spacekonijn
Badass junkie
vraag me af in hoeverre het slecht is om heel veel te nemen, pis je dit gewoon uit of wat?
L-tryptofaan
- Onderwerp starter spacekonijn
- Startdatum
Nah bij hele hoge doseringen verneuk je je lever.
Maar het heeft ook helemaal geen nut om dat spul overmatig te slikken, het nuttige effect ervan is niet inherent aan de hoeveelheid die je tot je neemt.
Dat eerste ben ik zeker van, dat tweede zou je in twijfel kunnen trekken, al vind ik het wel heel logisch.
Maar het heeft ook helemaal geen nut om dat spul overmatig te slikken, het nuttige effect ervan is niet inherent aan de hoeveelheid die je tot je neemt.
Dat eerste ben ik zeker van, dat tweede zou je in twijfel kunnen trekken, al vind ik het wel heel logisch.
spacekonijn
Badass junkie
dat tweede lijkt mij ook logisch maar in de praktijk pakt het iets anders uit, ik neem de laatste tijd dagelijks 500mg l-tryptofaan ik vind dit tot dusver het beste medicijn tegen onrust/ADD/stress wat ik gevonden heb, wanneer ik 1000mg neem werkt het toch echt nog beter( heb zitten twijfelen of dit placebo is maar ben toch ongever 80% zeker van niet).
weet je meer over bij welke dosering je lever echt gevaar loopt ?
ik heb overigens al flink ge-googled maar zo makkelijk is het niet te vinden!
weet je meer over bij welke dosering je lever echt gevaar loopt ?
ik heb overigens al flink ge-googled maar zo makkelijk is het niet te vinden!
spacekonijn
Badass junkie
dit is interessant
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Tryptophan, nature’s answer to Prozac
by James South MA
The "serotonin deficiency syndrome" is one of the most common and widespread disorders of human psychobiology in the modern world. Prozac allegedly increases the amount of serotonin in the synaptic gap that slightly separates nerve cells from each other. (For more on the "allegedly" see the excellent book; Talking back to Prozac by psychiatrist, Peter Breggin).
Greater amounts of serotonin in the synaptic gap increases communication between serotonin using neurons, allowing the brain’s multiple and critically important serotonin neural circuits to function more reliably, powerfully and effectively.
Tryptophan and serotonin action to order
Studies with humans and animals conducted over the past 30 years show that serotonin nerve circuits promote feelings of well being, calm, personal security, relaxation, confidence and concentration.
Serotonin neural circuits also help counterbalance the tendency of brain dopamine and noradrenaline circuits to encourage over-arousal, fear, anger, tension, aggression, violence, obsessive-compulsive actions, over-eating (especially carbohydrates), anxiety and sleep disturbances.
The serotonin deficiency syndrome has been shown to manifest as a broad array of emotional and behavioral problems, ranging from depression, PMS, anxiety, alcoholism, insomnia, violence, aggression, suicide and compulsive gambling.
Yet there is rarely a problem with the structure or "wiring" of the brain’s serotonin circuits. Rather the problem is caused by a chronic deficit of serotonin in the nerves that use it as their neurotransmitter. And this deficit in turn derives from various problems relating to the nutritional biochemistry of tryptophan.
Tryptophan the essential amino acid
Tryptophan is one of the eight essential amino acids found in the human diet. Essential amino acids must be gotten preformed from food or supplements; non-essential aminos (there are 14) can be made from the essential aminos, or other non-essential amino acids.
In any normal diet- animal or vegetarian- protein based tryptophan is the least plentiful of all 22 amino acids. A typical diet provides only 1 to 1.5 grams per day, yet there is much competition in the body for this scarce tryptophan. It is used to make various proteins, and in people with low to moderate intakes of vitamin B3 (niacin/ niacinamide), tryptophan may be used by the liver to make B3 at the expensive ratio of 60mg tryptophan to one-two mg B3.
In people who are even marginally vitamin B6 deficient, tryptophan may be rapidly degraded into mildly toxic metabolites such as hydroxykynurenine, xanthurenic acid and hydroxyanthranilic acid. Thus, the brain typically receives less than 1% of ingested tryptophan.
Yet even getting its meager share of tryptophan (the only normal dietary raw material for serotonin manufacture) proves a difficult task for the brain, due to the blood brain barrier (BBB).
The BBB serves as a protection to prevent toxins (and even excessive levels of nutrients which might temporally overwhelm and dysregulate brain function) from entering the brain.
Serotonin by itself cannot penetrate the BBB, its precursor tryptophan can. Yet the BBB makes it hard even for brain essential nutrients to enter the brain. Nutrients must be ferried through the BBB by transport molecules, like passengers on a bus. Unfortunately for the serotonin using nerves, tryptophan must share its "transport bus" with 5 other amino acids, tyrosine, phenylalanine, valine, leucine and isoleucine.
