Amazoniac
Member
Gurus,
It was only recently that I realized that stimulating activities at night can be counter-productive; those include long hot showers, prolonged red light therapy sessions, most exercises; basically everything that increases the metabolism too much, especially requiring a great deal of glycogen. If you engage on those activities, you'll need to eat afterwards to compensate, but at the same time eating and excessive warmth at night are a bit disruptive to natural cycles. Sometimes people have the metabolism so weak that every part of the day that offers a bit of momentary relief is prolonged to extend the reward; so people tend to overdo activities that are normally relaxing, and potentially exhausting, depending on the length/intensity.
It's not just a matter of weak metabolism. Another relevant thing is that many people take prolonged hot showers because it assists the body to keep the metabolism high and so people tend to have better brain function while taking their showers. So they stay more than they should and leave the showers in a jell-o consistency but with everything in their lives sorted.
And then I found this:
Temperature-responsive release of thyroxine and its environmental adaptation in Australians | Proceedings of the Royal Society of London B: Biological Sciences
“Although our data here and almost all the detailed knowledge of the physiology of thyroxine transport are derived from the human, there is clear evidence that the system is strongly conserved in all mammals. This is seen not only in the conservation of TBG sequence in diverse mammals [21] but also in the identity of molecular mechanisms based on crystal structures from the mouse [11] and the human [12,13]. Hence, the findings here (figures 1d and 2) have direct relevance to the hypothermia and torpor that occur in small animals [22,23]. Based on a saturation of TBG in the human of 20%, there will be a homoeostatic decrease in the concentration of free thyroxine as body temperature falls, with a fivefold drop from 20 pM at 37°C to a baseline 4 pM at 7°C. Similarly, as body temperature is restored, the thyroxine, stably stored in the TBG, will be increasingly released, rising to meet the needs of full activity at 37°C.”
“The critical metabolic demands of a much larger brain make humans especially sensitive to changes in the release of thyroxine and even mild hypothermia, if prolonged, is fatal. A physiological change in body temperature does, however, occur in humans with the fevers that are induced by inflammation and infection. The accelerated decrease in binding affinity that will accompany the increase in body temperature from 37° to 39°C and, exceptionally, to 42°C is seen in figure 1d. Evidence that this fever-induced decrease in binding affinity is specific and purposeful and comes from a similar but even greater acceleration of hormone release in the closely related CBG (figure 1c). The loss of affinity in TBG at fever temperatures has, however, even more direct physiological impact than that of CBG because of the much tighter hormone-binding affinity of TBG and the precisely defined limits of free-thyroxine concentration in the blood. Any changes in the Kd of TBG will be directly reflected in changes in free-thyroxine levels in the blood with a rise in body temperature to 39°C predictably giving a 23% increase in concentration, temporarily moving into the range seen in the clinical disorder of hyperthyroidism (figure 2).”
Then they ranted on some mutation found in some aboriginal Australians that diminishes the “accelerated release of thyroxine that takes place as the temperature rises above 37°C” and speculated that this adaptation is not random, and might be advantageous for survival:
“Thus, the paired polymorphisms provide the aboriginal Australian with a TBG that maintains its properties as a storage and carrier protein while having the additional local advantage of providing a reduced metabolic response to increased body temperatures. In a temperate climate, the boost to thyroxine release and increased metabolism that accompanies the rise in body temperatures in fevers will be an advantageous response to infection. But the same accelerated increase in metabolism could affect the survival of a population historically exposed to the arid environment of central Australia, with ambient temperatures of 45°C or above. There the life threatening risk is not so much the infection itself, but rather the dehydration and heat exhaustion that accompany dysentery and other common illnesses in infancy and childhood.”
“The demonstration that TBG, as with CBG [6,7], acts as a protein thermocouple, has direct physiological implications. Such temperature-sensitive regulation of hormone release will affect everyday lives. For example, the accelerated release that will take place as the body core temperature rises to 39°C in a hot-bath or sauna will contribute to an enhancement of the metabolism of body and mind—euphoria and eureka! A similar boost in hormone release also opens a contributory explanation for the common occurrence of febrile convulsions in infancy [29]. The brain is sensitive to changes in free thyroxine and raised levels in thyrotoxicosis in adults can result in convulsive seizures that cease, with no after-effects, when the thyroxine level returns to normal [30,31]. Comparable seizures also commonly occur in infants in conjunction with the spiking increases in temperature that accompany incidental infections at that age. The surge in thyroxine release that will occur in response to the increases in the temperature of the brain in fevers [32] poses a potential exacerbating factor in the childhood seizures—a conclusion reinforced by the prompt cessation of the convulsions as the infant's body temperature is cooled.”
Which is exactly what I commented and why I suspect that burtlan posts while showering.
