kindred
New member
There were no ducks so i ate them myself. I appreciate the help. Im afraid im a hopeless case. All my problems can be solved by execive alcohol consumption.
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Anyone dealing with depression of anxiety?
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- anxiety dealing depression
There were no ducks so i ate them myself. I appreciate the help. Im afraid im a hopeless case. All my problems can be solved by execive alcohol consumption.
Christian
Active Member, June10MOTM
Thats ridiculous mate, Alcohol only leads to more problems...
No matter how hopeless life seems sometimes there is always something you can do to better yourself.
**** i might have a brain tumour but i still stay optimisitc that there is hope for me.
You have to do the say, think positive and try and be positive there are supplements and therapies that can help you overcome what you are feeling you just need to explain a litte more exactly what is troubling you.
T
timmy_is_trying
Guest
sorry about bumping this thread, but i have been on Effexor for the last 7 years. I feel 'normal' now and have done for a while, but can certainly relate to the dark times, so im happy to have a chat if stuff is weighing ya down 
Christian
Active Member, June10MOTM
sorry about bumping this thread, but i have been on Effexor for the last 7 years. I feel 'normal' now and have done for a while, but can certainly relate to the dark times, so im happy to have a chat if stuff is weighing ya down
I thought i was fine on effexor, its not until im getting off it i realise how much better i am..
I have almost completley cured my self of Panic Disorder/Ocd
I am down to 35.7 mg from 150mg.. I have tried all anti depressants valium constantly..
5htp and melatonin and high dose niacin therapy and lifestyle change have saved mylife.. I hope to be off effexor soon and getting back into life..
no need to sorry about bumping the thread ,it is here for a reasonsorry about bumping this thread, but i have been on Effexor for the last 7 years. I feel 'normal' now and have done for a while, but can certainly relate to the dark times, so im happy to have a chat if stuff is weighing ya down
Grippy
Fat Member
Good luck to everyone dealing with these issues, they can be tough, I have dealt with anxiety for over 10 years now. I had a massive asthma attack where i went in to respiratory arrest, passed out and woke up in hospital on life support with all sorts of shit hanging off me and not being able to move due to the paralysis drug they pumped into me. After a few months and once I was back to normal I started freaking out all the time thinking I couldn't breathe, you know, tight chest, clenched fists, have to get away, the sweats. Alcohol and lots of it often fixed it for a while until it got really bad. Doctor put me on xanax and zoloft for a while but I stopped taking the zoloft as I hated the way it made me feel (not normal).
I have it under control now and have done for a few years, the thing that has worked is plenty of exercise, lots of sleep, eating clean and no booze. I find the day after drinking I have a hard time dealing with it and if I a heap of sugary shit I will get panicky.
I have it under control now and have done for a few years, the thing that has worked is plenty of exercise, lots of sleep, eating clean and no booze. I find the day after drinking I have a hard time dealing with it and if I a heap of sugary shit I will get panicky.
T
timmy_is_trying
Guest
you have done well to go down from 150mg to 37.5! Here a lot of horror stories of people coming off effexor. I was on 150, then 225, now have been back to 150 for the past 2 years. Im not sure if i want to go off of it, but i think thats a mental block of mine-i remember the dark times too vividly and feel that these meds are a safety net.
Last time i had a bout of depression i was exercising like i am now, so it wasnt the lack of physical activity or unhealthy lifestyle which caused it for me. Stress i believe, it builds on you i guess. That and every single member of my family (6 of us) are on anti-d's so i guess there may perhaps be a genetic link, i dont know.
zoloft is one nasty drug.