Thus, tryptophan is typically out-numbered about 8:1 in its competition to secure its transport through the BBB into the brain.
Tryptophan its affects on carbohydrates and obesity
Eating a high protein diet to provide more tryptophan only worsens the problem by even more increasing the intake of the 5 competing aminos. Ironically, the only dietary strategy that increases brain tryptophan supply is to eat a high carbohydrate diet.
When large amounts of carbos are eaten, the body secretes large amounts of the hormone insulin to lower the ensuing high blood sugar. The insulin also clears from the blood most of the 5 amino acids that compete with tryptophan for a ride to the brain. Tryptophan then has the "bus" all to itself, allowing more tryptophan to reach the brain.
This strategy is instinctively known and practiced by many people who eat large amounts of carbos like bread, cakes, pies, ice cream, chips, pizza, candy etc., especially when they are feeling depressed, stressed or anxious.
The increased brain serotonin this produces lowers arousal and anxiety, promoting a (temporary) sense of well being and security. However, this strategy comes at a price, the same insulin which enhances brain serotonin also enhances the conversion of the fats, carbos and aminos cleared from the blood into stored body fat!
Hence the carbo addition/ obesity serotonin connection.
Taking tryptophan as a supplement is the most natural way to defeat the brain’s serotonin production problems. Unlike ingesting a high protein diet, isolated supplemental tryptophan intake will not increase blood levels of its five amino competitors. Since the normal dietary intake is only 1 to 1.5 grams per day, even a modest amount of tryptophan supplementation (500mg to 3000mg) will have a significant effect in boosting blood and brain tryptophan levels.
Under normal conditions, the brain enzyme tryptophan hydroxylase (TH) is only 50% saturated. This means the serotonin production machinery is 50% idle; thus an increase in raw material (tryptophan) will tend to automatically increase brain serotonin production.
TH converts tryptophan to 5-hydroxy-tryptophan (5-HTP or Oxitriptan). A vitamin B6 dependant carboxylase enzyme then converts 5-HTP to serotonin, and more serotonin more effectively activates the calming, mood elevating, impulse and appetite controlling serotonin neural circuits.
Tryptophan when less is more!
In the case of tryptophan supplements, more is not always better. In the many human clinical studies using tryptophan to treat depression, published since the 1970’s, studies using moderate tryptophan doses (1g to 3g daily) have frequently shown better results than high doses (6 to 9g daily). This is due to a liver enzyme called "tryptophan pyrrolase" (TP). Tryptophan pyrrolase is a key enzyme in the normal liver tryptophan breakdown pathways. Tryptophan pyrrolase is known to be activated by at least two factors.
The first is the stress hormone cortisol. Cortisol, produced by the adrenal glands, is the "state of siege" stress hormone. It is released in response to unremitting chronic stress, which we can neither fight against, nor flee from. Cortisol is known to be frequently elevated in the very conditions, such as, depression, insomnia and obesity for which tryptophan/ serotonin might be helpful.
Thus, taking tryptophan while under elevated cortisol-stress conditions might supply little extra to the brain, because of cortisol’s activation of Tryptophan pyrrolase.
The other factor known to elevate liver Tryptophan pyrrolase activity is increased intake of tryptophan! Since the Tryptophan pyrrolase using kynurenine pathway is the major tryptophan degradation pathway, significantly elevated tryptophan intake automatically induces higher Tryptophan pyrrolase activity. Again, if liver Tryptophan pyrrolase activity seriously increases, more supplemental tryptophan will not necessarily translate into increased brain serotonin.
Thus, the lowest tryptophan dose that successfully alleviates serotonin-deficiency symptoms is the most efficacious.
Fortunately, clinical and anecdotal evidence shows that even 500mg to 1500mg of supplemental tryptophan, taken at bedtime on a regular basis, is frequently sufficient to ease serotonin-deficiency problems.
This low dose will usually not seriously elevate tryptophan destroying Tryptophan pyrrolase activity.
Niacinamide (vitamin B3) is known to inhibit liver Tryptophan pyrrolase ; it is also the vitamin that activates the enzyme that converts tryptophan to 5-HTP. Thus taking 100mg B3 several times daily with meals will also serve to enhance the effectiveness of low-moderate tryptophan doses.
Taking 25mg to 50mg vitamin B6 once or twice daily with meals will also augment tryptophan-serotonin conversion, since B6 activates the decarboxylase enzyme that converts 5-HTP to serotonin.
Tryptophan the anti-depressive
The published research of SN Young and HM Praag (two of the world’s chief experts on tryptophan-serotonin metabolism and psychobiology), suggest that tryptophan will likely be of most benefit to people suffering from depression of the type that Young refers to as "anxious-agitated." Young notes that increased brain production of serotonin through tryptophan supplementation does not automatically increase serotonin nerve activity.
