Question:
Rita, How sad you had to miss out on so many events with your children. I am sorry for you. One of the worst ones on your list was the parent teacher conferences – oh my good though were sotough. You and the teacher one on one – sheer hell for me. I always made my childrenstand out in the hall and I don’t know how I ever made it through those… But, you have a good day today and I am happy for you that your life has changed in a more positive direction. smiles, elise
– Hide quoted text — Show quoted text – Rand, you took up a lot of our time, so now let me take up some of yours. I just cannot keep quiet any longer. Let me tell you what NOT taking benzo’s can do to a persons life for 18 years. In 1970 while pregnant with my fourth child, I suddenly developed severe agoraphobia and panic attacks when ever I left my home. But I would not take any medications…I thought I was going crazy, so I never told anyone what was going on inside me for 3 years. Have you any idea the creative lies an agoraphobic can come up with? But better than that, let me list some of the things not taking a benzo did for me over the next 18 years…still with me? I hope so because I’m talking about not taking benzo’s and that’s your favorite topic. First thing it did for me was prevent me from taking my baby daughter out to buy her a baby bonnet. Now I know you think I’m being silly, but after 3 boys, I wanted to buy a frilly baby bonnet, but Grandmom had the thrill of her life buying those bonnets while I stayed home and twiddled my thumbs. Because I wouldn’t take a benzo, I never went to any of my kid’s teacher conferences…someone else had to go in my place..my husband, my Mom, and they had to sit there and listen to how great the kids were doing and looking at all the silly stuff the kids made in school…how dull. I did not go to the hospital when my biological mother lay dying for 3 months because I wouldn’t take a benzo…so my husband went every night without fail and had to comfort and encourage her. We all know how tiring that can be…meanwhile, I again stayed home and did my nails. I also didn’t go to the hospital when my daughter, now 8, broke her leg and had to be operated on…her Dad got the privilege of staying with her all night while I slept in my comfortable bed. Lucky me. I never says my son’s play football, run track and break some records…but I was home in my warm comfortable house, while their father and uncles had to stand in the cold. I never got the chance to go with my daughter to buy a prom gown…her Godmother had the fun of doing that…but who wants to be bothered by crowds of people in a store? I didn’t see my one son inducted in the National Honor Society…but my husband got a day off work, so it was worth it. I didn’t once see the inside of an orthodontist office for two of my kids, but who wants to sit around in a dentist’s office…again my husband got to get off work early for two years…he really enjoyed the time off. I didn’t have to sit in a crowded autitorium watching my 4 children graduate…the rest of my family had to endure the heat and emotion, but I got to stay in an air-conditioned house…wasn’t I the lucky one? I made it to my oldest son’s wedding and an hour of his reception, but then it was time for me to go…who wants to stand around and chitchat with family and friends and dance and have a good time….I got to see the video, so I didn’t miss a thing. These are just a few of the fun things that not taking a benzo afforded me. There’s lots of everyday things I didn’t do , but I was lucky…there was always someone else ready to take my place. My kids never even missed me. But sadly, here the story changes. In 1988 I had a doctor who insisted I take benzo’s for depression and Panic Disorder. I really had no choice in the matter. But taking a benzo forced me to attend the next 3 of my children’s weddings and I had to enjoy myself and dance and have a ball. I was forced to take my grandchildren to the playgrounds and play with them….and those soccor games and T-ball games…I had to sit and watch them play and laugh and have fun…how awful for me. Even though I got out of having to go to those horrible stores and buy a prom gown, now I had to go and buy a wedding dress…that was the worst of all. I even cried when I first saw her in her wedding gown…can you imagine that? Well, I could go on and on, but I’ve taken up enough of your time. But I think you get the drift of what I’ve been trying to say. In case you missed it…being off a benzo lost me the most valuable time of my life, never to be returned…but being on one gave me my life back and a second chance to enjoy what I had missed. Tell me, Rand, which life would you choose if you were in my shoes? Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon discontinuance there can be profound dysregulation of this stress axis. The neurotransmitters of the pons, medulla and basal ganglia are in a state of rebound excitability. The hypothalamus depends on the input from this area. It is the function of the hypothalamus to respond to these neurotransmitters as well as other modulators and peptides and maintain the body in homeostatic balance. All the body’s hormone regulation, appetite control, water and mineral balance, blood pressure and temperature regulation, immune response and more depend on the proper function of the hypothalamus. Exposure to benzodiazepines causes ligand induced changes (tolerance) and upregulation of peripheral-type benzodiazepine receptors especially in the hypothalamus and hippocampus, but also in the liver, kidney, gut and heart. Tolerance to benzodiazepines is defined as a decreased sensitivity of receptors and ligand induced changes in receptors rendering them unresponsive to the anxiolytic GABA – a shift in efficacy. These endogenous ligands for the benzodiazepine receptor exhibit inverse agonist properties. Tolerance can develop with repeat exposure, or in as little as 4 days as is the case with the short half life benzodiazepine Xanax, a triazalone benzodiazepine. It can also develop in one single exposure especially if given to the level of anaesthesia. Further exposure to benzodiazepines now produces anxiety. There