Christian
Active Member, June10MOTM
Hypothetical Explanation of Panic Disorder
--------------------------------------------------------------------------------
Copyright ã 2001 James Michael Howard and German Journal of Psychiatry 2001; 4: 40-42
--------------------------------------------------------------------------------
Abstract
Panic attacks may result from severe reduction of dehydroepiandrosterone (DHEA) in a person of low DHEA with normal or increased levels of cortisol. That is, an excessive ratio of cortisol to DHEA occurs which extinguishes the effects of unstable DHEA and magnifies the effects of cortisol. Prolactin increases during panic attacks and is correlated with attack severity. That is, prolactin increases to stimulate DHEA, but the response is inadequate to stabilize the DHEA to cortisol ratio and inhibit prolactin production. Therefore, prolactin remains elevated during an attack. Panic attacks occur when the effects of excessive cortisol excite prolactin stimulation of DHEA in a person who cannot respond with adequate DHEA.
Key words: cortisol, cholecystokinin, dehydroepiandrosterone, panic disorder, prolactin
The physiological mechanism of panic attacks is unexplained. I suggest panic attacks occur because of an acute reduction in availability of the major adrenal steroid hormone, dehydroepiandrosterone (DHEA) in people who already produce low levels. My primary hypothesis is DHEA optimizes transcription and replication of DNA. Therefore, all tissues are activated by DHEA. It follows that DHEA activates the brain. Therefore, consciousness is a function of times of high DHEA and sleep is a time of low DHEA. I think cortisol, the second major adrenal steroid hormone, evolved to counteract the effects of DHEA during aggressive, potentially harmful or lethal, conflicts. Antagonism of DHEA by cortisol may be the basis of "fight or flight," which has high survival value. Cortisol production causes stress. The ratio of DHEA to cortisol should affect all tissues, especially neurological tissues, and becomes pathological in individuals who experience panic attacks.
Cortisol is involved in panic attacks. One study of panic attacks reported "subtle but significant elevation of cortisol levels" compared to controls, however, these levels did not correlate significantly with the severity of panic attacks (Bandelow, et al., 2000a). A subsequent study found nocturnal cortisol levels tend to be higher and "occurred mainly in more severely ill panic patients." (Bandelow, et al., 2000b). Another study confirms lack of high cortisol levels with all panic attacks, i.e., plasma cortisol was elevated only during some attacks (Cameron, et al., 1987). Cortisol is connected to panic attacks, but cortisol levels, alone, do not cause panic attacks
Cholecystokinin (CCK) increases cortisol and provokes panic attacks, even in some healthy subjects. "In seven subjects, cholecystokinin-4 provoked a short-lasting (one to four minutes) panic-like attack (an intense unexplainable fear) at doses between 20 and 100 micrograms. In the other three subjects, doses of 80 to 100 micrograms induced severe anxiety, but no panic-like attack." (de Montigny, 1989). A larger study of healthy individuals of two different age groups (20-35 years- and 65-81 years-old) treated with CCK found "cortisol was significantly greater with CCK than with placebo," but the cortisol levels "were not correlated with symptom severity, suggesting that other factors may have contributed to the differential effect of panic on the HPA axis." (Flint, et al., 2000). In patients with panic disorder, CCK consistently stimulated panic attacks identical to spontaneous panic attacks (Bradwejn, et al., 1990).
Prolactin production increases during spontaneous panic attacks and panic attacks induced by CCK (de Montigny, 1989). In the study of CCK in healthy adults of differing ages, Flint, et al., found that "maximum increase in prolactin, ACTH and cortisol was significantly greater with CCK," compared to placebo (Flint, et al., 2000). More importantly, prolactin correlates with the severity of spontaneous panic attacks. "Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity." (Cameron, et al., 1987). Prolactin levels are directly tied to panic attacks and their severity.
