for me to remember/consider.
from the life-extension website, recommended by steven [of course, he lives according to that site].
One of the first theories to explain migraines was the classic theory of vasoconstriction/vasodilation. According to this theory, migraine headaches are caused by the constriction of blood vessels in the brain, followed by dilation (Spierings EL 2003; Deleu D et al 2000). Brain studies during migraine have shown that blood flow to the brain is in fact abnormal, which likely contributes to the symptoms (Kasper DL et al 2005).
The theory of hyperexcitability builds on the idea of vasoconstriction/vasodilation. According to the theory of hyperexcitability, the brains of migraine sufferers are extra susceptible to normal triggers, such as stress, and the frequency of migraines depends on the level of excitability. An external trigger, such as stress, causes the sudden constriction of the blood vessels in the brain, which launches the migraine headache. The cause of this excitability is thought to be abnormal brain chemistry, especially in the relationship between calcium and magnesium. During periods of excitability, calcium flows from the extracellular fluid to the intracellular space, resulting in vasoconstriction. Therefore, anything that blocks the flow of calcium or restores the balance of magnesium to calcium would be helpful in mitigating migraine. In fact, studies have shown calcium channel blockers, which block the flow of calcium into cells, can successfully prevent migraine attacks (Bartleson JD 1999).
Another theory proposes a derangement of serotonin metabolism and an excess of neurotransmitters (Beckett BE et al 2002). During migraine, serotonin levels are depressed in the brain, and certain drugs, called triptans, that selectively stimulate certain serotonin receptors, have been shown to reduce the symptoms of migraine (Kasper DL et al 2005). This theory is further supported by the fact that melatonin, which is secreted by the pineal gland along with serotonin, is also reduced during migraine, suggesting that the pineal gland is depressed in migraine patients (Claustrat B et al 1989). Finally, high levels of steroid hormones (e.g., estrogen) can interact with the serotonin transport system, further compromising the availability of serotonin.
Other parts of the nervous system, including the sympathetic nervous system, are also implicated in migraines. The sympathetic nervous system is responsible for various functions, including increasing the contractility of smooth muscle and increasing the heart rate. Many of the factors that trigger migraine, such as stress and hormonal changes, also act on the sympathetic nervous system (Kasper DL et al 2005). By the same token, drugs that mimic or enhance norepinephrine (a neurotransmitter in the sympathetic nervous system) can alleviate migraine (Kasper DL et al 2005).
And, as mentioned above, evidence implicates steroid hormonal imbalances in migraine. Many women note that their migraine attacks occur in connection with their menses, and abnormal hormone levels are closely associated with migraine headaches (Recober A et al 2005). This connection will be discussed in greater detail below.
Migraine Triggers
Several lifestyle factors may trigger a migraine headache. Implicated lifestyle factors include the following:
_Lack of sleep
_Consumption of alcohol, especially red wine and beer
_Excessive exercise
_Consumption of foods containing monosodium glutamate or nitrates
_Consumption of other potential food triggers, including chocolates, aged cheese, dairy foods, caffeine, fermented or pickled foods, shellfish, and wheat
_Emotional stress
Use of certain medications may trigger a migraine; these include the following:
_Birth control pills or conventional hormone replacement therapy with synthetic estrogens and progestins
_Drugs that dilate the blood vessels, such as Viagra ® (sildenafil)_
-Antimigraine drugs used excessively, which can cause rebound migraine
Migraines also may be triggered by the overreaction of blood vessels to a variety of factors, including the following:
-Menstruation
-Fatigue
-Changes in altitude, weather, or time zone
-Glaring lights
-Perfumes or other powerful odors
-Head trauma
well, i agreee!
....
This research suggests that it is not the absolute levels of estrogen that are associated with migraine among women but rather an imbalance between estrogen and progesterone. This theory would also help explain why conventional hormone replacement therapy among postmenopausal women sometimes exacerbates migraine headaches: it is not necessarily the withdrawal from estrogen but perhaps the imbalance between estrogen and progesterone that occurs when postmenopausal women take strong synthetic estrogens during conventional hormone replacement therapy.
Thus, to help balance progesterone and estrogen levels, Life Extension recommends comprehensive hormone testing and, if necessary, hormone restoration with bioidentical hormones that mimic a woman's natural balance of the various estrogens. When used as part of a multifactorial approach, this measure has been shown to help relieve migraine (Dzugan SA et al 2003).
hmmm....