may be a role for antagonists or inverse agonists in facilitating benzodiazepine withdrawal. The partial inverse agonist beta carboline passion flower has helped some with withdrawal anxiety. There is a beta carboline, abecarnil, being investigated as helpful in benzodiazepine withdrawal, the possibility exists that it can facilitate the re-adaptation of receptors to the benzo free state. However, there is a caution that tolerance may develop in as little as 3 weeks and there is a withdrawal as well. Dysregulation of this stress axis at the adrenals results in over production of glucocorticoids (which regulate carbohydrate metabolism and insulin responsiveness), mineralcorticoids (which regulate electrolytes and water balance) and androgens (sex and growth hormones). It is here that problems with acid/base balance emerge and further compound the metabolic disturbances at the liver. The hormone vasopressin (antidiuretic hormone) produced at the hypothalamus is responsible for keeping us continent. When we urinate all night long, it reflects a problem with ADH. It is unresponsive at the hypothalamus. We become dehydrated. Sodium and uric acid can increase as the kidney, sensing volume depletion, conserves sodium in an attempt to conserve water. Uric acid is conserved simultaneously. We lose potassium and magnesium in the diuresis. These effects are mediated by glucocorticoids (at the adrenal cortex) that cause hyperinsulinemia and insulin resistance. The decreased renal perfusion due to the action of excessive norepinephrine and epinephrine (at the adrenal medulla) also contributes by increasing the hormone rennin which in turn causes the production of another hormone angiotension II in the liver. This leads to increased kidney hormones aldosterone , cortisol and dehydrocorticosterone which causes further sodium retention. All body functions that depend on the correct ratio of minerals (electrolytes) is adversely affected. With increased sodium retention there is CNS disturbance and neuromuscular excitability. The fluid in our bodies begins to shift from the vascular compartment and cellular compartments to the interstitial spaces resulting in oedema. The neurochemical messages that depend on the right electrolyte being in the right compartment is now impaired. So we can see that another mechanism for cerebral ammonia accumulation is due to problems with the kidney and its relationship with the liver and the hormonal influence of the hypothalamus. It has been observed that haloperidol, a major tranquilliser, as well as tricyclic antidepressants, cocaine and amphetamines alter fluid and electrolyte balance. It is obvious to those of us suffering in benzodiazepine withdrawal that this oedema, frequent urination, thirst and much more is a reflection of a similar mechanism – a multimetabolic syndrome. Portal-systemic
… read more »
Response:
Rand, you took up a lot of our time, so now let me take up some of yours. I just cannot keep quiet any longer. Let me tell you what NOT taking benzo’s can do to a persons life for 18 years. In 1970 while pregnant with my fourth child, I suddenly developed severe agoraphobia and panic attacks when ever I left my home. But I would not take any medications…I thought I was going crazy, so I never told anyone what was going on inside me for 3 years. Have you any idea the creative lies an agoraphobic can come up with? But better than that, let me list some of the things not taking a benzo did for me over the next 18 years…still with me? I hope so because I’m talking about not taking benzo’s and that’s your favorite topic. First thing it did for me was prevent me from taking my baby daughter out to buy her a baby bonnet. Now I know you think I’m being silly, but after 3 boys, I wanted to buy a frilly baby bonnet, but Grandmom had the thrill of her life buying those bonnets while I stayed home and twiddled my thumbs. Because I wouldn’t take a benzo, I never went to any of my kid’s teacher conferences…someone else had to go in my place..my husband, my Mom, and they had to sit there and listen to how great the kids were doing and looking at all the silly stuff the kids made in school…how dull. I did not go to the hospital when my biological mother lay dying for 3 months because I wouldn’t take a benzo…so my husband went every night without fail and had to comfort and encourage her. We all know how tiring that can be…meanwhile, I again stayed home and did my nails. I also didn’t go to the hospital when my daughter, now 8, broke her leg and had to be operated on…her Dad got the privilege of staying with her all night while I slept in my comfortable bed. Lucky me. I never says my son’s play football, run track and break some records…but I was home in my warm comfortable house, while their father and uncles had to stand in the cold. I never got the chance to go with my daughter to buy a prom gown…her Godmother had the fun of doing that…but who wants to be bothered by crowds of people in a store? I didn’t see my one son inducted in the National Honor Society…but my husband got a day off work, so it was worth it. I didn’t once see the inside of an orthodontist office for two of my kids, but who wants to sit around in a dentist’s office…again my husband got to get off work early for two years…he really enjoyed the time off. I didn’t have to sit in a crowded autitorium watching my 4 children graduate…the rest of my family had to endure the heat and emotion, but I got to stay in an air-conditioned house…wasn’t I the lucky one? I made it to my oldest son’s wedding and an hour of his reception, but then it was time for me to go…who wants to stand around and chitchat with family and friends and dance and have a good time….I got to see the video, so I didn’t miss a thing. These are just a few of the fun things that not taking a benzo afforded me. There’s lots of everyday things I didn’t do , but I was lucky…there was always someone else ready to take my place. My kids never even missed me. But sadly, here the story changes. In 1988 I had a doctor who insisted I take benzo’s for depression and Panic Disorder. I really had no choice in the matter. But taking a benzo forced me