I suggest the increase in prolactin during spontaneous panic attacks and during "panic-like attacks in healthy volunteers" induced by CCK (de Montigny, 1989) represent a mechanism for increasing DHEA during attacks. In young baboons, prolactin specifically stimulates DHEA: "in contrast to ACTH, the action of PRL [prolactin] on the adrenal is apparently specific for androgen [DHEA] production." (Pepe, 1985). Hyperprolactinemia occurs with elevated DHEAS in women. When hyperprolactinemia is reduced with bromocriptine, DHEAS levels are reduced without changes in cortisol levels (Schiebinger, et al., 1986). Reducing prolactin reduces DHEAS. (DHEA sulfate, DHEAS, is the large supply of DHEA available in blood. The active molecule, DHEA, is derived from this supply.) >P? Fava, et al., measured the ratio of DHEAS to cortisol in panic disorder. They examined this ratio because the ratio had "been used as an index of adrenocortical function, [they hypothesized the ratio] would be altered in panic disorder patients and would change after treatment." They reported "No significant differences were noted between pretreatment and posttreatment DHEA-S/cortisol ratio values in patients treated with alprazolam(n = 8), in patients treated with clonazepam (n = 13), or in patients treated with placebo (n = 3)." Of importance to this treatise is their finding that "The DHEA-S/cortisol ratio values in the 24 patients with panic disorder (mean = 20.5, SD = 11.6) were significantly higher than those of a group of 60 normal controls (mean = 11.5, SD = 6.01) and were also significantly higher than those of a group of 22 depressed patients (mean = 10.6, SD = 6.33)." (Fava, et al., 1989)
If one assumes that DHEA is the active molecule, the findings of Fava, et al., may be explained. Patients with panic disorder may produce significantly less DHEA than controls and depressed patients because panic attack patients are not producing DHEA from DHEAS, so their DHEAS to cortisol ratio is very high. Fava, et al., also found no differences when their patients were treated with alprazolam. However, Kroboth, et al., report that alprazolam increases DHEA significantly in "healthy volunteers (25 young men, aged 22-35, and 13 elderly men, aged 65-75)." "Alprazolam produced (1) significant increases in DHEA concentrations at 7 hours in both young and elderly men; (2) significant decreases in cortisol concentrations; and (3) no change in DHEA-S concentrations." (Kroboth, et al., 1999). The lack of change in DHEAS levels may suggest the conversion from cortisol to DHEA in healthy individuals.
DHEA reduces prolactin levels (Milewich, et al., 1995). A sufficiently high level of DHEA inhibits prolactin production. This is a cyclic mechanism involving prolactin and DHEA. Healthy individuals produce sufficient DHEA to reduce prolactin levels. Patients with panic attack disorder who produce very low DHEA cannot reduce prolactin by feedback inhibition from DHEA. This is why "Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity." (Cameron, et al., 1987).
It is my hypothesis that DHEA stimulates consciousness during the day and declines at night, to allow sleep. During sleep, I think DHEA declines to lowest levels during delta (slow-wave) sleep, with levels maintained just sufficient to support cardiovascular activity. This level is maintained by the cyclic mechanism involving prolactin. When DHEA declines to low levels, prolactin increases and stimulates sufficient DHEA to maintain the brainstem. When this cycling occurs, DHEA levels overshoot and decrease prolactin. This extra DHEA stimulates the brain. This slight increase in DHEA during sleep activates the brain and produces REM sleep or dreaming. Therefore, according to my model of sleep, delta sleep represents a time of low DHEA and REM sleep represents a time of higher DHEA during sleep. Kronenberg, et al., administered CCK to healthy subjects during REM sleep and delta sleep. CCK produced panic attack-like effects of greater intensity during the time of lowest DHEA, that is, delta sleep. "In nine subjects, stimulation with 50 µg CCK-4 during REM sleep failed to elicit a full-blown panic awakening, while the same dose, administered during delta sleep, produced full-blown panic attacks in two participants. Similarly, stimulation of six subjects with 100 µg CCK-4 during REM sleep resulted in only one panic response, whereas four of nine subjects awoke experiencing a panic attack following stimulation with the identical dose during delta sleep. Severity of panic symptomatology, as measured by the self-rated Acute Panic Inventory, was also significantly increased when CCK-4 was administered during delta sleep." (Kronenberg, et al., 2001). This study supports a connection of low DHEA with panic attacks. Since Bandelow, et al., 2000b, found higher levels of nocturnal cortisol in "more severely ill panic patients" and Abelson and Curtis also reported "overnight hypercortisolemia" in panic disorder (Abelson and Curtis, 1996), this could indicate conversion from DHEA to cortisol in panic disorder.