Young’s research indicates that at low levels of psychobiologic arousal, there will be adequate neuronal serotonin to support the correlative low-level serotonin nerve activity, even when nerve serotonin levels are low.
At higher levels of arousal, however, the more rapid turnover of serotonin in the synaptic gap will require higher levels of serotonin production to adequately maintain the greater activity of serotonin circuits.
Those suffering depression of a more vegetative, passive, quiescent variety Young refers to as the "apathetic inhibited" type.
Given that serotonin neural circuits frequently serve to counterbalance the arousing activating dopamine/ noradrenaline circuits (the neural circuits cocaine and amphetamine and to a lessor extent coffee serve to activate), Young’s observations make perfect sense.
Anxious, agitated depression occurs when a person's dopamine/ noradrenaline activating arousal circuits (Yang) are functioning strongly, without the calming, relaxing, mellowing serotonin circuits (Yin) functioning strongly as a complementary counterbalance.
Tryptophan provides the anxious agitated depressive with that needed "Yin" counterbalance, restoring a sense of well being and behavioral self-control.
Van Praag’s research has shown that for many people suffering depression, combining the amino-acid tyrosine with tryptophan works much better than taking tryptophan alone. These would be Young’s "apathetic inhibited" types, where both the serotonin tranquillity/ well being circuits and the "get up and go" vigorous action dopamine/ noradrenaline circuits are underactive.
Tyrosine is the precursor for both dopamine and noradrenaline. The enzyme that converts tyrosine to its next step on the dopamine- noradrenaline pathway (tyrosine hydroxylase) is normally at least 25% unsaturated (i.e. 25% "idle"), so that providing supplemental tyrosine (100 to 500mg with meals) unregulated brain dopamine/ noradrenaline production and nerve activity.
The increased dopamine/ noradrenaline neural activity then requires greater complementary serotonin neural activity, which is provided by the tryptophan supplementation.
Tryptophan’s general uses
Research has shown that tryptophan/ serotonin is effective for more than depression. Various forms of defective impulse control and obsessive compulsive disorders are also strongly affected by serotonin nerve activity. Suicidal behavior, compulsive gambling, irrationally dangerous thrill seeking behavior and pyromania (compulsive fire starting), have been shown to be correlated with low serotonin neural activity, combined with excessive dopaminergic/ noradrenergic activity.
Chronic alcoholism may also have a serotonin component. Research with animals and humans has shown that alcohol initially increases serotonin nerve activity; yet chronic alcohol use impairs tryptophan entry into the brain. This chronic alcoholism may involve a vicious spiral of a brief alcohol induced increase of serotonin neural activity, with consequent sense of well being, combined with an ever worsening baseline state of serotonin nerve activity due to alcohol's impairment of brain tryptophan transport.
Tryptophan and sleep
In recent years, melatonin has gained the reputation as the natural answer to insomnia. Yet the fact that melatonin is made in the pineal gland from serotonin is frequently overlooked.
Thus supplemental tryptophan may induce one’s pineal gland to naturally increase its melatonin production. Also, important sleep regulating nerve circuits in the brainstem (the raphe nuclei) use serotonin as their neurotransmitter, so it is unreasonable to expect melatonin alone to provide optimal insomnia relief.
Low dose melatonin (0.5mg to 1mg) plus tryptophan (500mg to 1500mg) may prove more effective for many people with serious insomnia.
Tryptophan’s role in dementia
Recent research has shown that the depression that frequently accompanies and even predates the movement disorders of Parkinson's disease is primarily due to the hypofunction of serotonin nerves, so tryptophan may be a useful adjunct to L-Dopa/ deprenyl treatment of Parkinson’s.
In the latter stages of Alzheimer’s disease, heightened irritability and unprovoked aggression frequently accompany the mental decline, and recent research has shown partial destruction of key serotonergic neural circuits to be involved.
Supplemental tryptophan may optimize the activity of remaining serotonergic neurons, lessening the anger and aggression.
Tryptophan and 5-hydroxy-tryptophan
Supplemental 5-HTP (oxitriptan), the intermediary between tryptophan and serotonin, is also available as a natural remedy for the serotonin deficiency syndrome, yet tryptophan offers a major advantage over 5-HTP for many people.
There are nerves that line the intestinal tract, which use serotonin as their neurotransmitter. These nerves contain the carboxylase enzyme that converts 5-HTP to serotonin, but not the hydroxylase enzyme that coverts tryptophan to 5-HTP.
Thus, when 5-HTP is swallowed, large amounts of 5-HTP may be picked up by these intestinal serotonergic neurons and quickly converted to serotonin, leading to hyperactivity of these nerves.