to attend the next 3 of my children’s weddings and I had to enjoy myself and dance and have a ball. I was forced to take my grandchildren to the playgrounds and play with them….and those soccor games and T-ball games…I had to sit and watch them play and laugh and have fun…how awful for me. Even though I got out of having to go to those horrible stores and buy a prom gown, now I had to go and buy a wedding dress…that was the worst of all. I even cried when I first saw her in her wedding gown…can you imagine that? Well, I could go on and on, but I’ve taken up enough of your time. But I think you get the drift of what I’ve been trying to say. In case you missed it…being off a benzo lost me the most valuable time of my life, never to be returned…but being on one gave me my life back and a second chance to enjoy what I had missed. Tell me, Rand, which life would you choose if you were in my shoes? – Hide quoted text — Show quoted text – Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon discontinuance there can be profound dysregulation of this stress axis. The neurotransmitters of the pons, medulla and basal ganglia are in a state of rebound excitability. The hypothalamus depends on the input from this area. It is the function of the hypothalamus to respond to these neurotransmitters as well as other modulators and peptides and maintain the body in homeostatic balance. All the body’s hormone regulation, appetite control, water and mineral balance, blood pressure and temperature regulation, immune response and more depend on the proper function of the hypothalamus. Exposure to benzodiazepines causes ligand induced changes (tolerance) and upregulation of peripheral-type benzodiazepine receptors especially in the hypothalamus and hippocampus, but also in the liver, kidney, gut and heart. Tolerance to benzodiazepines is defined as a decreased sensitivity of receptors and ligand induced changes in receptors rendering them unresponsive to the anxiolytic GABA – a shift in efficacy. These endogenous ligands for the benzodiazepine receptor exhibit inverse agonist properties. Tolerance can develop with repeat exposure, or in as little as 4 days as is the case with the short half life benzodiazepine Xanax, a triazalone benzodiazepine. It can also develop in one single exposure especially if given to the level of anaesthesia. Further exposure to benzodiazepines now produces anxiety. There may be a role for antagonists or inverse agonists in facilitating benzodiazepine withdrawal. The partial inverse agonist beta carboline passion flower has helped some with withdrawal anxiety. There is a beta carboline, abecarnil, being investigated as helpful in benzodiazepine withdrawal, the possibility exists that it can facilitate the re-adaptation of receptors to the benzo free state. However, there is a caution that tolerance may develop in as little as 3 weeks and there is a withdrawal as well. Dysregulation of this stress axis at the adrenals results in over production of glucocorticoids (which regulate carbohydrate metabolism and insulin responsiveness), mineralcorticoids (which regulate electrolytes and water balance) and androgens (sex and growth hormones). It is here that problems with acid/base balance emerge and further compound the metabolic disturbances at the liver. The hormone vasopressin (antidiuretic hormone) produced at the hypothalamus is responsible for keeping us continent. When we urinate all night long, it reflects a problem with ADH. It is unresponsive at the hypothalamus. We become dehydrated. Sodium and uric acid can increase as the kidney, sensing volume depletion, conserves sodium in an attempt to conserve water. Uric acid is conserved simultaneously. We lose potassium and magnesium in the diuresis. These effects are mediated by glucocorticoids (at the adrenal cortex) that cause hyperinsulinemia and insulin resistance. The decreased renal perfusion due to the action of excessive norepinephrine and epinephrine (at the adrenal medulla) also contributes by increasing the hormone rennin which in turn causes the production of another hormone angiotension II in the liver. This leads to increased kidney hormones aldosterone , cortisol and dehydrocorticosterone which causes further sodium retention. All body functions that depend on the correct ratio of minerals (electrolytes) is adversely affected. With increased sodium retention there is CNS disturbance and neuromuscular excitability. The fluid in our bodies begins to shift from the vascular compartment and cellular compartments to the interstitial spaces resulting in oedema. The neurochemical messages that depend on the right electrolyte being in the right compartment is now impaired. So we can see that another mechanism for cerebral ammonia accumulation is due to problems with the kidney and its relationship with the liver and the hormonal influence of the hypothalamus. It has been observed that haloperidol, a major tranquilliser, as well as tricyclic antidepressants, cocaine and amphetamines alter fluid and electrolyte balance. It is obvious to those of us suffering in benzodiazepine withdrawal that this oedema, frequent urination, thirst and much more is a reflection of a similar mechanism – a multimetabolic syndrome. Portal-systemic shunting of venous blood with the development of extensive collaterals can result from exposure to tranquilliser / sedatives. Peripheral type benzodiazepine receptors and their endogenous ligands are implicated in decreased liver and renal perfusion and hypertrophy. However, shunting and brain ammonia can occur even in the absence of cirrhosis and liver function tests are often normal. The liver is the site of protein synthesis and ammonia detoxification through the "urea cycle". This process requires much water and vitamin B6 and energy in the form of ATP from the liver cells mitochondria, organelles that are responsible for cellular respiration and energy storage. There is a good deal of evidence of digestive problems in withdrawal. By-products of protein digestion produce ammonia. Brain ammonia is metabolised in astrocytes in the brain to glutamate with an accumulation of this contributing to brain oedema.