Panic attacks may be due to very low DHEA levels relative to cortisol levels, possibly resulting from conversion of DHEA to cortisol. Therefore, normal levels of cortisol may predispose an individual to panic attacks even without a triggering event. If cortisol levels are high relative to DHEA between attacks, the individual may experience intermittent or continuous anxiety. Therefore, any latent physiological or psychological change which increases the cortisol to DHEA ratio could excite a panic attack. Prolactin levels increase during panic attacks and are directly connected to severity. Prolactin increases to stimulate DHEA. Since prolactin levels are decreased by DHEA and panic attack sufferers cannot produce sufficient DHEA, prolactin levels remain high and connected with the panic attack. Panic attacks result from the inability to respond to excess cortisol relative to DHEA.
--------------------------------------------------------------------------------
Copyright ã 2001 James Michael Howard and German Journal of Psychiatry 2001; 4: 40-42
--------------------------------------------------------------------------------
Abstract
Panic attacks may result from severe reduction of dehydroepiandrosterone (DHEA) in a person of low DHEA with normal or increased levels of cortisol. That is, an excessive ratio of cortisol to DHEA occurs which extinguishes the effects of unstable DHEA and magnifies the effects of cortisol. Prolactin increases during panic attacks and is correlated with attack severity. That is, prolactin increases to stimulate DHEA, but the response is inadequate to stabilize the DHEA to cortisol ratio and inhibit prolactin production. Therefore, prolactin remains elevated during an attack. Panic attacks occur when the effects of excessive cortisol excite prolactin stimulation of DHEA in a person who cannot respond with adequate DHEA.
Key words: cortisol, cholecystokinin, dehydroepiandrosterone, panic disorder, prolactin
The physiological mechanism of panic attacks is unexplained. I suggest panic attacks occur because of an acute reduction in availability of the major adrenal steroid hormone, dehydroepiandrosterone (DHEA) in people who already produce low levels. My primary hypothesis is DHEA optimizes transcription and replication of DNA. Therefore, all tissues are activated by DHEA. It follows that DHEA activates the brain. Therefore, consciousness is a function of times of high DHEA and sleep is a time of low DHEA. I think cortisol, the second major adrenal steroid hormone, evolved to counteract the effects of DHEA during aggressive, potentially harmful or lethal, conflicts. Antagonism of DHEA by cortisol may be the basis of "fight or flight," which has high survival value. Cortisol production causes stress. The ratio of DHEA to cortisol should affect all tissues, especially neurological tissues, and becomes pathological in individuals who experience panic attacks.
Cortisol is involved in panic attacks. One study of panic attacks reported "subtle but significant elevation of cortisol levels" compared to controls, however, these levels did not correlate significantly with the severity of panic attacks (Bandelow, et al., 2000a). A subsequent study found nocturnal cortisol levels tend to be higher and "occurred mainly in more severely ill panic patients." (Bandelow, et al., 2000b). Another study confirms lack of high cortisol levels with all panic attacks, i.e., plasma cortisol was elevated only during some attacks (Cameron, et al., 1987). Cortisol is connected to panic attacks, but cortisol levels, alone, do not cause panic attacks
Cholecystokinin (CCK) increases cortisol and provokes panic attacks, even in some healthy subjects. "In seven subjects, cholecystokinin-4 provoked a short-lasting (one to four minutes) panic-like attack (an intense unexplainable fear) at doses between 20 and 100 micrograms. In the other three subjects, doses of 80 to 100 micrograms induced severe anxiety, but no panic-like attack." (de Montigny, 1989). A larger study of healthy individuals of two different age groups (20-35 years- and 65-81 years-old) treated with CCK found "cortisol was significantly greater with CCK than with placebo," but the cortisol levels "were not correlated with symptom severity, suggesting that other factors may have contributed to the differential effect of panic on the HPA axis." (Flint, et al., 2000). In patients with panic disorder, CCK consistently stimulated panic attacks identical to spontaneous panic attacks (Bradwejn, et al., 1990).
