- Lid geworden
- 8 jan 2005
- Berichten
- 12.252
- Waardering
- 559
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
-
Volg het forum via Google Nieuws
Sticky L-Tryptofaan en antidepressiva
- Topic starter Big-J
- Startdatum
- Volgers 9
Bezoekers in dit topic
Heb erg veel moeite met dat soort artikels. Waarom? Omdat mensen die wel antidepressiva gebruiken er niet veel aan hebben om dit soort artikels te lezen. Het kan mensen onrustig en uiteindelijk nog depressiever maken dan ze al zijn omdat ze lezen dat volgens de schrijver SSRI's niet helpen.
Ik begrijp je punt, maar men zou in medische kringen daar meer aandacht aan moeten besteden en indien nodig moeten optreden. Een patiënt heeft niks aan deze wetenschap want het is de psychiater die medicijnen voorschrijft.
Overigens kan ik het niemand aanraden om via zoekmachines naar ervaringen van anti-depressiva te gaan zoeken omdat iedereen er weer anders op reageert en je uiteindelijk door de bomen het bos niet meer ziet. Het kan een onbehaaglijk gevoel geven omdat je onbewust de meningen van anderen toch in je achterhoofd houdt en wellicht laat meewegen hoe jij de medicatie ervaart. Voel zelf aan of je klachten minder worden en geef het de tijd om het te laten inwerken. Heb je na enkele weken er geen profijt van, bespreek dan met de psychiater hoe je het beste kunt afbouwen en of er andere alternatieven zijn.
Laatst bewerkt:
- Lid geworden
- 8 jan 2005
- Berichten
- 12.252
- Waardering
- 559
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
Het grote probleem is dat psychiaters geen zak kennen van hoe antidepressiva precies werken, de ene SSRI na de andere gebruiken is vrijwel nutteloos, door bepaalde augmentatie strategieen toe te passen kan je SSRI's wel degelijk effectief maken.
Bijvoorbeeld, de reden waarom SSRI's zo slecht zijn is omdat ze serotonine verhogen en daarmee ook 5HT2C en 5HT7 activeren, deze receptoren hebben een tegenovergesteld dan wat de bedoeling is, ook worden 5HT1A autoreceptoren geactiveerd wat dan weer zegt dat de hoeveelheid serotonine minder word, na verloop van tijd worden die receptoren minder gevoelig wat dan zorgt dat de hoeveelheid serotonine verhoogt en zo de 5HT1A postsynaptische receptor geactiveerd word. Het probleem is alleen dat de presynaptische receptor altijd zal blijven tegenwerken.
Dit kan je omzeilen met het toevoegen van een lage dosis buspirone, die werkt als een partional agonist op 5HT1A en dus de plaats innenmen van serotonin wat een full agonist is wat op zijn beurt zorgt voor een verhoogde serotogene transmissie.
Nog een 5HT2C en 5HT7 antagonist en je hebt een krachtige serotogene antidepressiva combo (maar dat is iets voor de toekomst omdat er nog geen selectieve 5HT2 of 5HT7 antagonisten uit zijn.), alleen is er geen enkele psychiater die denkt aan zo'n augmentatie strategie en gewoon de ene antidepressiva na de andere gebruikt.
(beetje ingewikkelde text als je er niets van kent, maar wil maar zeggen dat met een beetje kennis je gemakkelijk wel aan combo's geraakt die zeker potent zijn.)
Ook zijn er genoeg meds die wel degelijk effectief zijn voor bepaalde stoornissen, alleen zijn ze daarvoor niet goedgekeurd.
Neem nu bijvoorbeeld OCD, er is enorm veel bewijs dat glutamate daarin betrokken is[1] toch bestaat de standaard behandeling uit SSRI's die alleen op serotonine werken. Er is een hoog effective glutamate antagonist beschikbaar namenlijk memantine, memantine word goed getolereerd en is verschillende studies effectief gebleken voor OCD[1][2] alleen gaat er nooit een psychiater zijn die memantine gaat uitproberen, alleen maar de SSRI's ondanks al het bewijs dat glutamate betrokken is bij OCD.
Dan nog iets anders, social angst. Er is aanzienlijk bewijs dat dopamine daarbij betrokken en dat mensen met sociale angst 6 keer meer kans hebben op het krijgen van parkinson. Toch is er geen enkele medicatie die werkt op dopamine goedgekeurd voor sociale angst.