… read more »
Response:
<snippity snip snip snip I’m afraid I was not able to make myself read past the first pararaph. Perhaps, had I taken a benzo I would have the patience. <Let me know when the cliffnotes version of that novel comes out
You gain strength, courage and confidence by every experience in whichyou really stop to look fear in the face.~~Eleanor Roosevelt
Response:
- Hide quoted text — Show quoted text – –WebTV-Mail-8026-1786 Content-Type: Text/Plain; Charset=US-ASCII Content-Transfer-Encoding: 7Bit <snippity snip snip snip I’m afraid I was not able to make myself read past the first pararaph. Perhaps, had I taken a benzo I would have the patience. <Let me know when the cliffnotes version of that novel comes out –xanax helps me with my anxiety and panic. they make you feel
better.(normal) donny
Response:
- Hide quoted text — Show quoted text – Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon lots of the usual Rand drivel snipped The problem with parroting concepts you don’t understand, Rand, is that you never know whether they are true or not. It seems to consist mainly of using dubious similarities between markedly different groups of medications to suggest benzos have some action during the withdrawal phase when there is very little, if any, direct evidence that they do have the effect this attributes to them. More of the usual anti medication snake oil. Ian Man i need another XANAX after reading that, maybe 2. donny
Response:
Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon
lots of the usual Rand drivel snipped The problem with parroting concepts you don’t understand, Rand, is that you never know whether they are true or not. It seems to consist mainly of using dubious similarities between markedly different groups of medications to suggest benzos have some action during the withdrawal phase when there is very little, if any, direct evidence that they do have the effect this attributes to them. More of the usual anti medication snake oil. Ian
Response:
I wrote 10 seconds ago: <total snip Whoops sorry I didn’t realize that Rand actually wrote that post when I first replied. I should have suspected though LOL — Steve
Response:
- Hide quoted text — Show quoted text – <snip Well put! Thank you! Have you considered a legal career! Thanks for the great thoughts. David ps: I went throught the wife’s pantyhose drawer and found some bright red fishnet hose, I think that would match up well with my plaid kilt you go man!!!!!!! donny
Response:
- Hide quoted text — Show quoted text – Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon discontinuance there can be profound dysregulation of this stress axis. The neurotransmitters of the pons, medulla and basal ganglia are in a state of rebound excitability. The hypothalamus depends on the input from this area. It is the function of the hypothalamus to respond to these neurotransmitters as well as other modulators and peptides and maintain the body in homeostatic balance. All the body’s hormone regulation, appetite control, water and mineral balance, blood pressure and temperature regulation, immune response and more depend on the proper function of the hypothalamus. Exposure to benzodiazepines causes ligand induced changes (tolerance) and upregulation of peripheral-type benzodiazepine receptors especially in the hypothalamus and hippocampus, but also in the liver, kidney, gut and heart. Tolerance to benzodiazepines is defined as a decreased sensitivity of receptors and ligand induced changes in receptors rendering them unresponsive to the anxiolytic GABA – a shift in efficacy. These endogenous ligands for the benzodiazepine receptor exhibit inverse agonist properties. Tolerance can develop with repeat exposure, or in as little as 4 days as is the case with the short half life benzodiazepine Xanax, a triazalone benzodiazepine. It can also develop in one single exposure especially if given to the level of anaesthesia. Further exposure to benzodiazepines now produces anxiety. There may be a role for antagonists or inverse agonists in facilitating benzodiazepine withdrawal. The partial inverse agonist beta carboline passion flower has helped some with withdrawal anxiety. There is a beta carboline, abecarnil, being investigated as helpful in benzodiazepine withdrawal, the possibility exists that it can facilitate the re-adaptation of receptors to the benzo free state. However, there is a caution that tolerance may develop in as little as 3 weeks and there is a withdrawal as well. Dysregulation of this stress axis at the adrenals results in over production of glucocorticoids (which regulate carbohydrate metabolism and insulin responsiveness), mineralcorticoids (which regulate electrolytes and water balance) and androgens (sex and growth hormones). It is here that problems with acid/base balance emerge and further compound the metabolic disturbances at the liver. The hormone vasopressin (antidiuretic hormone) produced at the hypothalamus is responsible for keeping us continent. When we urinate all night long, it reflects a problem with ADH. It is unresponsive at the hypothalamus. We become dehydrated. Sodium and uric acid can increase as the kidney, sensing volume depletion, conserves sodium in an attempt to conserve water. Uric acid is conserved simultaneously. We lose potassium and magnesium in the diuresis. These effects are mediated by glucocorticoids (at the adrenal cortex) that cause hyperinsulinemia and insulin resistance. The decreased renal perfusion due to the action of excessive norepinephrine and epinephrine (at the adrenal medulla) also contributes by increasing the hormone rennin which in turn causes the production of another hormone angiotension II in the liver. This leads to increased kidney hormones aldosterone , cortisol and dehydrocorticosterone which causes further sodium retention. All body functions that depend on the correct ratio of minerals (electrolytes) is adversely affected. With increased sodium retention there is CNS disturbance and neuromuscular excitability. The fluid in our bodies begins to shift from the vascular compartment and cellular compartments to the interstitial spaces resulting in oedema. The neurochemical messages that depend on the right electrolyte being in the right compartment is now impaired. So we can see that another mechanism for cerebral ammonia accumulation is due to problems with the kidney and its relationship with the liver and the hormonal influence of the hypothalamus. It has been observed that haloperidol, a major tranquilliser, as well as tricyclic antidepressants, cocaine and amphetamines alter fluid and electrolyte balance. It is obvious to those of us suffering in benzodiazepine withdrawal that this oedema, frequent urination, thirst and much more is a reflection of a similar mechanism – a multimetabolic syndrome. Portal-systemic shunting of venous blood with the development of extensive collaterals can result from exposure to tranquilliser / sedatives. Peripheral type benzodiazepine receptors and their endogenous ligands are implicated in decreased liver and renal perfusion and hypertrophy. However, shunting and brain ammonia can occur even in the absence