causes the clock to advance while the person's circadian clock stays in the time zone of takeoff. The person is now at danger of developing insomnia. Cortisol levels in the evening and early hours of sleep are significantly higher in those with insomnia whose ratio of total time asleep to total time in bed is less than 70% of normal. In a study of young people whose circadian rhythms were thrown off by a travel from Europe to the US, GH secretory patterns adjusted to the new sleep-wake cycle within a few days, while cortisol levels persisted in their dissociated state for two weeks. It is believed that this dissociation plays a role in the manifestations of jet lag syndrome. The hypothalamic-thyroid axis' disruption during protracted flight has also been researched. Long-haul flight travel may negate the inhibitory effects of sleep on TSH release, resulting in an overall elevation of TSH and a slight, brief elevation of triiodothyronine (T3) levels. The study linked persistent elevations of thyroid hormone and the dissynchronization of several circadian rhythms to the weariness and pain of jet lag syndrome. What is Endocrinology - Why are TSH and cortisol levels not constant throughout the day and night given that their release is circadian?
Basically, TSH is impacted by the time of day, as well as the quantity and quality of sleep (SWH) (circadian). However, the time of day has a significant impact on the release of corticotropin (adrenocorticotropic hormone [ACTH]). Thus, the circadian process and Process-S both have a significant impact on cortisol. When compared to people who experience daytime sleep deprivation followed by daytime recovery sleep, the typical 24-hour cortisol profile does not significantly vary in shape. TSH begins to rise immediately before sleep begins and is maximum in SWS, whereas cortisol starts to rise in REM-predominant sleep, followed by a burst on awakening. The wave shape of the two hormone profiles is highest during sleep compared to daytime. TSH does not reveal this explosion. As a result, altering one's sleep-wake cycle has varying effects on the release of both hormones. TSH changes typically occur before cortisol fluctuations; cortisol peaks later and bursts upon awakening. TSH starts to increase in accordance with circadian rhythm, peaks between midnight and two in the morning, and troughs at 1.5 mU/L by mid-afternoon. TSH then stabilises, preventing what would have been a rise following sleep onset, reflecting TSH suppression during sleep. TSH increased by more than doubling in a study of healthy young men after nocturnal sleep deprivation from 10 pm to 6 am (SWS suppression eliminated). TSH climbed from its afternoon low of around 1.5 mU/L to a new peak of about 3.8 mU/L at 2 am. TSH rebounded to a mean of 1.25 mU/L during the subsequent recovery sleep (10 am to 6 pm). Contrarily, cortisol rises rapidly after midnight, peaks between 6 and 9 am, and then falls during the day (reaching a nadir at midnight). It is widely known that nocturnal sleep disruptions are linked to transient TSH increases. When regular nocturnal sleep is restored, TSH levels return to normal. Increases in cortisol are brought on by frequent and protracted nocturnal sleep disruptions. What is Endocrinology -What elements affect the secretion of thyroid-stimulating hormone (TSH)?9/19/2022 What is Endocrinology -What elements affect the secretion of thyroid-stimulating hormone (TSH)? Although there is a significant influence from Process-S, the circadian rhythm is principally responsible for TSH release. TSH release in young, healthy male participants exhibits an early-evening circadian increase, followed by a fall in levels that lasts until the nadir in the late afternoon. Sleep is thought to have an inhibitory effect on TSH in SWS. As a result, doctors may want to think twice before making therapeutic recommendations based solely on mid-afternoon TSH readings. Acute sleep loss causes TSH to rise normally in the early evening at around 6 pm, but it continues to rise into the middle of the typical sleep phase, reaching nearly double the normal maximum. When this sleep-deprived person gets daytime recovery sleep, TSH returns to normal. The higher TSH readings found in critically unwell hospitalised patients may be caused by the lack of a sleep-inhibitory influence on circadian TSH elevation.
What is Endocrinology - Do the changes in LH and FSH mentioned in the preceding questions also occur in the gonadal steroid hormones?