Prolactin production increases during spontaneous panic attacks and panic attacks induced by CCK (de Montigny, 1989). In the study of CCK in healthy adults of differing ages, Flint, et al., found that "maximum increase in prolactin, ACTH and cortisol was significantly greater with CCK," compared to placebo (Flint, et al., 2000). More importantly, prolactin correlates with the severity of spontaneous panic attacks. "Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity." (Cameron, et al., 1987). Prolactin levels are directly tied to panic attacks and their severity.
I suggest the increase in prolactin during spontaneous panic attacks and during "panic-like attacks in healthy volunteers" induced by CCK (de Montigny, 1989) represent a mechanism for increasing DHEA during attacks. In young baboons, prolactin specifically stimulates DHEA: "in contrast to ACTH, the action of PRL [prolactin] on the adrenal is apparently specific for androgen [DHEA] production." (Pepe, 1985). Hyperprolactinemia occurs with elevated DHEAS in women. When hyperprolactinemia is reduced with bromocriptine, DHEAS levels are reduced without changes in cortisol levels (Schiebinger, et al., 1986). Reducing prolactin reduces DHEAS. (DHEA sulfate, DHEAS, is the large supply of DHEA available in blood. The active molecule, DHEA, is derived from this supply.) >P? Fava, et al., measured the ratio of DHEAS to cortisol in panic disorder. They examined this ratio because the ratio had "been used as an index of adrenocortical function, [they hypothesized the ratio] would be altered in panic disorder patients and would change after treatment." They reported "No significant differences were noted between pretreatment and posttreatment DHEA-S/cortisol ratio values in patients treated with alprazolam(n = 8), in patients treated with clonazepam (n = 13), or in patients treated with placebo (n = 3)." Of importance to this treatise is their finding that "The DHEA-S/cortisol ratio values in the 24 patients with panic disorder (mean = 20.5, SD = 11.6) were significantly higher than those of a group of 60 normal controls (mean = 11.5, SD = 6.01) and were also significantly higher than those of a group of 22 depressed patients (mean = 10.6, SD = 6.33)." (Fava, et al., 1989)
If one assumes that DHEA is the active molecule, the findings of Fava, et al., may be explained. Patients with panic disorder may produce significantly less DHEA than controls and depressed patients because panic attack patients are not producing DHEA from DHEAS, so their DHEAS to cortisol ratio is very high. Fava, et al., also found no differences when their patients were treated with alprazolam. However, Kroboth, et al., report that alprazolam increases DHEA significantly in "healthy volunteers (25 young men, aged 22-35, and 13 elderly men, aged 65-75)." "Alprazolam produced (1) significant increases in DHEA concentrations at 7 hours in both young and elderly men; (2) significant decreases in cortisol concentrations; and (3) no change in DHEA-S concentrations." (Kroboth, et al., 1999). The lack of change in DHEAS levels may suggest the conversion from cortisol to DHEA in healthy individuals.
DHEA reduces prolactin levels (Milewich, et al., 1995). A sufficiently high level of DHEA inhibits prolactin production. This is a cyclic mechanism involving prolactin and DHEA. Healthy individuals produce sufficient DHEA to reduce prolactin levels. Patients with panic attack disorder who produce very low DHEA cannot reduce prolactin by feedback inhibition from DHEA. This is why "Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity." (Cameron, et al., 1987).
