Don’t be too hard on yourself. Stupid Mistakes are gonna happen if you are doing anything worthwhile. As you say, relax into a smile and let it go. Thanks for smart and interesting posts.
I personally prefer aspirin against headaches because it’s based on a natural molecule that comes from a tree originally. Then herbal tea with lemon is also one of the things my body craves when having headaches, from herbs like thyme, stinging nettle, St. John’s wort, sage
I'm not sure yet if these are run by different people. .net is associated with Ann Blake-Tracy: "“Help! I Can’t Get Off My Antidepressant! (drugawareness.org) by our Executive Director, Ann Blake Tracy,"
drugawareness.org (ssristories.net) Our Executive Director, Ann Blake-Tracy, has been researching, writing, and lecturing about serotoneric medications since 1990. And since 1992 she has been testifying in court cases as an expert witness, in both the US and Canada, involving serotonergic medications – antidepressants, some pain killers, & the newer atypical antipsychotics.
Just yesterday i was making notes for myself, making possible connections. I’m going to post these here, knowing that i did not include the references from which i pulled these quotes. This is all from common sources like verywell.
I am interested in lipofuscin, calcification and fibrosis. I started looking at lipofuscin and found “piracetam appears to significantly reduce accumulation of lipofuscin in the brain tissue of rats.” Interesting. In a very layperson terminology (mine), GABA receptors can be activated by many different molecules. The receptor itself changes shape. “ Herbal benzodiazepines” (apparently so named because they bind to the GABA receptor and are calming to humans) include but not limited to chamomile and valerian. It seems an interesting thing that without enough GABA/receptor-activation, symptoms can be tension, Stiff Man Syndrome type things (definitely not relaxed). But then when people take some of these benzodiazepines they can get this intense need to MOVE their body at a pathological level and it’s a horrible experience. To me, this sounds like the drugs bind to the GABA receptors and send some kind of a commensal signal “we are now fully relaxed” and “we are now too much relaxed” and then the body compensates somehow with this akithisia—the intense need to MOVE. I believe that we have a basic need for movement; just imagine being held in a straight jacket—just that thought feels unbearable. It’s an intuitive concept in my mind, but it seems that amount of movement is one of the factors being monitored in a body for what we call “homeostasis.” I’m guessing there are experts who have better terminology for this concept.
===========
clonazepam is the drug JBP had to detoxify from in Russia.
(i have heard this story from a couple of different videos/sources).
Clonazepam is a benzodiazepine. I.e. GABA agonist.
Piracetam
Piracetam is in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It is a derivative of the neurotransmitter GABA[9] and shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid. Piracetam is a cyclic derivative of GABA (gamma-aminobutyric acid). Related drugs include the anticonvulsants levetiracetam and brivaracetam, and the putative nootropics aniracetam and phenylpiracetam. More info racetams group: https://drugs.selfdecode.com/blog/comparison-aniracetam-oxiracetam-phenylracetam-pramiracetam/
Side effects
Symptoms of general excitability, including anxiety, insomnia, irritability, headache, agitation, nervousness, tremor, and hyperkinesia, are occasionally reported.[14][20][21] Other reported side effects include somnolence, weight gain, clinical depression, weakness, increased libido, and hypersexuality.[14]
According to a 2005 review, piracetam has been observed to have the following side effects: hyperkinesia, weight gain, nervousness, somnolence, depression and asthenia.[9]
Piracetam reduces platelet aggregation as well as fibrinogen concentration, and thus is contraindicated to patients with cerebral hemorrhage.[9][3]
Hyperkinesia? Is that like Akathisia? akathisia
Possible therapies for lipofuscin
Calorie restriction,[4] vitamin E,[4] and increased glutathione appear to reduce or halt the production of lipofuscin.
The nootropic drug piracetam appears to significantly reduce accumulation of lipofuscin in the brain tissue of rats.[18]
Other possible treatments:
• Centrophenoxine[19]
• Acetyl-L-carnitine[20]
• Ginkgo biloba[21]
• Dimethylethanolamine [22]
• Curcumin[23]
Wet macular degeneration can be treated using selective photothermolysis where a pulsed unfocused laser predominantly heats and kills lipofuscin-rich cells, leaving untouched healthy cells to multiply and fill in the gaps.[citation needed] The technique is also used as a skin treatment to remove tattoos, liverspots, and in general make skin appear younger. This ability to selectively target lipofuscin has opened up research opportunities in the field of anti-aging medicine.