of cirrhosis and liver function tests are often normal. The liver is the site of protein synthesis and ammonia detoxification through the "urea cycle". This process requires much water and vitamin B6 and energy in the form of ATP from the liver cells mitochondria, organelles that are responsible for cellular respiration and energy storage. There is a good deal of evidence of digestive problems in withdrawal. By-products of protein digestion produce ammonia. Brain ammonia is metabolised in astrocytes in the brain to glutamate with an accumulation of this contributing to brain oedema. EEG shows diffuse slow wave activity even in mild cases. Elevated serum levels of astroglial S100beta is an early diagnostic indicator even in the absence of elevated arterial ammonia – pNH(3). Brain SPECT (perfusion testing) is more sensitive than MRI but T1-weighted magnetic resonance (MR) can reveal high intensity in the basal ganglia with hyperammonemia. Cerebral blood flow is decreased rendering these areas of the brain susceptible to damage by toxic metabolites (ammonia and other short chain fatty acids and other enteric products). Additionally, liver perfusion is compromised. Ammonia induced glial swelling results in reduced glutamic transporter (GTL-1) with extracellular glutamate unable to be removed from the synapse. The result is neuronal excitability which the precipitates even more glial cell dysfunction and oedema. This is a circular process. It is limited to neurotransmitter malfunction without neuronal death in most cases but can result in beta amyloid production and neuronal death in severe instances. Tranquilizers can precipitate this even without cirrhosis. Alterations in cerebrovascular permeability may play a role. The result is multiple neurotransmitter system disorder with derangement of the serotonergic system specifically and basal ganglia dysfunction in general. The corpus striatum and nucleus accumbens at the basal ganglia contain large amounts of GABA and are very strongly affected by benzodiazepines. The triazone benzos have the most effect on this area (Xanax, Halcion). The substantia nigra, a dopamine nucleus in the brainstem, is considered part of the basal ganglia and it also contains GABA and the enzyme glutamic decarboxylase which is necessary to convert glutamate (excitatory) to GABA (inhibitory). The profound sleep dysfunction in withdrawal may be directly related to this derangement of serotonin at the basal ganglia and not to peripheral tryptophan. In addition, this upregulation of benzodiazepine peripheral-type receptors increases cholesterol uptake and the synthesis of brain neurosteroids that positively affect GABA A receptors. These are allopregnonolone, alpha THDOC, pregnalone sulphate and others. This, in addition to the cerebral oedema, may contribute to the somnolence and reduced pain we experience as withdrawal progresses. This "drugged" or "tired" phase can last a few weeks or many months. It is followed by a profound insomnia and increase in pain. As was previously stated, the detoxification of ammonia in the liver is an expensive process. The urea cycle requires much water, B6 and energy (as ATP from the mitochondria). These mitochondria are the respiratory centre and energy storage organelles of the cell. It is likely that the profound fatigue phase that follows the pain, hyperactivity and insomnia may be due to depletion of the mitochondria energy stores. There are many articles implicating benzodiazepines and peripheral type benzodiazepine receptors in the pathogenesis of CNS problems characteristic of portal-systemic encephalopathy. R F Butterworth, University of Montreal, Neuroscience Research Unit, Hospital St Luc, Quebec writes extensively on the subject. If , indeed, this is part of the process there may be some benefit in treating the brain oedema with a protein restricted diet and supplementing with branched chain amino acids and L-orthinine-L-aspartate. Colonics are also recommended to eliminate toxic enteric products. The gut and muscle become the primary way the body rids itself of ammonia when the liver is compromised. Exercise, massage and even sauna can aid in riding the body of ammonia. Maintaining gut flora with probiotics and supplementing with B vitamins may be helpful. The dipeptide carnosine may be useful as both an antioxidant of aldehydes and ketones and protection from amyloid beta which can result from prolonged glial cell dysfunction and exposure to ammonia. It may protect the endothelial cells and maintain the blood brain barrier. However, there is some caution that this GABA analogue may switch off GABA in susceptible people and cause excitability. DHA, an omega 3 fatty acid, may ameliorate the prostaglandin (PGE2) inflammation caused by arachidonic acid and protect the brain from inflammatory cytokines. Antioxidants tocopherol, ascorbic acid, S.O.D. and catalase as well as flavonoids are protective of oxidative stress.
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Response:
<snip They allow me to drive, have job, sleep, and lead a semi-normal life (not to neglect the fine support, and a great therapist). Anyone else care to comment? David
Response:
– TC3
<snip They allow me to drive, have job, sleep, and lead a semi-normal life (not to neglect the fine support, and a great therapist). Anyone else care to comment?
Yeah…read my hell in the Chocolate thread. I am so glad they helped me among other things/people get me back on my Fred Flintstone feet. :o) – Hide quoted text — Show quoted text – David
Response:
<snip Well put! Thank you! Have you considered a legal career! Thanks for the great thoughts. David ps: I went throught the wife’s pantyhose drawer and found some bright red fishnet hose, I think that would match up well with my plaid kilt
Response:
Rand wrote" <<Snipped What do benzo`s do? Hmm…..from reading this newsgroup I will tell you what I have seen benzo`s do. I have seen benzo`s save peoples lives. I have seen people do things they haven`t done in years because of benzo`s. I have seen people be able to hold down jobs because of benzo`s. It has freed many people from living life that is tormented by anxiety and panic, which is a living hell by the way. You have to be a anxiety and panic sufferer to understand that living hell though. It has enabled people who have been trapped in their house due to fear, to be able to take a few steps out their door. Rand have you ever been unable to leave your house because you are scared out of your mind? I wonder how many people would have killed themselves if it wasn`t for these meds? Bottom line, benzo`s have given so many people quality in their lives again. Yes, there are people who have had problems with benzo`s, that can be said about ""any"" med there is. But not one person can deny that millions and millions of people have been helped by benzo`s…. You refuse to acknowledge that benzo`s help people. You are a victim of benzo`s not your enemy, you yourself are your own worst enemy. Jackie ~*~Man must exist in a state of balance between risk and safety. Pure risk leads to self-destruction. Pure safety leads to stagnation. In between lies survival and progress.