In kort, kennis is essentieel om veel progressie te maken.
Laatst bewerkt:
- Lid geworden
- 8 jan 2005
- Berichten
- 12.252
- Waardering
- 559
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
Physicians Are Talking About: SSRI's and the Choice to Numb Out
Selective serotonin reuptake inhibitors (SSRIs), mainstays of psychopharmacology, effectively eliminate suicidal ideation -- not to mention feelings of exhilaration, caring, and desire.
A recent study published in the British Journal of Psychiatry found that the majority of patients taking SSRIs experienced emotional detachment, feelings of indifference, personality changes, and a reduction in positive and negative emotions.[1]
Currently, tens of millions of patients in the United States take SSRIs daily. However, evidence pertaining to the long-term effects of these drugs is scant. "In a few decades, as many as 15% of the world's population might be on SSRIs," comments a psychiatrist. "Although the suicide rate might decrease, I wonder what the long-term effect will be."
The conjecture posited on Medscape's Physician Connect (MPC), an all-physician discussion board, launches a discussion about the apparent choice in SSRI use -- to be crippled by depression or functional and emotionally numb.
MPC contributors commented that their anecdotal experience aligns with that of the British study.
"In several patients on long-term SSRIs, I have noticed some subtle personality changes," says a psychiatrist. "Of course, there's no way of ascertaining cause and effect without a good, long-term study, but this is what I've observed: (1) SSRIs decrease pain (irritability, depression) but also seem to increase the threshold for what constitutes an exciting event (a person needs more novelty than previously for the same effect); and (2) SSRIs increase apathy and have the potential to decrease empathy."
"It would be unrealistic," adds another psychiatrist, "to think that taking a medication which significantly impacts a major neurotransmitter would not have, in some cases if not many, a significant effect on a person's personality, either short- or long-term." The psychiatrist comments that case studies documented in Peter Kramer's book Listening to Prozac indicate that SSRIs strongly impact a patient's feeling of "caring," which can affect the patient's relationships with friends and family.
An endocrinologist suggests that his colleagues view the film Numb, which documents filmmaker Phil Lawrence's struggle to stop taking the popular SSRI Paxil. In the trailer for the film, Lawrence says, "I'm flatlined. This isn't me. This is me on Paxil®."[2]
"These are the wonder drugs of psychiatry," argues a psychiatrist. "They continue to benefit people over the long term, even at low doses. They help with anxiety, much more robustly than with depression, but they help in depression too. If I had my way Prozac®, Zoloft®, and Celexa® would be sold over the counter." The psychiatrist comments that the life-time prevalence of depression is between 15% and 30%,[3] and most people remain untreated for fear of persecution and judgment formation about their need to take antidepressant drugs. Over-the-counter distribution, he reasons, would make SSRIs more readily available to people who need them.
"I disagree about the OTC [over-the-counter] issue," replies Stephen Grcevich, MD, a child and adolescent psychiatrist. "I think there are untoward effects of SSRIs that are still poorly understood, such as the very small but statistically significant risk of suicidal behavior in persons aged 25 and under. We also saw a subgroup of kids who displayed significant disinhibition and indifference to academics in a large, open-label, federally funded study looking at SSRI safety." He comments that he hopes to present the study data at the 2010 annual meeting of the American Academy of Child and Adolescent Psychiatry (AACAP).
An internist who frequently prescribes SSRIs, reports that she repeatedly experienced suicidal thoughts while taking an SSRI for depression. "I have been placed by my physician on Lexapro® 3 times. In each instance, my mood lifted and crying decreased. I could sleep. In 3 days' time, I started having thoughts that came out of the blue, such as 'I want to drive off this bridge.' Stopping the medication stopped the thoughts." She says that she tells her patients about this potential side effect, but no patient has related having a similar response.
"SSRIs and then SNRIs [serotonin noradrenaline reuptake inhibitors] nearly killed me," says an obstetrician/gynecologist. "They caused narcolepsy, and I fell asleep and drove off the road." He comments that his level of apathy while taking the drugs was so extreme as to appear parkinsonian. "In my opinion as a patient, mild to moderate depression should be treated by cognitive behavioral therapy, not meds."
A surgeon comments that, in many cases, SSRIs are given to patients who are only mildly depressed. "The drugs are given as mood elevators," he says. "We essentially are giving out the drug for the same reason people self-medicate or abuse alcohol."