--
http://www.altmedrev.com/publications/12/1/49.pdf
It was only recently that I realized that stimulating activities at night can be counter-productive; those include long hot showers, prolonged red light therapy sessions, most exercises; basically everything that increases the metabolism too much, especially requiring a great deal of glycogen. If you engage on those activities, you'll need to eat afterwards to compensate, but at the same time eating and excessive warmth at night are a bit disruptive to natural cycles. Sometimes people have the metabolism so weak that every part of the day that offers a bit of momentary relief is prolonged to extend the reward; so people tend to overdo activities that are normally relaxing, and potentially exhausting, depending on the length/intensity.
It's not just a matter of weak metabolism. Another relevant thing is that many people take prolonged hot showers because it assists the body to keep the metabolism high and so people tend to have better brain function while taking their showers. So they stay more than they should and leave the showers in a jell-o consistency but with everything in their lives sorted.
And then I found this:
Temperature-responsive release of thyroxine and its environmental adaptation in Australians | Proceedings of the Royal Society of London B: Biological Sciences
“Although our data here and almost all the detailed knowledge of the physiology of thyroxine transport are derived from the human, there is clear evidence that the system is strongly conserved in all mammals. This is seen not only in the conservation of TBG sequence in diverse mammals [21] but also in the identity of molecular mechanisms based on crystal structures from the mouse [11] and the human [12,13]. Hence, the findings here (figures 1d and 2) have direct relevance to the hypothermia and torpor that occur in small animals [22,23]. Based on a saturation of TBG in the human of 20%, there will be a homoeostatic decrease in the concentration of free thyroxine as body temperature falls, with a fivefold drop from 20 pM at 37°C to a baseline 4 pM at 7°C. Similarly, as body temperature is restored, the thyroxine, stably stored in the TBG, will be increasingly released, rising to meet the needs of full activity at 37°C.”
“The critical metabolic demands of a much larger brain make humans especially sensitive to changes in the release of thyroxine and even mild hypothermia, if prolonged, is fatal. A physiological change in body temperature does, however, occur in humans with the fevers that are induced by inflammation and infection. The accelerated decrease in binding affinity that will accompany the increase in body temperature from 37° to 39°C and, exceptionally, to 42°C is seen in figure 1d. Evidence that this fever-induced decrease in binding affinity is specific and purposeful and comes from a similar but even greater acceleration of hormone release in the closely related CBG (figure 1c). The loss of affinity in TBG at fever temperatures has, however, even more direct physiological impact than that of CBG because of the much tighter hormone-binding affinity of TBG and the precisely defined limits of free-thyroxine concentration in the blood. Any changes in the Kd of TBG will be directly reflected in changes in free-thyroxine levels in the blood with a rise in body temperature to 39°C predictably giving a 23% increase in concentration, temporarily moving into the range seen in the clinical disorder of hyperthyroidism (figure 2).”
Then they ranted on some mutation found in some aboriginal Australians that diminishes the “accelerated release of thyroxine that takes place as the temperature rises above 37°C” and speculated that this adaptation is not random, and might be advantageous for survival:
“Thus, the paired polymorphisms provide the aboriginal Australian with a TBG that maintains its properties as a storage and carrier protein while having the additional local advantage of providing a reduced metabolic response to increased body temperatures. In a temperate climate, the boost to thyroxine release and increased metabolism that accompanies the rise in body temperatures in fevers will be an advantageous response to infection. But the same accelerated increase in metabolism could affect the survival of a population historically exposed to the arid environment of central Australia, with ambient temperatures of 45°C or above. There the life threatening risk is not so much the infection itself, but rather the dehydration and heat exhaustion that accompany dysentery and other common illnesses in infancy and childhood.”
“The demonstration that TBG, as with CBG [6,7], acts as a protein thermocouple, has direct physiological implications. Such temperature-sensitive regulation of hormone release will affect everyday lives. For example, the accelerated release that will take place as the body core temperature rises to 39°C in a hot-bath or sauna will contribute to an enhancement of the metabolism of body and mind—euphoria and eureka! A similar boost in hormone release also opens a contributory explanation for the common occurrence of febrile convulsions in infancy [29]. The brain is sensitive to changes in free thyroxine and raised levels in thyrotoxicosis in adults can result in convulsive seizures that cease, with no after-effects, when the thyroxine level returns to normal [30,31]. Comparable seizures also commonly occur in infants in conjunction with the spiking increases in temperature that accompany incidental infections at that age. The surge in thyroxine release that will occur in response to the increases in the temperature of the brain in fevers [32] poses a potential exacerbating factor in the childhood seizures—a conclusion reinforced by the prompt cessation of the convulsions as the infant's body temperature is cooled.”
Which is exactly what I commented and why I suspect that burtlan posts while showering.
--
http://www.altmedrev.com/publications/12/1/49.pdf