One of the first theories to explain migraines was the classic theory of vasoconstriction/vasodilation. According to this theory, migraine headaches are caused by the constriction of blood vessels in the brain, followed by dilation (Spierings EL 2003; Deleu D et al 2000). Brain studies during migraine have shown that blood flow to the brain is in fact abnormal, which likely contributes to the symptoms (Kasper DL et al 2005).
The theory of hyperexcitability builds on the idea of vasoconstriction/vasodilation. According to the theory of hyperexcitability, the brains of migraine sufferers are extra susceptible to normal triggers, such as stress, and the frequency of migraines depends on the level of excitability. An external trigger, such as stress, causes the sudden constriction of the blood vessels in the brain, which launches the migraine headache. The cause of this excitability is thought to be abnormal brain chemistry, especially in the relationship between calcium and magnesium. During periods of excitability, calcium flows from the extracellular fluid to the intracellular space, resulting in vasoconstriction. Therefore, anything that blocks the flow of calcium or restores the balance of magnesium to calcium would be helpful in mitigating migraine. In fact, studies have shown calcium channel blockers, which block the flow of calcium into cells, can successfully prevent migraine attacks (Bartleson JD 1999).
Another theory proposes a derangement of serotonin metabolism and an excess of neurotransmitters (Beckett BE et al 2002). During migraine, serotonin levels are depressed in the brain, and certain drugs, called triptans, that selectively stimulate certain serotonin receptors, have been shown to reduce the symptoms of migraine (Kasper DL et al 2005). This theory is further supported by the fact that melatonin, which is secreted by the pineal gland along with serotonin, is also reduced during migraine, suggesting that the pineal gland is depressed in migraine patients (Claustrat B et al 1989). Finally, high levels of steroid hormones (e.g., estrogen) can interact with the serotonin transport system, further compromising the availability of serotonin.
Other parts of the nervous system, including the sympathetic nervous system, are also implicated in migraines. The sympathetic nervous system is responsible for various functions, including increasing the contractility of smooth muscle and increasing the heart rate. Many of the factors that trigger migraine, such as stress and hormonal changes, also act on the sympathetic nervous system (Kasper DL et al 2005). By the same token, drugs that mimic or enhance norepinephrine (a neurotransmitter in the sympathetic nervous system) can alleviate migraine (Kasper DL et al 2005).
And, as mentioned above, evidence implicates steroid hormonal imbalances in migraine. Many women note that their migraine attacks occur in connection with their menses, and abnormal hormone levels are closely associated with migraine headaches (Recober A et al 2005). This connection will be discussed in greater detail below.
Migraine Triggers
Several lifestyle factors may trigger a migraine headache. Implicated lifestyle factors include the following:
_Lack of sleep
_Consumption of alcohol, especially red wine and beer
_Excessive exercise
_Consumption of foods containing monosodium glutamate or nitrates
_Consumption of other potential food triggers, including chocolates, aged cheese, dairy foods, caffeine, fermented or pickled foods, shellfish, and wheat
_Emotional stress
Use of certain medications may trigger a migraine; these include the following:
_Birth control pills or conventional hormone replacement therapy with synthetic estrogens and progestins
_Drugs that dilate the blood vessels, such as Viagra ® (sildenafil)_
-Antimigraine drugs used excessively, which can cause rebound migraine
Migraines also may be triggered by the overreaction of blood vessels to a variety of factors, including the following:
-Menstruation
-Fatigue
-Changes in altitude, weather, or time zone
-Glaring lights
-Perfumes or other powerful odors
-Head trauma
well, i agreee!
....
This research suggests that it is not the absolute levels of estrogen that are associated with migraine among women but rather an imbalance between estrogen and progesterone. This theory would also help explain why conventional hormone replacement therapy among postmenopausal women sometimes exacerbates migraine headaches: it is not necessarily the withdrawal from estrogen but perhaps the imbalance between estrogen and progesterone that occurs when postmenopausal women take strong synthetic estrogens during conventional hormone replacement therapy.
Thus, to help balance progesterone and estrogen levels, Life Extension recommends comprehensive hormone testing and, if necessary, hormone restoration with bioidentical hormones that mimic a woman's natural balance of the various estrogens. When used as part of a multifactorial approach, this measure has been shown to help relieve migraine (Dzugan SA et al 2003).
hmmm....