"I do agree we are pushed to start meds too early on mild cases sometimes," says a family medicine physician. "We must ask the tough questions of patients about suicidal thoughts to determine the severity of their illness. Then start a multipronged approach to treatment and not just write a script and send them out the door."
A neurosurgeon comments that clearly there are a number of questions about SSRIs that need to be addressed:
Should we treat mild depression knowing the risks?
Are we educating patients about the possibility that they will experience apathy?
Are we increasing the risk for substance abuse in patients who attempt to counterbalance induced conditions of apathy and boredom?
Are the artificially high levels of serotonin caused by the use of SSRIs chronically changing the brain and making it impossible to withdraw from these drugs?
"I agree that higher doses and long-term use does blunt emotions," says a pediatrician. "I used Effexor® for about 7 years and tried to wean off during that time, but at very low doses would redevelop extreme sadness that resolved when I upped the dose." He says that working with his psychiatrist, he switched to Wellbutrin® and now experiences a wider range of appropriate emotions. "However, if I did not have another option, I would prefer Effexor® side effects over the chronic anxiety and sadness I experienced for much of my life without it."
The authors of the British study reported a similar finding. Many participants in the study considered whether they should stop taking their medication, but viewed the side effects as preferable to the illness for which they were being treated.
"And that is the problem, isn't it?" comments an MPC contributor. "We just don't have meds that treat without some side effects."
Selective serotonin reuptake inhibitors (SSRIs), mainstays of psychopharmacology, effectively eliminate suicidal ideation -- not to mention feelings of exhilaration, caring, and desire.
A recent study published in the British Journal of Psychiatry found that the majority of patients taking SSRIs experienced emotional detachment, feelings of indifference, personality changes, and a reduction in positive and negative emotions.[1]
Currently, tens of millions of patients in the United States take SSRIs daily. However, evidence pertaining to the long-term effects of these drugs is scant. "In a few decades, as many as 15% of the world's population might be on SSRIs," comments a psychiatrist. "Although the suicide rate might decrease, I wonder what the long-term effect will be."
The conjecture posited on Medscape's Physician Connect (MPC), an all-physician discussion board, launches a discussion about the apparent choice in SSRI use -- to be crippled by depression or functional and emotionally numb.
MPC contributors commented that their anecdotal experience aligns with that of the British study.
"In several patients on long-term SSRIs, I have noticed some subtle personality changes," says a psychiatrist. "Of course, there's no way of ascertaining cause and effect without a good, long-term study, but this is what I've observed: (1) SSRIs decrease pain (irritability, depression) but also seem to increase the threshold for what constitutes an exciting event (a person needs more novelty than previously for the same effect); and (2) SSRIs increase apathy and have the potential to decrease empathy."
"It would be unrealistic," adds another psychiatrist, "to think that taking a medication which significantly impacts a major neurotransmitter would not have, in some cases if not many, a significant effect on a person's personality, either short- or long-term." The psychiatrist comments that case studies documented in Peter Kramer's book Listening to Prozac indicate that SSRIs strongly impact a patient's feeling of "caring," which can affect the patient's relationships with friends and family.
An endocrinologist suggests that his colleagues view the film Numb, which documents filmmaker Phil Lawrence's struggle to stop taking the popular SSRI Paxil. In the trailer for the film, Lawrence says, "I'm flatlined. This isn't me. This is me on Paxil®."[2]
"These are the wonder drugs of psychiatry," argues a psychiatrist. "They continue to benefit people over the long term, even at low doses. They help with anxiety, much more robustly than with depression, but they help in depression too. If I had my way Prozac®, Zoloft®, and Celexa® would be sold over the counter." The psychiatrist comments that the life-time prevalence of depression is between 15% and 30%,[3] and most people remain untreated for fear of persecution and judgment formation about their need to take antidepressant drugs. Over-the-counter distribution, he reasons, would make SSRIs more readily available to people who need them.
"I disagree about the OTC [over-the-counter] issue," replies Stephen Grcevich, MD, a child and adolescent psychiatrist. "I think there are untoward effects of SSRIs that are still poorly understood, such as the very small but statistically significant risk of suicidal behavior in persons aged 25 and under. We also saw a subgroup of kids who displayed significant disinhibition and indifference to academics in a large, open-label, federally funded study looking at SSRI safety." He comments that he hopes to present the study data at the 2010 annual meeting of the American Academy of Child and Adolescent Psychiatry (AACAP).