No. Gonadal steroids do not reflect the pulse amplitude and frequency of gonadotropins (i.e., gonadal steroids do not have similar pulsations). There is an increase in midday estradiol among pubescent girls. For adolescent boys, the rise in testosterone occurs concurrently with the reported elevation of the gonadotropins, with the lowest testosterone levels occurring in the late evening and peak levels occurring in the morning. There is no consistent circadian gonadotropin pattern in postmenopausal women because their gonadotropin levels rise in an effort to produce estradiol. What is Endocrinology -Do women have the same LH pattern as men?
The menstrual cycle has a considerable impact on plasma LH in females. However, because the LH pulse frequency decreases when you sleep, there is some sleep-related LH level modulation. Although the frequency of the LH pulse drops in the early follicular and early luteal phases, the amplitude actually increases, making the nocturnal LH pulse frequency slowing more obvious. This slowdown is less noticeable or not present throughout the middle and late follicular and luteal phases. FSH and LH levels are higher in postmenopausal women without any diurnal fluctuation. What is Endocrinology - Does testosterone release exclusively depend on the LH maturity pattern of release, and how does gonadotropin release alter from adolescence to adulthood?
Sleep patterns differ depending on the person's gender and level of maturity. Daytime pulsatile gonadotropin release, which is boosted by the beginning of sleep, occurs before puberty. Increased nocturnal amplitude of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) pulses is one of the telltale signs of puberty in children. This nocturnal spike in pubertal youngsters is caused by both Process-S and Process-C. The daytime LH also increases as the pubescent boy approaches adulthood, masking the 24-hour cycle's fluctuation. NREM-REM cycling has a major impact on the testosterone profile in adult men, according to mounting research. The overnight LH surges of puberty become shorter and less frequent as people age. The early morning rise in male testosterone begins with the initiation of sleep and peaks during the second part of sleep (REM predominant). Contrary to cortisol, which is quiescent during the first stages of sleep, testosterone is in a surge. Additionally, there is no equivalent LH spike in the early stages of sleep. Later, in the second half of sleep, the typical midnight LH bursts take place. During adult daytime recovery sleep, testosterone was found to increase; however, as the patient remained awake following the midday recovery sleep, testosterone levels began to decline. All of this implies that testosterone release is influenced by sleep itself and not just by LH bursts. The underlying causes of this growth are not yet understood. The 24-hour testosterone profile is more similar to PRL, as is the reaction to sleep deprivation and daytime recovery sleep. For instance, when a male internal medicine resident who has been sleep deprived finally gets some sleep, his testosterone levels will spike during his recovery sleep; yet, during a typical day and in someone who has not slept, testosterone levels are on the fall. Applying this example in a clinical setting, it is possible that shift work, OSA, or sleep deprivation are the causes of low testosterone in a person. Based on the findings that sleep boosts testosterone, awake decreases it, and the circadian influence may be less powerful than SWH, it is reasonable to advise our patients to have their testosterone levels measured first thing in the morning while they are rested. What is Endocrinology -Identify the two hormones that are raised before sleep and the two hormones that are elevated after sleep.
During the first third of sleep, the SWS predominates, while during the second half of sleep, REM predominates. Prolactin (PRL) and growth hormone (GH) are entrained to SWS. No of the person's age or gender, when they are asleep, they release the majority of their PRL. The initial period of SWS is connected to the nighttime GH and PRL surges. Although girls and women burst less than boys and men, both genders have the highest 24-hour GH surge right after the start of sleep. Girls and women have two nighttime GH bursts: the first happens just before sleep sets in and the second occurs with SWS. Compared to girls and women, boys and men have fewer GH pulses during the day. If the patient is unable to sleep, the surge of PRL and GH is gone; but, if the patient is able to sleep, it returns. The beginning of sleep, not the hour of the day, initiates the release of these hormones. Cortisol and testosterone are the hormones that rise later in the sleep cycle. Just after midnight, testosterone starts to climb, while cortisol starts to rise around 2 am before peaking between 6 and 9 am. The late-sleep surge of these two hormones in men is correlated with the timing and duration of REM sleep. However, circadian rhythmicity (Process-C) and not SWH is what essentially regulates the 24-hour rhythm for both testosterone and cortisol (Process-S). |
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