This in turn may lead to nausea, vomiting, cramping, constipation and/ or diarrhea, and indeed, the research published on 5-HTP since the 1970’s has consistently shown various forms of intestinal discomfort to be the main side effect of 5-HTP use.
Yet, because these intestinal neurons cannot convert tryptophan to 5-HTP, tryptophan does not cause intestinal distress.
Tryptophan its synergistic combinations
A practical program to relieve the many forms of serotonin deficiency syndrome will ideally combine moderate amounts of tryptophan (500mg to 1500mg), 5-HTP at 33mg to 100mg, and melatonin (0.5mg to 1mg) taken at bedtime.
Melatonin actually promotes increased brain serotonin through its ability to reduce cortisol levels, and reduced cortisol levels will lessen the activity of liver pyrrolase, the enzyme that degrades tryptophan.
GH3/ KH3, Dilantin (phenytoin) and magnesium may also lower cortisol activity.
Standardized extracts of St. John’s Wort (0.3% hypercin) may also synergise with tryptophan to optimize serotonin levels. Research summarized in Hypericum and Depression by H. Bloomfield and colleagues suggests three complementary mechanisms of action, whereby St. John’s Wort may increase serotonin. It seems to be a weak serotonin reuptake inhibitor (and thus a more natural and safer equivalent of Prozac), a weak MAO inhibitor (MAO enzymes break down neuronal serotonin), and a cortisol inhibitor. The standard St. John’s Wort dosage is 300mg three times daily; however, less may be needed when combined with tryptophan.
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Tryptophan, nature’s answer to Prozac
by James South MA
The "serotonin deficiency syndrome" is one of the most common and widespread disorders of human psychobiology in the modern world. Prozac allegedly increases the amount of serotonin in the synaptic gap that slightly separates nerve cells from each other. (For more on the "allegedly" see the excellent book; Talking back to Prozac by psychiatrist, Peter Breggin).
Greater amounts of serotonin in the synaptic gap increases communication between serotonin using neurons, allowing the brain’s multiple and critically important serotonin neural circuits to function more reliably, powerfully and effectively.
Tryptophan and serotonin action to order
Studies with humans and animals conducted over the past 30 years show that serotonin nerve circuits promote feelings of well being, calm, personal security, relaxation, confidence and concentration.
Serotonin neural circuits also help counterbalance the tendency of brain dopamine and noradrenaline circuits to encourage over-arousal, fear, anger, tension, aggression, violence, obsessive-compulsive actions, over-eating (especially carbohydrates), anxiety and sleep disturbances.
The serotonin deficiency syndrome has been shown to manifest as a broad array of emotional and behavioral problems, ranging from depression, PMS, anxiety, alcoholism, insomnia, violence, aggression, suicide and compulsive gambling.
Yet there is rarely a problem with the structure or "wiring" of the brain’s serotonin circuits. Rather the problem is caused by a chronic deficit of serotonin in the nerves that use it as their neurotransmitter. And this deficit in turn derives from various problems relating to the nutritional biochemistry of tryptophan.
Tryptophan the essential amino acid
Tryptophan is one of the eight essential amino acids found in the human diet. Essential amino acids must be gotten preformed from food or supplements; non-essential aminos (there are 14) can be made from the essential aminos, or other non-essential amino acids.
In any normal diet- animal or vegetarian- protein based tryptophan is the least plentiful of all 22 amino acids. A typical diet provides only 1 to 1.5 grams per day, yet there is much competition in the body for this scarce tryptophan. It is used to make various proteins, and in people with low to moderate intakes of vitamin B3 (niacin/ niacinamide), tryptophan may be used by the liver to make B3 at the expensive ratio of 60mg tryptophan to one-two mg B3.
In people who are even marginally vitamin B6 deficient, tryptophan may be rapidly degraded into mildly toxic metabolites such as hydroxykynurenine, xanthurenic acid and hydroxyanthranilic acid. Thus, the brain typically receives less than 1% of ingested tryptophan.
Yet even getting its meager share of tryptophan (the only normal dietary raw material for serotonin manufacture) proves a difficult task for the brain, due to the blood brain barrier (BBB).
The BBB serves as a protection to prevent toxins (and even excessive levels of nutrients which might temporally overwhelm and dysregulate brain function) from entering the brain.
Serotonin by itself cannot penetrate the BBB, its precursor tryptophan can. Yet the BBB makes it hard even for brain essential nutrients to enter the brain. Nutrients must be ferried through the BBB by transport molecules, like passengers on a bus. Unfortunately for the serotonin using nerves, tryptophan must share its "transport bus" with 5 other amino acids, tyrosine, phenylalanine, valine, leucine and isoleucine.
Thus, tryptophan is typically out-numbered about 8:1 in its competition to secure its transport through the BBB into the brain.
