Night Sweats and High Adrenaline

[Velve921]

Why would an individual have night sweats but low temperature (95s)? For years he's always been burning up with tremendous night sweats...how would this be different from myself who is in high 97s at night but have to wear socks, pajamas, hoody, and skull cap?

 

[tara]

I used to think I was waking up sweating because I had too many blankets. Since I started eating more sugar etc, attended to night time mouth-breathing, and had warmer bedclothes, it does not happen any more.

My understanding is that in a hypothyroid state, it is common to have low core temperature, and poor glycogen storage. Low glycogen stores can also result from not eating enough carbs, or from an overloaded and undernourished liver. Peat says sugar is easier to convert to glycogen than starch is. Poor glycogen storage means running out of glycogen during the night. This usually results in an increase in adrenaline and/or cortisol. These stress hormones liberate more blood sugar to maintain basic functions, and can also set of sudden night sweats. There may be other hormones involved in this - others may be able to fill in more.
Mitigation: eat enough sugar through day and before bed to help provide for glycogen refill, and helps keep cortisol down. Salt helps lower adrenaline. Both can help raise core temperature. If he wakes up before the sweats, a small sweet and salt snack may help prevent them. Having more bedclothes/warmer bed helps conserve glycogen because you don't have to burn so much of it just to keep warm. Make sure overall nutrition is good to support healthy thyroid function etc. Monitor body temp and pulse to see if these measures are enough to bring it up over a period. If not, get thyroid hormones tested, and if indicated by symptoms and test, consider cautious thyroid supplementation.

 

[messtafarian]

Hey there:

This is what RP says about hot flashes:

One of the animal "models" used to study hot flashes is morphine withdrawal. The model seems relevant to human hot flashes, because estrogen can stop the morphine withdrawal flushing, and estrogen's acute and chronic effects on the brain-pituitary-ovary system involve the endorphins and the opioidergic nerves (Merchenthaler, et al., 1998; Holinka, et al., 2008).
In young rats, sudden morphine withdrawal caused by injecting the anti-opiate naloxone, causes the tail skin to flush, with a temperature increase of a few degrees, and causes the core body temperature to fall slightly. However, old animals respond to the withdrawal in two different ways. One group responded to the naloxone with an exaggerated flushing and decrease of core temperature. The other group of old rats, which already had a lower body temperature, didn't flush at all (Simpkins, 1994). I think this provides an insight into the reason that menopausal treatment with estrogen can relieve some hot flashes--estrogen treatment might create a flush resistant state similar to that of the cooler old animals in Simpkins' experiment.
It has been known for a long time, from studies in animals and people, that estrogen lowers body temperature, and that this involves a tendency to increase blood flow to the skin in response to a given environmental temperature, that is, the temperature "set-point" is lowered by estrogen. Besides increasing heat loss, estrogen decreases heat production. These physiological effects of estrogen can be seen in the normal menstrual cycle, with progesterone having the opposite effect of estrogen on metabolic rate, skin circulation, body temperature, and heat loss. This causes the familiar rise in temperature when ovulation occurs. Occasionally, young women will experience hot flashes during the luteal phase of their menstrual cycle because of insufficient progesterone production, or at menstruation, when the corpus luteus stops producing progesterone.
Estrogen increases the free fatty acids circulating in the blood, and this shifts metabolism away from oxidation of glucose to oxidation of fat, and it also reduces oxidative metabolism, for example by lowering thyroid function (Vandorpe and Kühn, 1989). These changes are analogous to those of fasting, in which metabolism shifts to the oxidation of fatty acids for energy, causes decreased body temperature, and in some animals leads to a state of torpor or hibernation.
Despite decreasing oxidative metabolism, estrogen stimulates the adrenal cortex, both directly and indirectly through the brain and pituitary, increasing the production of cortisol. Cortisol, by increasing protein turnover, can increase heat production, but this effect isn't necessarily sufficient to maintain a normal body temperature. It increases blood glucose, mainly by blocking its use for energy production, but the glucose is derived from the breakdown of muscle protein. It allows some glucose to be stored as fat. Sudden increases in the amount of glucose can lower adrenaline, and chronically excessive cortisol tends to suppress adrenaline. Cushing's syndrome (produced by excessive cortisol) commonly involves flushing and depression, both of which are likely to be related to the decreased action of adrenaline.
While the biological changes occurring at menopause and during hot flashes are very similar to some of the direct actions of estrogen, and although the menopause itself is the result of prolonged exposure to estrogen, very large doses of estrogen can, in many women (as well as in morphine addicted rats), stop the flushing. In some of the published animal experiments, effective doses of estrogen were about 2000 times normal, and in some human studies, the dose was 30 times normal. By blocking the production of heat, the estrogen treatments might be creating conditions similar to those in Simpkin's cooler old rats, which failed to flush during morphine withdrawal. Menopausal estrogen treatment is known to lower temperature (Brooks, et al., 1994).
Since the Women's Health Initiative publicized the dangers of estrogen, there has been some interest in alternative treatments for hot flashes. Since a reduced production of progesterone has been associated with hot flushes for several decades, it isn't surprising that it is now being tested as an alternative to estrogen. Recently, 300 mg of oral progesterone was found to be effective for decreasing hot flashes, and a month after discontinuing it, the hot flushes were still less frequent than before using it (Prior and Hitchcock, 2012). Previously, transdermal progesterone was found to be effective (Leonetti, et al., 1999).
One of the things progesterone does is to stabilize blood sugar. In one experiment, hot flashes were found to be increased by lowering blood sugar, and decreased by moderately increasing blood sugar (Dormire and Reame, 2003).
Hypoglycemia increases the brain hormone, corticotropin release hormone, CRH (Widmaier, et al., 1988), which increases ACTH and cortisol. CRH causes vasodilation (Clifton, et al., 2005), and is more active in the presence of estrogen. Menopausal women are more responsive to its effects, and those with the most severe hot flushes are the most responsive (Yakubo, et al., 1990).
The first reaction to a decrease of blood glucose, at least in healthy individuals, is to increase the activity of the sympathetic nervous system, with an increase of adrenaline, which causes the liver to release glucose from its glycogen stores. The effect of adrenaline on the liver is very quick, but adrenaline also acts on the brain, stimulating CRH, which causes the pituitary to secrete ACTH, which stimulates the adrenal cortex to release cortisol, which by various means causes blood sugar to increase, consequently causing the sympathetic nervous activity to decrease. Even when the liver's glycogen stores are adequate, the system cycles rhythmically, usually repeating about every 90 minutes throughout the day.
Sympathetic nervous activity typically causes vasoconstriction in the skin and extremities, reducing heat loss, but the small cycles in the system normally aren't noticed, except as small changes in alertness or appetite. With advancing age, most tissues become less sensitive to adrenaline and the sympathetic nervous stimulation, and the body relies increasingly on the production of cortisol to maintain blood glucose. Many of the changes occurring around the menopause, such as the rise of free fatty acids and decrease of glucose availability, increase the sensitivity of the CRH nerves, causing the fluctuations of the adrenergic system to cause larger increases of ACTH and cortisol. Estrogen is another factor that increases the sensitivity of the CRH nerves, and unsaturated fatty acids (Widmaier, et al. 1995) and serotonin (Buckingham, et al., 1982) are other factors stimulating it. Serotonin, like noradrenalin, rises with hypoglycemia (Vahabzadeh, et al., 1995), and estrogen contributes to hypoglycemia, by impairing the counterregulatory system (Cheng and Mobbs, 2009).