Soraprazan (remofuscin) has been found to remove lipofuscin from retinal pigment epithelial cells in animals.[24] This opens up a new therapy option for the treatment of dry age-related macular degeneration and Stargardt disease, for which there is currently no treatment. The drug has now been granted orphan drug designation for the treatment of Stargardt disease by the European Medicines Agency.[25]
Akathisia is estimated to affect approximately 15%–35% of people who use antipsychotic medications.2
…
The goal of antipsychotic medications is to help control mental disorders like schizophrenia.4 While these medications work well in treating mental disorders, many are avoided because they can cause severe side effects. Extrapyramidal symptoms [EPS] develop when dopamine is suppressed, which is what antipsychotic medications do.1
Extrapyramidal symptoms can appear with other conditions, like Parkinson's disease, but tardive dyskinesia is specific to the use of antipsychotics.1
Tardive dyskinesia develops within the first year in 6% to 12% of people who take even low-dose antipsychotics.1 Age can impact the likelihood of developing TD, with 25% to 45% of people over age 45 developing TD after a year of treatment.
Beyond antipsychotics, several other medications have also been linked to tardive dyskinesia. These include:2
Antidepressants, such as Prozac (fluoxetine) and Desyrel (trazodone)
Anti-epileptic drugs (AEDs), such as Dilantin (phenytoin) and Tegretol (carbamazepine)
Anticholinergics, such as Cogentin (benztropine)
Antiemetics (anti-nausea medications), such as Reglan (metoclopramide) and Compazine (prochlorperazine)
Patient Rights
Many people who are prescribed antipsychotics have conditions like schizophrenia or dementia. Since these conditions can impair your ability to make decisions, concerns have been raised about the forceful administration of these medications.
The sedating nature of these medications and the risk of side effects have led to the creation of legal protections for people who are prescribed antipsychotics. Specifics vary by state, but in most cases—outside of a medical emergency—people have the right to refuse psychiatric treatment, including the use of antipsychotic medications.
Recap
Remember, you have the right to refuse medications, especially ones that are sedating.
Schizophrenia and other conditions that present with psychotic episodes can be difficult to manage, but for many people with these conditions, the medications used to treat them are even harder to bear. More than 20 years of studies revealed that up to 50% of people who take antipsychotic medications don't take them as they should, largely because of the negative side effects they produce.6
Up to half of people with tardive dyskinesia may experience worsening symptoms when stopping medications, although many see improvement over time. In some cases, symptoms are permanent. Arguments can be made both for maintaining and stopping antipsychotic use for tardive dyskinesia because stopping may or may not result in improvement. Stopping antipsychotics, on the other hand, can lead to increases in the psychotic symptoms the medications are prescribed to treat in the first place.1
Wait a second.
So, antipsychotic drugs suppress dopamine. Which would mean that in schizophrenia, dopamine is too high. Why? Low methylation?? !!
COMT DEFECT?? !!
Antipsychotics might work by blocking the effects of the overactivity of a brain chemical called dopamine. This chemical affects emotions, planning, and memory. The overactivity of dopamine is thought to contribute to psychotic symptoms.9
Why not treat COMT defect effects by supporting COMT methylation??
Treatment for schizophrenia (hallucinations and delusions—distantly caused from high dopamine), [and, off-label Alzheimer’s with aggression and agitation] then prescribed antipsychotic drugs, which commonly cause EPS (includes akathisia).
They are trying to treat the brain, and end up messing up the entire neurological system throughout the body.
Identifying and treating EPS as soon as possible is very important because these side effects can be permanent in some people.
List of drugs given for schizophrenia is alarming to me because the more common ones are given to people without schizophrenia. I know people who have been Rxd these drugs and they do not have schizophrenia, not even psychosis.
They are very bad, no good drugs, and schizophrenia is nutrient deficiencies some related to gene differences probably. I have a huge series from this summer on factors that may be involved in schizophrenia and it seems like Alzheimer’s is just the next step if the underlying issue isn't treated.
Don’t be too hard on yourself. Stupid Mistakes are gonna happen if you are doing anything worthwhile. As you say, relax into a smile and let it go. Thanks for smart and interesting posts.
aww thanks and writing gives me a sense of purpose.
Interesting post. I do have a prescription for chlorpromazine for migraines but I don’t take it often. Started taking more supplements & vitamins 👍
I personally prefer aspirin against headaches because it’s based on a natural molecule that comes from a tree originally. Then herbal tea with lemon is also one of the things my body craves when having headaches, from herbs like thyme, stinging nettle, St. John’s wort, sage
Aspirin was recommended. I use some of those herbs too.