Tryptophan its affects on carbohydrates and obesity
Eating a high protein diet to provide more tryptophan only worsens the problem by even more increasing the intake of the 5 competing aminos. Ironically, the only dietary strategy that increases brain tryptophan supply is to eat a high carbohydrate diet.
When large amounts of carbos are eaten, the body secretes large amounts of the hormone insulin to lower the ensuing high blood sugar. The insulin also clears from the blood most of the 5 amino acids that compete with tryptophan for a ride to the brain. Tryptophan then has the "bus" all to itself, allowing more tryptophan to reach the brain.
This strategy is instinctively known and practiced by many people who eat large amounts of carbos like bread, cakes, pies, ice cream, chips, pizza, candy etc., especially when they are feeling depressed, stressed or anxious.
The increased brain serotonin this produces lowers arousal and anxiety, promoting a (temporary) sense of well being and security. However, this strategy comes at a price, the same insulin which enhances brain serotonin also enhances the conversion of the fats, carbos and aminos cleared from the blood into stored body fat!
Hence the carbo addition/ obesity serotonin connection.
Taking tryptophan as a supplement is the most natural way to defeat the brain’s serotonin production problems. Unlike ingesting a high protein diet, isolated supplemental tryptophan intake will not increase blood levels of its five amino competitors. Since the normal dietary intake is only 1 to 1.5 grams per day, even a modest amount of tryptophan supplementation (500mg to 3000mg) will have a significant effect in boosting blood and brain tryptophan levels.
Under normal conditions, the brain enzyme tryptophan hydroxylase (TH) is only 50% saturated. This means the serotonin production machinery is 50% idle; thus an increase in raw material (tryptophan) will tend to automatically increase brain serotonin production.
TH converts tryptophan to 5-hydroxy-tryptophan (5-HTP or Oxitriptan). A vitamin B6 dependant carboxylase enzyme then converts 5-HTP to serotonin, and more serotonin more effectively activates the calming, mood elevating, impulse and appetite controlling serotonin neural circuits.
Tryptophan when less is more!
In the case of tryptophan supplements, more is not always better. In the many human clinical studies using tryptophan to treat depression, published since the 1970’s, studies using moderate tryptophan doses (1g to 3g daily) have frequently shown better results than high doses (6 to 9g daily). This is due to a liver enzyme called "tryptophan pyrrolase" (TP). Tryptophan pyrrolase is a key enzyme in the normal liver tryptophan breakdown pathways. Tryptophan pyrrolase is known to be activated by at least two factors.
The first is the stress hormone cortisol. Cortisol, produced by the adrenal glands, is the "state of siege" stress hormone. It is released in response to unremitting chronic stress, which we can neither fight against, nor flee from. Cortisol is known to be frequently elevated in the very conditions, such as, depression, insomnia and obesity for which tryptophan/ serotonin might be helpful.
Thus, taking tryptophan while under elevated cortisol-stress conditions might supply little extra to the brain, because of cortisol’s activation of Tryptophan pyrrolase.
The other factor known to elevate liver Tryptophan pyrrolase activity is increased intake of tryptophan! Since the Tryptophan pyrrolase using kynurenine pathway is the major tryptophan degradation pathway, significantly elevated tryptophan intake automatically induces higher Tryptophan pyrrolase activity. Again, if liver Tryptophan pyrrolase activity seriously increases, more supplemental tryptophan will not necessarily translate into increased brain serotonin.
Thus, the lowest tryptophan dose that successfully alleviates serotonin-deficiency symptoms is the most efficacious.
Fortunately, clinical and anecdotal evidence shows that even 500mg to 1500mg of supplemental tryptophan, taken at bedtime on a regular basis, is frequently sufficient to ease serotonin-deficiency problems.
This low dose will usually not seriously elevate tryptophan destroying Tryptophan pyrrolase activity.
Niacinamide (vitamin B3) is known to inhibit liver Tryptophan pyrrolase ; it is also the vitamin that activates the enzyme that converts tryptophan to 5-HTP. Thus taking 100mg B3 several times daily with meals will also serve to enhance the effectiveness of low-moderate tryptophan doses.
Taking 25mg to 50mg vitamin B6 once or twice daily with meals will also augment tryptophan-serotonin conversion, since B6 activates the decarboxylase enzyme that converts 5-HTP to serotonin.
Tryptophan the anti-depressive
The published research of SN Young and HM Praag (two of the world’s chief experts on tryptophan-serotonin metabolism and psychobiology), suggest that tryptophan will likely be of most benefit to people suffering from depression of the type that Young refers to as "anxious-agitated." Young notes that increased brain production of serotonin through tryptophan supplementation does not automatically increase serotonin nerve activity.