An internist who frequently prescribes SSRIs, reports that she repeatedly experienced suicidal thoughts while taking an SSRI for depression. "I have been placed by my physician on Lexapro® 3 times. In each instance, my mood lifted and crying decreased. I could sleep. In 3 days' time, I started having thoughts that came out of the blue, such as 'I want to drive off this bridge.' Stopping the medication stopped the thoughts." She says that she tells her patients about this potential side effect, but no patient has related having a similar response.
"SSRIs and then SNRIs [serotonin noradrenaline reuptake inhibitors] nearly killed me," says an obstetrician/gynecologist. "They caused narcolepsy, and I fell asleep and drove off the road." He comments that his level of apathy while taking the drugs was so extreme as to appear parkinsonian. "In my opinion as a patient, mild to moderate depression should be treated by cognitive behavioral therapy, not meds."
A surgeon comments that, in many cases, SSRIs are given to patients who are only mildly depressed. "The drugs are given as mood elevators," he says. "We essentially are giving out the drug for the same reason people self-medicate or abuse alcohol."
"I do agree we are pushed to start meds too early on mild cases sometimes," says a family medicine physician. "We must ask the tough questions of patients about suicidal thoughts to determine the severity of their illness. Then start a multipronged approach to treatment and not just write a script and send them out the door."
A neurosurgeon comments that clearly there are a number of questions about SSRIs that need to be addressed:
Should we treat mild depression knowing the risks?
Are we educating patients about the possibility that they will experience apathy?
Are we increasing the risk for substance abuse in patients who attempt to counterbalance induced conditions of apathy and boredom?
Are the artificially high levels of serotonin caused by the use of SSRIs chronically changing the brain and making it impossible to withdraw from these drugs?
"I agree that higher doses and long-term use does blunt emotions," says a pediatrician. "I used Effexor® for about 7 years and tried to wean off during that time, but at very low doses would redevelop extreme sadness that resolved when I upped the dose." He says that working with his psychiatrist, he switched to Wellbutrin® and now experiences a wider range of appropriate emotions. "However, if I did not have another option, I would prefer Effexor® side effects over the chronic anxiety and sadness I experienced for much of my life without it."
The authors of the British study reported a similar finding. Many participants in the study considered whether they should stop taking their medication, but viewed the side effects as preferable to the illness for which they were being treated.
"And that is the problem, isn't it?" comments an MPC contributor. "We just don't have meds that treat without some side effects."
- Lid geworden
- 8 jan 2005
- Berichten
- 12.252
- Waardering
- 559
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
- Lid geworden
- 8 jan 2005
- Berichten
- 12.252
- Waardering
- 559
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
Agomelatine ownt de SSRI's once again!
J Clin Psychiatry. 2010 Feb;71(2):109-120.
Efficacy of the novel antidepressant agomelatine on the circadian rest-activity cycle and depressive and anxiety symptoms in patients with major depressive disorder: a randomized, double-blind comparison with sertraline.
Kasper S, Hajak G, Wulff K, Hoogendijk WJ, Montejo AL, Smeraldi E, Rybakowski JK, Quera-Salva MA, Wirz-Justice AM, Picarel-Blanchot F, Baylé FJ.
Department of Psychiatry and Psychotherapy, Medical University Vienna, MUV, AKH, Währinger Gürtel 18-20, A-1090 Wien, Austria. biol-psychiatry@meduniwien.ac.at.