Response:
Your point would be? How many times do we have to flush before these go away? R – Hide quoted text — Show quoted text – Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon discontinuance there can be profound dysregulation of this stress axis. The neurotransmitters of the pons, medulla and basal ganglia are in a state of rebound excitability. The hypothalamus depends on the input from this area. It is the function of the hypothalamus to respond to these neurotransmitters as well as other modulators and peptides and maintain the body in homeostatic balance. All the body’s hormone regulation, appetite control, water and mineral balance, blood pressure and temperature regulation, immune response and more depend on the proper function of the hypothalamus. Exposure to benzodiazepines causes ligand induced changes (tolerance) and upregulation of peripheral-type benzodiazepine receptors especially in the hypothalamus and hippocampus, but also in the liver, kidney, gut and heart. Tolerance to benzodiazepines is defined as a decreased sensitivity of receptors and ligand induced changes in receptors rendering them unresponsive to the anxiolytic GABA – a shift in efficacy. These endogenous ligands for the benzodiazepine receptor exhibit inverse agonist properties. Tolerance can develop with repeat exposure, or in as little as 4 days as is the case with the short half life benzodiazepine Xanax, a triazalone benzodiazepine. It can also develop in one single exposure especially if given to the level of anaesthesia. Further exposure to benzodiazepines now produces anxiety. There may be a role for antagonists or inverse agonists in facilitating benzodiazepine withdrawal. The partial inverse agonist beta carboline passion flower has helped some with withdrawal anxiety. There is a beta carboline, abecarnil, being investigated as helpful in benzodiazepine withdrawal, the possibility exists that it can facilitate the re-adaptation of receptors to the benzo free state. However, there is a caution that tolerance may develop in as little as 3 weeks and there is a withdrawal as well. Dysregulation of this stress axis at the adrenals results in over production of glucocorticoids (which regulate carbohydrate metabolism and insulin responsiveness), mineralcorticoids (which regulate electrolytes and water balance) and androgens (sex and growth hormones). It is here that problems with acid/base balance emerge and further compound the metabolic disturbances at the liver. The hormone vasopressin (antidiuretic hormone) produced at the hypothalamus is responsible for keeping us continent. When we urinate all night long, it reflects a problem with ADH. It is unresponsive at the hypothalamus. We become dehydrated. Sodium and uric acid can increase as the kidney, sensing volume depletion, conserves sodium in an attempt to conserve water. Uric acid is conserved simultaneously. We lose potassium and magnesium in the diuresis. These effects are mediated by glucocorticoids (at the adrenal cortex) that cause hyperinsulinemia and insulin resistance. The decreased renal perfusion due to the action of excessive norepinephrine and epinephrine (at the adrenal medulla) also contributes by increasing the hormone rennin which in turn causes the production of another hormone angiotension II in the liver. This leads to increased kidney hormones aldosterone , cortisol and dehydrocorticosterone which causes further sodium retention. All body functions that depend on the correct ratio of minerals (electrolytes) is adversely affected. With increased sodium retention there is CNS disturbance and neuromuscular excitability. The fluid in our bodies begins to shift from the vascular compartment and cellular compartments to the interstitial spaces resulting in oedema. The neurochemical messages that depend on the right electrolyte being in the right compartment is now impaired. So we can see that another mechanism for cerebral ammonia accumulation is due to problems with the kidney and its relationship with the liver and the hormonal influence of the hypothalamus. It has been observed that haloperidol, a major tranquilliser, as well as tricyclic antidepressants, cocaine and amphetamines alter fluid and electrolyte balance. It is obvious to those of us suffering in benzodiazepine withdrawal that this oedema, frequent urination, thirst and much more is a reflection of a similar mechanism – a multimetabolic syndrome. Portal-systemic shunting of venous blood with the development of extensive collaterals can result from exposure to tranquilliser / sedatives. Peripheral type benzodiazepine receptors and their endogenous ligands are implicated in decreased liver and renal perfusion and hypertrophy. However, shunting and brain ammonia can occur even in the absence of cirrhosis and liver function tests are often normal. The liver is the site of protein synthesis and ammonia detoxification through the "urea cycle". This process requires much water and vitamin B6 and energy in the form of ATP from the liver cells mitochondria, organelles that are responsible for cellular respiration and energy storage. There is a good deal of evidence of digestive problems in withdrawal. By-products of protein digestion produce ammonia. Brain ammonia is metabolised in astrocytes in the brain to glutamate with an accumulation of this contributing to brain oedema. EEG shows diffuse slow wave activity even in mild cases. Elevated serum levels of astroglial S100beta is an early diagnostic indicator even in the absence of elevated arterial ammonia – pNH(3). Brain SPECT (perfusion testing) is more sensitive than MRI but T1-weighted magnetic resonance (MR) can reveal high intensity in the basal ganglia with hyperammonemia. Cerebral blood flow is decreased rendering these areas of the brain susceptible to damage by toxic metabolites (ammonia and other short chain fatty acids and other enteric products). Additionally, liver perfusion is compromised. Ammonia induced glial swelling results in reduced glutamic transporter (GTL-1) with extracellular glutamate unable to be removed from the synapse. The result is neuronal excitability which the precipitates even more glial cell dysfunction and oedema. This is a circular process. It is limited to neurotransmitter malfunction without neuronal death in most cases but can result in beta amyloid production and neuronal death in severe instances. Tranquilizers can precipitate this even without cirrhosis. Alterations in cerebrovascular permeability may play a role. The result is multiple