Young’s research indicates that at low levels of psychobiologic arousal, there will be adequate neuronal serotonin to support the correlative low-level serotonin nerve activity, even when nerve serotonin levels are low.
At higher levels of arousal, however, the more rapid turnover of serotonin in the synaptic gap will require higher levels of serotonin production to adequately maintain the greater activity of serotonin circuits.
Those suffering depression of a more vegetative, passive, quiescent variety Young refers to as the "apathetic inhibited" type.
Given that serotonin neural circuits frequently serve to counterbalance the arousing activating dopamine/ noradrenaline circuits (the neural circuits cocaine and amphetamine and to a lessor extent coffee serve to activate), Young’s observations make perfect sense.
Anxious, agitated depression occurs when a person's dopamine/ noradrenaline activating arousal circuits (Yang) are functioning strongly, without the calming, relaxing, mellowing serotonin circuits (Yin) functioning strongly as a complementary counterbalance.
Tryptophan provides the anxious agitated depressive with that needed "Yin" counterbalance, restoring a sense of well being and behavioral self-control.
Van Praag’s research has shown that for many people suffering depression, combining the amino-acid tyrosine with tryptophan works much better than taking tryptophan alone. These would be Young’s "apathetic inhibited" types, where both the serotonin tranquillity/ well being circuits and the "get up and go" vigorous action dopamine/ noradrenaline circuits are underactive.
Tyrosine is the precursor for both dopamine and noradrenaline. The enzyme that converts tyrosine to its next step on the dopamine- noradrenaline pathway (tyrosine hydroxylase) is normally at least 25% unsaturated (i.e. 25% "idle"), so that providing supplemental tyrosine (100 to 500mg with meals) unregulated brain dopamine/ noradrenaline production and nerve activity.
The increased dopamine/ noradrenaline neural activity then requires greater complementary serotonin neural activity, which is provided by the tryptophan supplementation.
Tryptophan’s general uses
Research has shown that tryptophan/ serotonin is effective for more than depression. Various forms of defective impulse control and obsessive compulsive disorders are also strongly affected by serotonin nerve activity. Suicidal behavior, compulsive gambling, irrationally dangerous thrill seeking behavior and pyromania (compulsive fire starting), have been shown to be correlated with low serotonin neural activity, combined with excessive dopaminergic/ noradrenergic activity.
Chronic alcoholism may also have a serotonin component. Research with animals and humans has shown that alcohol initially increases serotonin nerve activity; yet chronic alcohol use impairs tryptophan entry into the brain. This chronic alcoholism may involve a vicious spiral of a brief alcohol induced increase of serotonin neural activity, with consequent sense of well being, combined with an ever worsening baseline state of serotonin nerve activity due to alcohol's impairment of brain tryptophan transport.
Tryptophan and sleep
In recent years, melatonin has gained the reputation as the natural answer to insomnia. Yet the fact that melatonin is made in the pineal gland from serotonin is frequently overlooked.
Thus supplemental tryptophan may induce one’s pineal gland to naturally increase its melatonin production. Also, important sleep regulating nerve circuits in the brainstem (the raphe nuclei) use serotonin as their neurotransmitter, so it is unreasonable to expect melatonin alone to provide optimal insomnia relief.
Low dose melatonin (0.5mg to 1mg) plus tryptophan (500mg to 1500mg) may prove more effective for many people with serious insomnia.
Tryptophan’s role in dementia
Recent research has shown that the depression that frequently accompanies and even predates the movement disorders of Parkinson's disease is primarily due to the hypofunction of serotonin nerves, so tryptophan may be a useful adjunct to L-Dopa/ deprenyl treatment of Parkinson’s.
In the latter stages of Alzheimer’s disease, heightened irritability and unprovoked aggression frequently accompany the mental decline, and recent research has shown partial destruction of key serotonergic neural circuits to be involved.
Supplemental tryptophan may optimize the activity of remaining serotonergic neurons, lessening the anger and aggression.
Tryptophan and 5-hydroxy-tryptophan
Supplemental 5-HTP (oxitriptan), the intermediary between tryptophan and serotonin, is also available as a natural remedy for the serotonin deficiency syndrome, yet tryptophan offers a major advantage over 5-HTP for many people.
There are nerves that line the intestinal tract, which use serotonin as their neurotransmitter. These nerves contain the carboxylase enzyme that converts 5-HTP to serotonin, but not the hydroxylase enzyme that coverts tryptophan to 5-HTP.
Thus, when 5-HTP is swallowed, large amounts of 5-HTP may be picked up by these intestinal serotonergic neurons and quickly converted to serotonin, leading to hyperactivity of these nerves.
This in turn may lead to nausea, vomiting, cramping, constipation and/ or diarrhea, and indeed, the research published on 5-HTP since the 1970’s has consistently shown various forms of intestinal discomfort to be the main side effect of 5-HTP use.