OBJECTIVE: This study evaluates the efficacy of agomelatine, the first antidepressant to be an agonist at MT(1)/MT(2) receptors and an antagonist at 5-HT(2C) receptors, versus sertraline with regard to the amplitude of the circadian rest-activity cycle and depressive and anxiety symptoms in patients with major depressive disorder (MDD). METHOD: Outpatients with DSM-IV-TR-defined MDD received either agomelatine 25 to 50 mg (n = 154) or sertraline 50 to 100 mg (n = 159) during a 6-week, randomized, double-blind treatment period. The study was conducted from 2005 to 2006. The main outcome measure was the relative amplitude of the individual rest-activity cycles, expressed as change from baseline to week 6 and collected from continuous records using wrist actigraphy and sleep logs. Secondary outcome measures were sleep efficiency and sleep latency, both derived from actigraphy, and efficacy on depression symptoms (17-Item Hamilton Depression Rating Scale total score and Clinical Global Impressions scale scores) and anxiety symptoms (Hamilton Anxiety Rating Scale total score and subscores). RESULTS: A significant difference in favor of agomelatine compared to sertraline on the relative amplitude of the circadian rest-activity cycle was observed at the end of the first week (P = .01). In parallel, a significant improvement of sleep latency (P <.001) and sleep efficiency (P <.001) from week 1 to week 6 was observed with agomelatine as compared to sertraline. Over the 6-week treatment period, depressive symptoms improved significantly more with agomelatine than with sertraline (P <.05), as did anxiety symptoms (P <.05). CONCLUSIONS: The favorable effect of agomelatine on the relative amplitude of the circadian rest-activity/sleep-wake cycle in depressed patients at week 1 reflects early improvement in sleep and daytime functioning. Higher efficacy results were observed with agomelatine as compared to sertraline on both depressive and anxiety symptoms over the 6-week treatment period, together with a good tolerability profile. These findings indicate that agomelatine offers promising benefits for MDD patients. TRIAL REGISTRATION: www.isrctn.org: ISRCTN49376288. © Copyright 2010 Physicians Postgraduate Press, Inc.
Jammer dat ago nog niet beschikbaar is in Belgie.
J Clin Psychiatry. 2010 Feb;71(2):109-120.
Efficacy of the novel antidepressant agomelatine on the circadian rest-activity cycle and depressive and anxiety symptoms in patients with major depressive disorder: a randomized, double-blind comparison with sertraline.
Kasper S, Hajak G, Wulff K, Hoogendijk WJ, Montejo AL, Smeraldi E, Rybakowski JK, Quera-Salva MA, Wirz-Justice AM, Picarel-Blanchot F, Baylé FJ.
Department of Psychiatry and Psychotherapy, Medical University Vienna, MUV, AKH, Währinger Gürtel 18-20, A-1090 Wien, Austria. biol-psychiatry@meduniwien.ac.at.
OBJECTIVE: This study evaluates the efficacy of agomelatine, the first antidepressant to be an agonist at MT(1)/MT(2) receptors and an antagonist at 5-HT(2C) receptors, versus sertraline with regard to the amplitude of the circadian rest-activity cycle and depressive and anxiety symptoms in patients with major depressive disorder (MDD). METHOD: Outpatients with DSM-IV-TR-defined MDD received either agomelatine 25 to 50 mg (n = 154) or sertraline 50 to 100 mg (n = 159) during a 6-week, randomized, double-blind treatment period. The study was conducted from 2005 to 2006. The main outcome measure was the relative amplitude of the individual rest-activity cycles, expressed as change from baseline to week 6 and collected from continuous records using wrist actigraphy and sleep logs. Secondary outcome measures were sleep efficiency and sleep latency, both derived from actigraphy, and efficacy on depression symptoms (17-Item Hamilton Depression Rating Scale total score and Clinical Global Impressions scale scores) and anxiety symptoms (Hamilton Anxiety Rating Scale total score and subscores). RESULTS: A significant difference in favor of agomelatine compared to sertraline on the relative amplitude of the circadian rest-activity cycle was observed at the end of the first week (P = .01). In parallel, a significant improvement of sleep latency (P <.001) and sleep efficiency (P <.001) from week 1 to week 6 was observed with agomelatine as compared to sertraline. Over the 6-week treatment period, depressive symptoms improved significantly more with agomelatine than with sertraline (P <.05), as did anxiety symptoms (P <.05). CONCLUSIONS: The favorable effect of agomelatine on the relative amplitude of the circadian rest-activity/sleep-wake cycle in depressed patients at week 1 reflects early improvement in sleep and daytime functioning. Higher efficacy results were observed with agomelatine as compared to sertraline on both depressive and anxiety symptoms over the 6-week treatment period, together with a good tolerability profile. These findings indicate that agomelatine offers promising benefits for MDD patients. TRIAL REGISTRATION: www.isrctn.org: ISRCTN49376288. © Copyright 2010 Physicians Postgraduate Press, Inc.
Jammer dat ago nog niet beschikbaar is in Belgie.
Laatst bewerkt:
Amaiii, wat een TOPIC dit!!! 