Smile 😊... 🌻https://twitter.com/upliftingvids/status/1627125818420764673?s=46&t=5tMNRPOYYDIWOC-x8zoaBQ
https://www.ssristories.net/ - SSRIstories.com was abandoned as-is because Rosie Meysenburg died in 2012. https://ssristories.org/about-us/ So, SSRIstories.net was formed, and this site currently says that it is maintained by a group of people including Dr. David Healy, author of 2012 book Pharmageddon, and RxISK.org.
SSRIstories.com
I'm not sure yet if these are run by different people. .net is associated with Ann Blake-Tracy: "“Help! I Can’t Get Off My Antidepressant! (drugawareness.org) by our Executive Director, Ann Blake Tracy,"
drugawareness.org (ssristories.net) Our Executive Director, Ann Blake-Tracy, has been researching, writing, and lecturing about serotoneric medications since 1990. And since 1992 she has been testifying in court cases as an expert witness, in both the US and Canada, involving serotonergic medications – antidepressants, some pain killers, & the newer atypical antipsychotics.
Ssristories
Just yesterday i was making notes for myself, making possible connections. I’m going to post these here, knowing that i did not include the references from which i pulled these quotes. This is all from common sources like verywell.
I am interested in lipofuscin, calcification and fibrosis. I started looking at lipofuscin and found “piracetam appears to significantly reduce accumulation of lipofuscin in the brain tissue of rats.” Interesting. In a very layperson terminology (mine), GABA receptors can be activated by many different molecules. The receptor itself changes shape. “ Herbal benzodiazepines” (apparently so named because they bind to the GABA receptor and are calming to humans) include but not limited to chamomile and valerian. It seems an interesting thing that without enough GABA/receptor-activation, symptoms can be tension, Stiff Man Syndrome type things (definitely not relaxed). But then when people take some of these benzodiazepines they can get this intense need to MOVE their body at a pathological level and it’s a horrible experience. To me, this sounds like the drugs bind to the GABA receptors and send some kind of a commensal signal “we are now fully relaxed” and “we are now too much relaxed” and then the body compensates somehow with this akithisia—the intense need to MOVE. I believe that we have a basic need for movement; just imagine being held in a straight jacket—just that thought feels unbearable. It’s an intuitive concept in my mind, but it seems that amount of movement is one of the factors being monitored in a body for what we call “homeostasis.” I’m guessing there are experts who have better terminology for this concept.
===========
clonazepam is the drug JBP had to detoxify from in Russia.
https://www.cbc.ca/news/canada/jordan-peterson-treatment-russia-1.5456939
(i have heard this story from a couple of different videos/sources).
Clonazepam is a benzodiazepine. I.e. GABA agonist.
Piracetam
Piracetam is in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It is a derivative of the neurotransmitter GABA[9] and shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid. Piracetam is a cyclic derivative of GABA (gamma-aminobutyric acid). Related drugs include the anticonvulsants levetiracetam and brivaracetam, and the putative nootropics aniracetam and phenylpiracetam. More info racetams group: https://drugs.selfdecode.com/blog/comparison-aniracetam-oxiracetam-phenylracetam-pramiracetam/
Side effects
Symptoms of general excitability, including anxiety, insomnia, irritability, headache, agitation, nervousness, tremor, and hyperkinesia, are occasionally reported.[14][20][21] Other reported side effects include somnolence, weight gain, clinical depression, weakness, increased libido, and hypersexuality.[14]
According to a 2005 review, piracetam has been observed to have the following side effects: hyperkinesia, weight gain, nervousness, somnolence, depression and asthenia.[9]
Piracetam reduces platelet aggregation as well as fibrinogen concentration, and thus is contraindicated to patients with cerebral hemorrhage.[9][3]
Hyperkinesia? Is that like Akathisia? akathisia
Possible therapies for lipofuscin
Calorie restriction,[4] vitamin E,[4] and increased glutathione appear to reduce or halt the production of lipofuscin.
The nootropic drug piracetam appears to significantly reduce accumulation of lipofuscin in the brain tissue of rats.[18]
Other possible treatments:
• Centrophenoxine[19]
• Acetyl-L-carnitine[20]
• Ginkgo biloba[21]
• Dimethylethanolamine [22]
• Curcumin[23]
Wet macular degeneration can be treated using selective photothermolysis where a pulsed unfocused laser predominantly heats and kills lipofuscin-rich cells, leaving untouched healthy cells to multiply and fill in the gaps.[citation needed] The technique is also used as a skin treatment to remove tattoos, liverspots, and in general make skin appear younger. This ability to selectively target lipofuscin has opened up research opportunities in the field of anti-aging medicine.