Yet, because these intestinal neurons cannot convert tryptophan to 5-HTP, tryptophan does not cause intestinal distress.
Tryptophan its synergistic combinations
A practical program to relieve the many forms of serotonin deficiency syndrome will ideally combine moderate amounts of tryptophan (500mg to 1500mg), 5-HTP at 33mg to 100mg, and melatonin (0.5mg to 1mg) taken at bedtime.
Melatonin actually promotes increased brain serotonin through its ability to reduce cortisol levels, and reduced cortisol levels will lessen the activity of liver pyrrolase, the enzyme that degrades tryptophan.
GH3/ KH3, Dilantin (phenytoin) and magnesium may also lower cortisol activity.
Standardized extracts of St. John’s Wort (0.3% hypercin) may also synergise with tryptophan to optimize serotonin levels. Research summarized in Hypericum and Depression by H. Bloomfield and colleagues suggests three complementary mechanisms of action, whereby St. John’s Wort may increase serotonin. It seems to be a weak serotonin reuptake inhibitor (and thus a more natural and safer equivalent of Prozac), a weak MAO inhibitor (MAO enzymes break down neuronal serotonin), and a cortisol inhibitor. The standard St. John’s Wort dosage is 300mg three times daily; however, less may be needed when combined with tryptophan.
DreamerOfDreams
Bewuste gebruiker
ik zit al een tijdje te denken om ze eens aan te schaffen
wat denken jullie dat het 'beste' werkt
L-tryptofaan of 5-HTP?
wat denken jullie dat het 'beste' werkt
L-tryptofaan of 5-HTP?
Heb niet heel bovenstaand verhaal gelezen, maar heb even gegoogelt op tryptofaan en 5-HTP. Tryptofaan wordt daarin omgezet. Dus ik vraag me af of het dan zo veel uitmaakt. Ik lees ook al een aantal dagen dit (viewtopic.php?f=10&t=19437) topic, en die tryptofaan is voor mij misschien ook wel iets, ook gezien de vele positieve reacties erover.DreamerOfDreams zei:
spacekonijn
Badass junkie
tryptofaan is een stuk beter dan 5htp zowel voor je lever als het lichamelijk proces l-tryp-5 htp wat gewoon ontbreekt als je puur 5htp neemt. maar lees vooral dat stuk text ( het is zwaar maar toch een zeer goed en leerzaam stuk).
tryptofaan is een aminozuur ( bouwstof in je lichaam ), je kunt dit ook uit eten halen maar je haalt dan automatisch een aantal andere aminozuren erbij binnen die samen door de doorvoer gaan waardoor je alsnog niet een flinke lading tryptofaan binnenkrijgt. vandaar dat supplementen aan te raden zijn (vrij goedkoop online te vinden maar zoek wel naar een betrouwebare pharma source).
sry ben te high voor een uitgebreid antwoord
tryptofaan is een aminozuur ( bouwstof in je lichaam ), je kunt dit ook uit eten halen maar je haalt dan automatisch een aantal andere aminozuren erbij binnen die samen door de doorvoer gaan waardoor je alsnog niet een flinke lading tryptofaan binnenkrijgt. vandaar dat supplementen aan te raden zijn (vrij goedkoop online te vinden maar zoek wel naar een betrouwebare pharma source).
sry ben te high voor een uitgebreid antwoord
Angramar Temenos
Badass junkie
Ik mik zelf elke dag:
750 mg L-Tryptofaan
50 mg 5-HTP
1 MG Melatonine
500 MG L-Tyrosine
naar binnen. Ik vind het zeker helpen. Ik ben ook een stuk minder psychotisch als ik het neem.
750 mg L-Tryptofaan
50 mg 5-HTP
1 MG Melatonine
500 MG L-Tyrosine
naar binnen. Ik vind het zeker helpen. Ik ben ook een stuk minder psychotisch als ik het neem.
L
Lid 6909
Gast
Helpen die dingen tegen psychose's dan?
Melatonine zijn toch slaaptabletten? Die zou een gezond mens van jou leeftijd niet nodig moeten hebben lijkt me!