neurotransmitter system disorder with derangement of the serotonergic system specifically and basal ganglia dysfunction in general. The corpus striatum and nucleus accumbens at the basal ganglia contain large amounts of GABA and are very strongly affected by benzodiazepines. The triazone benzos have the most effect on this area (Xanax, Halcion). The substantia nigra, a dopamine nucleus in the brainstem, is considered part of the basal ganglia and it also contains GABA and the enzyme glutamic decarboxylase which is necessary to convert glutamate (excitatory) to GABA (inhibitory). The profound sleep dysfunction in withdrawal may be directly related to this derangement of serotonin at the basal ganglia and not to peripheral tryptophan. In addition, this upregulation of benzodiazepine peripheral-type receptors increases cholesterol uptake and the synthesis of brain neurosteroids that positively affect GABA A receptors. These are allopregnonolone, alpha THDOC, pregnalone sulphate and others. This, in addition to the cerebral oedema, may contribute to the somnolence and reduced pain we experience as withdrawal progresses. This "drugged" or "tired" phase can last a few weeks or many months. It is followed by a profound insomnia and increase in pain. As was previously stated, the detoxification of ammonia in the liver is an expensive process. The urea cycle requires much water, B6 and energy (as ATP from the mitochondria). These mitochondria are the respiratory centre and energy storage organelles of the cell. It is likely that the profound fatigue phase that follows the pain, hyperactivity and insomnia may be due to depletion of the mitochondria energy stores. There are many articles implicating benzodiazepines and peripheral type benzodiazepine receptors in the pathogenesis of CNS problems characteristic of portal-systemic encephalopathy. R F Butterworth, University of Montreal, Neuroscience Research Unit, Hospital St Luc, Quebec writes extensively on the subject. If , indeed, this is part of the process there may be some benefit in treating the brain oedema with a protein restricted diet and supplementing with branched chain amino acids and L-orthinine-L-aspartate. Colonics are also recommended to eliminate toxic enteric products. The gut and muscle become the primary way the body rids itself of ammonia when the liver is compromised. Exercise, massage and even sauna can aid in riding the body of ammonia. Maintaining gut flora with probiotics and supplementing with B vitamins may be helpful. The dipeptide carnosine may be useful as both an antioxidant of aldehydes and ketones and protection from amyloid beta which can result from prolonged glial cell dysfunction and exposure to ammonia. It may protect the endothelial cells and maintain the blood brain barrier. However, there is some caution that this GABA analogue may switch off GABA in susceptible people and cause excitability. DHA, an omega 3 fatty acid, may ameliorate the prostaglandin (PGE2) inflammation caused by arachidonic acid and protect the brain from
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Response:
Benzodiazepines (sedative/hypnotics) cause a variety of homeostatic problems. They profoundly affect the reticular activating system, the hypothalamus, pituitary and adrenal stress axis in particular. Upon discontinuance there can be profound dysregulation of this stress axis. The neurotransmitters of the pons, medulla and basal ganglia are in a state of rebound excitability. The hypothalamus depends on the input from this area. It is the function of the hypothalamus to respond to these neurotransmitters as well as other modulators and peptides and maintain the body in homeostatic balance. All the body’s hormone regulation, appetite control, water and mineral balance, blood pressure and temperature regulation, immune response and more depend on the proper function of the hypothalamus. Exposure to benzodiazepines causes ligand induced changes (tolerance) and upregulation of peripheral-type benzodiazepine receptors especially in the hypothalamus and hippocampus, but also in the liver, kidney, gut and heart. Tolerance to benzodiazepines is defined as a decreased sensitivity of receptors and ligand induced changes in receptors rendering them unresponsive to the anxiolytic GABA – a shift in efficacy. These endogenous ligands for the benzodiazepine receptor exhibit inverse agonist properties. Tolerance can develop with repeat exposure, or in as little as 4 days as is the case with the short half life benzodiazepine Xanax, a triazalone benzodiazepine. It can also develop in one single exposure especially if given to the level of anaesthesia. Further exposure to benzodiazepines now produces anxiety. There may be a role for antagonists or inverse agonists in facilitating benzodiazepine withdrawal. The partial inverse agonist beta carboline passion flower has helped some with withdrawal anxiety. There is a beta carboline, abecarnil, being investigated as helpful in benzodiazepine withdrawal, the possibility exists that it can facilitate the re-adaptation of receptors to the benzo free state. However, there is a caution that tolerance may develop in as little as 3 weeks and there is a withdrawal as well. Dysregulation of this stress axis at the adrenals results in over production of glucocorticoids (which regulate carbohydrate metabolism and insulin responsiveness), mineralcorticoids (which regulate electrolytes and water balance) and androgens (sex and growth hormones). It is here that problems with acid/base balance emerge and further compound the metabolic disturbances at the liver. The hormone vasopressin (antidiuretic hormone) produced at the hypothalamus is responsible for keeping us continent. When we urinate all night long, it reflects a problem with ADH. It is unresponsive at the hypothalamus. We become dehydrated. Sodium and uric acid can increase as the kidney, sensing volume depletion, conserves sodium in an attempt to conserve water. Uric acid is conserved simultaneously. We lose potassium and magnesium in the diuresis. These effects are mediated by glucocorticoids (at the adrenal cortex) that cause hyperinsulinemia and insulin resistance. The decreased renal perfusion due to the action of excessive norepinephrine and epinephrine (at the adrenal medulla) also contributes by increasing the hormone rennin which in turn causes the production of another hormone angiotension II in the liver. This leads to increased kidney hormones aldosterone , cortisol and dehydrocorticosterone which causes further