Soraprazan (remofuscin) has been found to remove lipofuscin from retinal pigment epithelial cells in animals.[24] This opens up a new therapy option for the treatment of dry age-related macular degeneration and Stargardt disease, for which there is currently no treatment. The drug has now been granted orphan drug designation for the treatment of Stargardt disease by the European Medicines Agency.[25]
Akathisia is estimated to affect approximately 15%–35% of people who use antipsychotic medications.2
…
The goal of antipsychotic medications is to help control mental disorders like schizophrenia.4 While these medications work well in treating mental disorders, many are avoided because they can cause severe side effects. Extrapyramidal symptoms [EPS] develop when dopamine is suppressed, which is what antipsychotic medications do.1
Extrapyramidal symptoms can appear with other conditions, like Parkinson's disease, but tardive dyskinesia is specific to the use of antipsychotics.1
Tardive dyskinesia develops within the first year in 6% to 12% of people who take even low-dose antipsychotics.1 Age can impact the likelihood of developing TD, with 25% to 45% of people over age 45 developing TD after a year of treatment.
Beyond antipsychotics, several other medications have also been linked to tardive dyskinesia. These include:2
Antidepressants, such as Prozac (fluoxetine) and Desyrel (trazodone)
Anti-epileptic drugs (AEDs), such as Dilantin (phenytoin) and Tegretol (carbamazepine)
Anticholinergics, such as Cogentin (benztropine)
Antiemetics (anti-nausea medications), such as Reglan (metoclopramide) and Compazine (prochlorperazine)
Patient Rights
Many people who are prescribed antipsychotics have conditions like schizophrenia or dementia. Since these conditions can impair your ability to make decisions, concerns have been raised about the forceful administration of these medications.
The sedating nature of these medications and the risk of side effects have led to the creation of legal protections for people who are prescribed antipsychotics. Specifics vary by state, but in most cases—outside of a medical emergency—people have the right to refuse psychiatric treatment, including the use of antipsychotic medications.
Recap
Remember, you have the right to refuse medications, especially ones that are sedating.
Schizophrenia and other conditions that present with psychotic episodes can be difficult to manage, but for many people with these conditions, the medications used to treat them are even harder to bear. More than 20 years of studies revealed that up to 50% of people who take antipsychotic medications don't take them as they should, largely because of the negative side effects they produce.6
Up to half of people with tardive dyskinesia may experience worsening symptoms when stopping medications, although many see improvement over time. In some cases, symptoms are permanent. Arguments can be made both for maintaining and stopping antipsychotic use for tardive dyskinesia because stopping may or may not result in improvement. Stopping antipsychotics, on the other hand, can lead to increases in the psychotic symptoms the medications are prescribed to treat in the first place.1
Wait a second.
So, antipsychotic drugs suppress dopamine. Which would mean that in schizophrenia, dopamine is too high. Why? Low methylation?? !!
COMT DEFECT?? !!
Antipsychotics might work by blocking the effects of the overactivity of a brain chemical called dopamine. This chemical affects emotions, planning, and memory. The overactivity of dopamine is thought to contribute to psychotic symptoms.9
Why not treat COMT defect effects by supporting COMT methylation??
Treatment for schizophrenia (hallucinations and delusions—distantly caused from high dopamine), [and, off-label Alzheimer’s with aggression and agitation] then prescribed antipsychotic drugs, which commonly cause EPS (includes akathisia).
They are trying to treat the brain, and end up messing up the entire neurological system throughout the body.
Identifying and treating EPS as soon as possible is very important because these side effects can be permanent in some people.
List of drugs given for schizophrenia is alarming to me because the more common ones are given to people without schizophrenia. I know people who have been Rxd these drugs and they do not have schizophrenia, not even psychosis.
https://www.verywellhealth.com/undifferentiated-schizophrenia-5095937
They are very bad, no good drugs, and schizophrenia is nutrient deficiencies some related to gene differences probably. I have a huge series from this summer on factors that may be involved in schizophrenia and it seems like Alzheimer’s is just the next step if the underlying issue isn't treated.
How do you account for people who get Alzheimer’s but didn’t have schizophrenia symptoms during their lifetime?
😊https://twitter.com/atexan575/status/1635288095984848897?s=46&t=5tMNRPOYYDIWOC-x8zoaBQ
Thanks 😊