Melatonine zijn toch slaaptabletten? Die zou een gezond mens van jou leeftijd niet nodig moeten hebben lijkt me!
spacekonijn
Badass junkie
dit wil ik ook aanschaffen, weet je een goede goedkope leverancier in Nederland ?Angramar Temenos zei:
hier nog een handige pagina over de gevaren van aminozuren supplementen, tryptofaan en tyrosine is niet gevaarlijk
http://jn.nutrition.org/cgi/content/full/134/6/1633S
Tryptophan
High intake levels of tryptophan depress food intake and growth in animals fed low-protein but not higher-protein diets (1,2). In addition, adult rats fed 20% casein diets supplemented with 28.5% tryptophan showed rapid weight loss (105). However, pigs given tryptophan as 1% of diet showed no effects on growth or intake (106). In biochemical studies, rats given 5% tryptophan in diet for 6 wk showed increases in serotonin and 5-hydroxyindole acetic acid in the lower brain stem (107). Moreover, behavioral effects that are mediated through serotonergic neurons, e.g., reduced sleep latency, reduced food intake, depressed motor activity, and improved maze-test performance were observed in animal studies (10
. Despite these reported effects in animals, no evidence exists of serious adverse effects attributable directly to tryptophan in humans, and some potentially beneficial effects, e.g., sleep enhancement (109), have been reported, so tryptophan is widely sold as a sleep aid. The most important negative evidence is the outbreak of eosinophlia-myalgia syndrome in the 1980s that occurred in subjects taking tryptophan supplements (110). However, this is now believed to be unrelated to tryptophan itself; rather, the syndrome appears to have resulted from a contaminant in the tryptophan produced by a single supplier (5).Tyrosine
In young rats on low-protein diets, depression of growth and food intake occur when additional tyrosine is given, which is followed by death at higher tyrosine intake levels. A unique effect of this amino acid is to induce corneal and paw lesions in rats fed low-protein diets with 3–5% tyrosine, but histopathological changes also occur in a variety of other tissues (1). These effects are moderated with time and higher levels of dietary protein or by limiting amino acids (1). The eye lesions were shown to consist of tyrosine crystals resulting from the high concentration and low solubility of tyrosine in tissue fluids (111,112). In addition, changes in catecholamine-mediated functions, e.g., blood pressure, were reported (113). After female rats were given additional tyrosine during gestation, neurological and behavioral changes were detected in the pups (114).
The genetic disorder tyrosinemia II is associated with very high plasma tyrosine levels due to the deficiency of hepatic tyrosine aminotransferase. It results in mental retardation and lesions of the eye and soles of the feet that are analogous to those reported in animal studies (4). However, experimental studies of high tyrosine intake in humans have not in general reproduced these effects or the adverse effects seen in animals. Oral doses of 100 mg/kg in adults did not change blood pressure or pulse rate, and there were no other reported side effects (115,116). Although a 14-g dose resulted in increases in plasma epinephrine, norepinephrine, and dopamine concentrations, no physical or psychological effects were detected (117). Moreover, a single 100 mg/kg dose of tyrosine led to improvement in cognitive and performance tasks at high altitude (11
. During these studies, no side effects were reported. However, in babies there may be some cause for concern. A follow-up study of premature infants who had suffered transient neonatal tyrosinemia revealed an association between elevated plasma tyrosine in infancy, impaired perceptual function, and reduced achievement scores when they reached 7–8 y of age (119). Also, in a study of transient neonatal tyrosinemia attributed to a high-protein formula plus a lack of supplemental vitamin C, children whose tyrosinemia persisted for >45 d showed lower scores on some tests of intellectual ability (120). This suggests that supplemental tyrosine should be avoided by pregnant women and infants.Ik gebruik het ook af en toe, let wel op wanneer je het gebruik en enig effect wil hebben je best ook vitamine B3 en B6 bijneemt, omdat - zoals aangegeven in het artikel hierboven - een tekort aan deze vitamines zorgt dat de Tryptofaan zich omzet naar die vitamines (met groot verlies) en dat willen we natuurlijk niet.
Ook zien dat voor- en na inname gedurende 1,5 uur lang geen proteïne rijke producten inneemt (melk, yoghurt, kwark, eieren, tonijn, zalm,...). Best neem je het voor het slapen gaan.
Ook zien dat voor- en na inname gedurende 1,5 uur lang geen proteïne rijke producten inneemt (melk, yoghurt, kwark, eieren, tonijn, zalm,...). Best neem je het voor het slapen gaan.
Angramar Temenos
Badass junkie
Misschien placebo, maar bij mij in ieder geval wel. Misschien ligt het aan het feit dat hele erge pieken depressie bij mij nauwlijks voorkomen met die middelen (depressie sowieso bijna niet als ik braaf mn crap slik), en die hele extreme pieken kunnen bij mij vaak triggers zijn om psychotisch te worden.
l-triptofaan is ook verkrijgbaar met toegevoegde vitamine B6 (bv van VitOrtho). bter dan ook nog bv multivitamines te slikken waarvan je 90% van de ingredienten in principe niet nodig hebt!
miss voor de een placebo, maar verwacht niet dat met één pilletje je hele depressie weg is (daar is het sowieso ook niet voor bedoeld )
miss voor de een placebo, maar verwacht niet dat met één pilletje je hele depressie weg is (daar is het sowieso ook niet voor bedoeld
)www.azarius.nl Neem het al lange tijd en werkt echt goed.