It is my hypothesis that DHEA stimulates consciousness during the day and declines at night, to allow sleep. During sleep, I think DHEA declines to lowest levels during delta (slow-wave) sleep, with levels maintained just sufficient to support cardiovascular activity. This level is maintained by the cyclic mechanism involving prolactin. When DHEA declines to low levels, prolactin increases and stimulates sufficient DHEA to maintain the brainstem. When this cycling occurs, DHEA levels overshoot and decrease prolactin. This extra DHEA stimulates the brain. This slight increase in DHEA during sleep activates the brain and produces REM sleep or dreaming. Therefore, according to my model of sleep, delta sleep represents a time of low DHEA and REM sleep represents a time of higher DHEA during sleep. Kronenberg, et al., administered CCK to healthy subjects during REM sleep and delta sleep. CCK produced panic attack-like effects of greater intensity during the time of lowest DHEA, that is, delta sleep. "In nine subjects, stimulation with 50 µg CCK-4 during REM sleep failed to elicit a full-blown panic awakening, while the same dose, administered during delta sleep, produced full-blown panic attacks in two participants. Similarly, stimulation of six subjects with 100 µg CCK-4 during REM sleep resulted in only one panic response, whereas four of nine subjects awoke experiencing a panic attack following stimulation with the identical dose during delta sleep. Severity of panic symptomatology, as measured by the self-rated Acute Panic Inventory, was also significantly increased when CCK-4 was administered during delta sleep." (Kronenberg, et al., 2001). This study supports a connection of low DHEA with panic attacks. Since Bandelow, et al., 2000b, found higher levels of nocturnal cortisol in "more severely ill panic patients" and Abelson and Curtis also reported "overnight hypercortisolemia" in panic disorder (Abelson and Curtis, 1996), this could indicate conversion from DHEA to cortisol in panic disorder.
Panic attacks may be due to very low DHEA levels relative to cortisol levels, possibly resulting from conversion of DHEA to cortisol. Therefore, normal levels of cortisol may predispose an individual to panic attacks even without a triggering event. If cortisol levels are high relative to DHEA between attacks, the individual may experience intermittent or continuous anxiety. Therefore, any latent physiological or psychological change which increases the cortisol to DHEA ratio could excite a panic attack. Prolactin levels increase during panic attacks and are directly connected to severity. Prolactin increases to stimulate DHEA. Since prolactin levels are decreased by DHEA and panic attack sufferers cannot produce sufficient DHEA, prolactin levels remain high and connected with the panic attack. Panic attacks result from the inability to respond to excess cortisol relative to DHEA.
kindred
New member
Nothing numbs the pain I feel on a daily basis. I cry everyday and think about death multiple times a day. I have no reason to feel this way and the mental health system is reluctant to assist me. Do i get depressed? I dont know if depressed is the right word to describe how I feel. All I have left is randomly typing bullshit into random forums and chat sites on the net.
Christian
Active Member, June10MOTM
You need help kindred...
Please look for it.
Buy this book kindred...
The UltraMind Solution by Mark Hyman, M.D.
You might find it helpfull
Please look for it.
Buy this book kindred...
The UltraMind Solution by Mark Hyman, M.D.
You might find it helpfull
well get out there and do something!!!! dont just sit there, as much as your mind or body is saying to just sit there actually do the opposite as hard as it may be and get out there and just do something.. buy a plane ticket to the goldie or something and so something completely different.
kindred
New member
The book looks interesting I may read it thank you.
I would like to add I have sought help from doctors, counsellors psychologists and psychiatrists all told me to suck it up. What am I to do? You tell me.
kindred
New member
Thank you for your advice. I will consider it carefully.
Christian
Active Member, June10MOTM
Read that book and fix your problrems...
GO to amazon now and buy it.
If u dont like to read go find the audio book online.
its pretty much up to you kindred.. other people can only do so much its up to you as an individual to change how you are... YOU are the only one who can do it, people can give you ideas or help you how to think or sort through things but that is all pointless if the individual will not help themself...
ITS ALL YOU! break the cycle and actually fix the issue
ITS ALL YOU! break the cycle and actually fix the issue