Oké, nu even mijn beurt
Binnen enkele weken zal ik beginnen met een SNRI kuur,
dus geen SSRI maar wel SNRI
http://nl.wikipedia.org/wiki/SNRI
Ik heb hier thuis Whey Perfection liggen van Body & Fit Sportsnutrition
http://www.bodyenfitshop.nl/eiwitten-alle/body-fit-sportsnutrition/whey-perfection
En ik lees bij de ingrediënten dat daar inderdaad "Tryptophane" (Tryptofaan)
aanwezig is...
Hierbij heb ik 4 vragen:
1) Ik weeg amper 59/60kg voor een lengte van 1m81 en ik vroeg mij
ERNSTIG af of het innemen van 60gram Whey Perfection samen met die SNRI
een probleem kan veroorzaken
2) Wat is nu EXACT het verschil tussen Tryptofaan en L-Tryptofaan
3) In Whey Perfection zitten ook nog andere essentiële aminozuren, namelijk:
Isoleucine, Leucine, Lysine, Methionine,
Fenylalanine, Threonine, Tryptofaan (1068mg) en Valine.
Ik had graag willen weten of er nog andere interacties kunnen ontstaan bij het
innemen van één van die andere essentiële aminozuren naast die Tryptofaan in
combinatie met SSRI of SNRI antidepressiva Of kan het gewoon geen kwaad?
4) Misschien een domme vraag maar toch even vragen: bestaan er whey
shakes zonder die extra toevoeging van essentiële aminozuren die eventueel
af te raden zijn bij combinatie met antidepressiva
God help.....
Nee, ik heb even jullie hulp, tips en adviezen nodig hieromtrent,
misschien leer ik weer iets bij
P.S.: die whey shake ben ik van plan om 's ochtends 30gr bij mijn havermout te
eten en 's avonds 30gr na de training...
Gemeende groetjes
en hopelijk krijg ik wat reacties te lezen hieromtrent
Oké, nu even mijn beurt
Binnen enkele weken zal ik beginnen met een SNRI kuur,
dus geen SSRI maar wel SNRI
http://nl.wikipedia.org/wiki/SNRI
Ik heb hier thuis Whey Perfection liggen van Body & Fit Sportsnutrition
http://www.bodyenfitshop.nl/eiwitten-alle/body-fit-sportsnutrition/whey-perfection
En ik lees bij de ingrediënten dat daar inderdaad "Tryptophane" (Tryptofaan)
aanwezig is...
Hierbij heb ik 4 vragen:
1) Ik weeg amper 59/60kg voor een lengte van 1m81 en ik vroeg mij
ERNSTIG af of het innemen van 60gram Whey Perfection samen met die SNRI
een probleem kan veroorzaken
2) Wat is nu EXACT het verschil tussen Tryptofaan en L-Tryptofaan
3) In Whey Perfection zitten ook nog andere essentiële aminozuren, namelijk:
Isoleucine, Leucine, Lysine, Methionine,
Fenylalanine, Threonine, Tryptofaan (1068mg) en Valine.
Ik had graag willen weten of er nog andere interacties kunnen ontstaan bij het
innemen van één van die andere essentiële aminozuren naast die Tryptofaan in
combinatie met SSRI of SNRI antidepressiva
Of kan het gewoon geen kwaad?4) Misschien een domme vraag maar toch even vragen: bestaan er whey
shakes zonder die extra toevoeging van essentiële aminozuren die eventueel
af te raden zijn bij combinatie met antidepressiva
God help.....
Nee, ik heb even jullie hulp, tips en adviezen nodig hieromtrent,
misschien leer ik weer iets bij
P.S.: die whey shake ben ik van plan om 's ochtends 30gr bij mijn havermout te
eten en 's avonds 30gr na de training...
Gemeende groetjes
en hopelijk krijg ik wat reacties te lezen hieromtrent
Laatst bewerkt:
- Lid geworden
- 29 okt 2010
- Berichten
- 8.610
- Waardering
- 894
- Lengte
- 1m90
supermegagroteergeflinkewaanzinnigeuberbump
ff serieus a.u.b.
- Lid geworden
- 20 dec 2007
- Berichten
- 730
- Waardering
- 15
- Lengte
- 1m74
- Massa
- 83kg
- Vetpercentage
- 11%
Amaiii, wat een TOPIC dit!!!
Oké, nu even mijn beurt
Binnen enkele weken zal ik beginnen met een SNRI kuur,
dus geen SSRI maar wel SNRI
http://nl.wikipedia.org/wiki/SNRI
Ik heb hier thuis Whey Perfection liggen van Body & Fit Sportsnutrition
http://www.bodyenfitshop.nl/eiwitten-alle/body-fit-sportsnutrition/whey-perfection
En ik lees bij de ingrediënten dat daar inderdaad "Tryptophane" (Tryptofaan)
aanwezig is...