sodium retention. All body functions that depend on the correct ratio of minerals (electrolytes) is adversely affected. With increased sodium retention there is CNS disturbance and neuromuscular excitability. The fluid in our bodies begins to shift from the vascular compartment and cellular compartments to the interstitial spaces resulting in oedema. The neurochemical messages that depend on the right electrolyte being in the right compartment is now impaired. So we can see that another mechanism for cerebral ammonia accumulation is due to problems with the kidney and its relationship with the liver and the hormonal influence of the hypothalamus. It has been observed that haloperidol, a major tranquilliser, as well as tricyclic antidepressants, cocaine and amphetamines alter fluid and electrolyte balance. It is obvious to those of us suffering in benzodiazepine withdrawal that this oedema, frequent urination, thirst and much more is a reflection of a similar mechanism – a multimetabolic syndrome. Portal-systemic shunting of venous blood with the development of extensive collaterals can result from exposure to tranquilliser / sedatives. Peripheral type benzodiazepine receptors and their endogenous ligands are implicated in decreased liver and renal perfusion and hypertrophy. However, shunting and brain ammonia can occur even in the absence of cirrhosis and liver function tests are often normal. The liver is the site of protein synthesis and ammonia detoxification through the "urea cycle". This process requires much water and vitamin B6 and energy in the form of ATP from the liver cells mitochondria, organelles that are responsible for cellular respiration and energy storage. There is a good deal of evidence of digestive problems in withdrawal. By-products of protein digestion produce ammonia. Brain ammonia is metabolised in astrocytes in the brain to glutamate with an accumulation of this contributing to brain oedema. EEG shows diffuse slow wave activity even in mild cases. Elevated serum levels of astroglial S100beta is an early diagnostic indicator even in the absence of elevated arterial ammonia – pNH(3). Brain SPECT (perfusion testing) is more sensitive than MRI but T1-weighted magnetic resonance (MR) can reveal high intensity in the basal ganglia with hyperammonemia. Cerebral blood flow is decreased rendering these areas of the brain susceptible to damage by toxic metabolites (ammonia and other short chain fatty acids and other enteric products). Additionally, liver perfusion is compromised. Ammonia induced glial swelling results in reduced glutamic transporter (GTL-1) with extracellular glutamate unable to be removed from the synapse. The result is neuronal excitability which the precipitates even more glial cell dysfunction and oedema. This is a circular process. It is limited to neurotransmitter malfunction without neuronal death in most cases but can result in beta amyloid production and neuronal death in severe instances. Tranquilizers can precipitate this even without cirrhosis. Alterations in cerebrovascular permeability may play a role. The result is multiple neurotransmitter system disorder with derangement of the serotonergic system specifically and basal ganglia dysfunction in general. The corpus striatum and nucleus accumbens at the basal ganglia contain large amounts of GABA and are very strongly affected by benzodiazepines. The triazone benzos have the most effect on this area (Xanax, Halcion). The substantia nigra, a dopamine nucleus in the brainstem, is considered part of the basal ganglia and it also contains GABA and the enzyme glutamic decarboxylase which is necessary to convert glutamate (excitatory) to GABA (inhibitory). The profound sleep dysfunction in withdrawal may be directly related to this derangement of serotonin at the basal ganglia and not to peripheral tryptophan. In addition, this upregulation of benzodiazepine peripheral-type receptors increases cholesterol uptake and the synthesis of brain neurosteroids that positively affect GABA A receptors. These are allopregnonolone, alpha THDOC, pregnalone sulphate and others. This, in addition to the cerebral oedema, may contribute to the somnolence and reduced pain we experience as withdrawal progresses. This "drugged" or "tired" phase can last a few weeks or many months. It is followed by a profound insomnia and increase in pain. As was previously stated, the detoxification of ammonia in the liver is an expensive process. The urea cycle requires much water, B6 and energy (as ATP from the mitochondria). These mitochondria are the respiratory centre and energy storage organelles of the cell. It is likely that the profound fatigue phase that follows the pain, hyperactivity and insomnia may be due to depletion of the mitochondria energy stores. There are many articles implicating benzodiazepines and peripheral type benzodiazepine receptors in the pathogenesis of CNS problems characteristic of portal-systemic encephalopathy. R F Butterworth, University of Montreal, Neuroscience Research Unit, Hospital St Luc, Quebec writes extensively on the subject. If , indeed, this is part of the process there may be some benefit in treating the brain oedema with a protein restricted diet and supplementing with branched chain amino acids and L-orthinine-L-aspartate. Colonics are also recommended to eliminate toxic enteric products. The gut and muscle become the primary way the body rids itself of ammonia when the liver is compromised. Exercise, massage and even sauna can aid in riding the body of ammonia. Maintaining gut flora with probiotics and supplementing with B vitamins may be helpful. The dipeptide carnosine may be useful as both an antioxidant of aldehydes and ketones and protection from amyloid beta which can result from prolonged glial cell dysfunction and exposure to ammonia. It may protect the endothelial cells and maintain the blood brain barrier. However, there is some caution that this GABA analogue may switch off GABA in susceptible people and cause excitability. DHA, an omega 3 fatty acid, may ameliorate the prostaglandin (PGE2) inflammation caused by arachidonic acid and protect the brain from inflammatory cytokines. Antioxidants tocopherol, ascorbic acid, S.O.D. and catalase as well as flavonoids are protective of oxidative stress. Magnesium is protective and can oppose calcium induced excitability. The amino acids taurine and glycine are neuroprotective, possibly maintaining nitric oxide in the brain and … read more »
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