Hierbij heb ik 4 vragen:
1) Ik weeg amper 59/60kg voor een lengte van 1m81 en ik vroeg mij
ERNSTIG af of het innemen van 60gram Whey Perfection samen met die SNRI
een probleem kan veroorzaken
2) Wat is nu EXACT het verschil tussen Tryptofaan en L-Tryptofaan
3) In Whey Perfection zitten ook nog andere essentiële aminozuren, namelijk:
Isoleucine, Leucine, Lysine, Methionine,
Fenylalanine, Threonine, Tryptofaan (1068mg) en Valine.
Ik had graag willen weten of er nog andere interacties kunnen ontstaan bij het
innemen van één van die andere essentiële aminozuren naast die Tryptofaan in
combinatie met SSRI of SNRI antidepressiva
4) Misschien een domme vraag maar toch even vragen: bestaan er whey
shakes zonder die extra toevoeging van essentiële aminozuren die eventueel
af te raden zijn bij combinatie met antidepressiva
God help.....
Nee, ik heb even jullie hulp, tips en adviezen nodig hieromtrent,
misschien leer ik weer iets bij
P.S.: die whey shake ben ik van plan om 's ochtends 30gr bij mijn havermout te
eten en 's avonds 30gr na de training...
Gemeende groetjes
en hopelijk krijg ik wat reacties te lezen hieromtrent
1)Nee.
Reden dat L-Tryptofaan op bijsluiter staat is dat het een precursor is voor serotonine.
Een ssri en snri verhogen serotonine in de hersenen.
Dus het kan kans verhogen op een serotonine vergiftiging.
Zou me er niet druk om maken een serotonine vergiftiging krijg je niet zo snel.
en zeker niet van dat beetje L-Tryptofaan wat je met voeding,eiwitten binnen krijgt.
En als je het krijgt een serotonine vergiftiging voel direct.
2)Zelfde stof.
3)Kan geen kwaad.
4)Er is geen extra toevoeging van essentiële aminozuren.een eiwit bestaat uit aminozuren.
Beste,
ik lees net op de volgende pagina:
http://nl.wikipedia.org/wiki/Essentiële_aminozuren
Aanbevolen dagelijkse hoeveelheden
Bij "Tryptofaan" staat er 4mg per kg lichaamsgewicht!!!
Als ik er 59 weeg dan is dat maal 4 = 236mg ADH Tryptofaan/dag
dat ik mag nuttigen...
In 100 gram Whey Perfection zit er 1068mg "Tryptofaan" !!!!!
Als ik op een dag 60gr whey zou gebruiken dan is dat nog steeds 640mg :S
Wat nu
- Lid geworden
- 20 dec 2007
- Berichten
- 730
- Waardering
- 15
- Lengte
- 1m74
- Massa
- 83kg
- Vetpercentage
- 11%
Beste,
ik lees net op de volgende pagina:
http://nl.wikipedia.org/wiki/Essentiële_aminozuren
Aanbevolen dagelijkse hoeveelheden
Bij "Tryptofaan" staat er 4mg per kg lichaamsgewicht!!!
Als ik er 59 weeg dan is dat maal 4 = 236mg ADH Tryptofaan/dag
dat ik mag nuttigen...
In 100 gram Whey Perfection zit er 1068mg "Tryptofaan" !!!!!
Als ik op een dag 60gr whey zou gebruiken dan is dat nog steeds 640mg :S
Wat nu
Er zijn genoeg bbers die ssri's nemen.
Waarvan die gasten makkelijk 2-3+g eiwit per kg vvm(vet vrije massa) binnen krijgen.
Die gasten krijgen heel wat meer l-tryptofaan binnen als jij.
60 g eiwit krijgt een niet bber al snel binnen op een dag.
Als het niet kon zou iedereen die vlees eet en een ssri neemt een serotonine vergiftiging krijgen.
Kijk probeer het gewoon,dit gaat normaal echt geen problemen geven.
Als je toevallig toch symptomen van serotonine vergiftiging krijgt weet je waar het aan ligt en kan je nog altijd eiwit beperken.
Als je dit krijgt merk je het toch direct.
